2,089 results on '"Murray, Melissa"'
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2. Epigenetic and genetic risk of Alzheimer disease from autopsied brains in two ethnic groups.
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Ma, Yiyi, Reyes-Dumeyer, Dolly, Piriz, Angel, Recio, Patricia, Mejia, Diones Rivera, Medrano, Martin, Lantigua, Rafael A, Vonsattel, Jean Paul G, Tosto, Giuseppe, Teich, Andrew F, Ciener, Benjamin, Leskinen, Sandra, Sivakumar, Sharanya, DeTure, Michael, Ranjan, Duara, Dickson, Dennis, Murray, Melissa, Lee, Edward, Wolk, David A, Jin, Lee-Way, Dugger, Brittany N, Hiniker, Annie, Rissman, Robert A, Mayeux, Richard, and Vardarajan, Badri N
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Biomedical and Clinical Sciences ,Neurosciences ,Acquired Cognitive Impairment ,Neurodegenerative ,Alzheimer's Disease ,Human Genome ,Genetics ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Dementia ,Aging ,Brain Disorders ,Clinical Research ,Prevention ,2.1 Biological and endogenous factors ,Neurological ,Humans ,Alzheimer Disease ,Female ,Male ,Epigenesis ,Genetic ,Aged ,White People ,Genetic Predisposition to Disease ,Brain ,Polymorphism ,Single Nucleotide ,Hispanic or Latino ,Aged ,80 and over ,Genome-Wide Association Study ,DNA Methylation ,Autopsy ,Caribbean Region ,Alzheimer's disease ,Epigenetics ,Hispanics ,Non-Hispanic Whites ,CpG-related single nucleotide polymorphism ,Alzheimer’s disease ,Clinical Sciences ,Neurology & Neurosurgery - Abstract
Genetic variants and epigenetic features both contribute to the risk of Alzheimer's disease (AD). We studied the AD association of CpG-related single nucleotide polymorphisms (CGS), which act as a hub of both the genetic and epigenetic effects, in Caribbean Hispanics (CH) and generalized the findings to Non-Hispanic Whites (NHW). First, we conducted a genome-wide, sliding-window-based association with AD, in 7,155 CH and 1,283 NHW participants. Next, using data from the dorsolateral prefrontal cortex in 179 CH brains, we tested the cis- and trans-effects of AD-associated CGS on brain DNA methylation to mRNA expression. For the genes with significant cis- and trans-effects, we investigated their enriched pathways. We identified six genetic loci in CH with CGS dosage associated with AD at genome-wide significance levels: ADAM20 (Score = 55.19, P = 4.06 × 10-8), the intergenic region between VRTN and SYNDIG1L (Score = - 37.67, P = 2.25 × 10-9), SPG7 (16q24.3) (Score = 40.51, P = 2.23 × 10-8), PVRL2 (Score = 125.86, P = 1.64 × 10-9), TOMM40 (Score = - 18.58, P = 4.61 × 10-8), and APOE (Score = 75.12, P = 7.26 × 10-26). CGSes in PVRL2 and APOE were also significant in NHW. Except for ADAM20, CGSes in the other five loci were associated with CH brain methylation levels (mQTLs) and CGSes in SPG7, PVRL2, and APOE were also mQTLs in NHW. Except for SYNDIG1L (P = 0.08), brain methylation levels in the other five loci affected downstream mRNA expression in CH (P
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- 2024
3. Biomarker-based staging of Alzheimer disease: rationale and clinical applications
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Therriault, Joseph, Schindler, Suzanne E., Salvadó, Gemma, Pascoal, Tharick A., Benedet, Andréa Lessa, Ashton, Nicholas J., Karikari, Thomas K., Apostolova, Liana, Murray, Melissa E., Verberk, Inge, Vogel, Jacob W., La Joie, Renaud, Gauthier, Serge, Teunissen, Charlotte, Rabinovici, Gil D., Zetterberg, Henrik, Bateman, Randall J., Scheltens, Philip, Blennow, Kaj, Sperling, Reisa, Hansson, Oskar, Jack, Jr, Clifford R., and Rosa-Neto, Pedro
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- 2024
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4. 49. Dobbs, Democracy, and Distortion
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Murray, Melissa, primary
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- 2024
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5. STARE DECISIS AND REMEDY
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Murray, Melissa
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Religious Right (American politics) -- Remedies -- Laws, regulations and rules ,Minorities -- Remedies -- Laws, regulations and rules ,Whites -- Remedies -- Laws, regulations and rules ,Reverse discrimination -- Remedies -- Laws, regulations and rules ,Working class in television -- Remedies -- Laws, regulations and rules ,Working class -- Remedies -- Laws, regulations and rules ,Proletariat -- Remedies -- Laws, regulations and rules ,Stare decisis -- Analysis ,Race discrimination -- Remedies -- Laws, regulations and rules ,Government regulation ,Law - Abstract
Much ink has been spilled on the Roberts Court's approach to stare decisis and precedent. Such commentary is hardly surprising. In just the last five years, the Court has overruled extant precedents on issues that range from abortion and jury convictions to property rights and public unions. It has also substantially narrowed and limited existing precedents, curbing the reach of earlier decisions in ways that disrupt and distort the jurisprudential landscape. Some view the Court's uneven approach to precedent as ideologically determined. As these critics maintain, the Court adheres to precedents that are consistent with the views of its six-member conservative supermajority while jettisoning or narrowing those precedents that do not accord with those ideological priors. This Essay takes a different tack. Specifically, it argues for reading the Roberts Court's approach to precedent and stare decisis through the lens of remedy. That is, the Court's treatment of precedent might be understood, whether in whole or in part, as animated by a desire to rectify an earlier error or injustice. To be sure, this impulse is not merely corrective--the Court's approach to stare decisis goes beyond correcting what it views as jurisprudential errors. Instead, the Court's approach seems marked by an interest in identifying and righting a past wrong. Recent cases like Dobbs v. Jackson Women's Health Organization, New York State Rifle & Pistol Association, Inc. v. Bruen, and Ramos v. Louisiana accord with this interpretive frame. In these cases, the Court departed from--or overruled--earlier decisions in part to remedy past racial injustices. Likewise, in Students for Fair Admissions, Inc. v. President & Fellows of Harvard College, the Court dismissed the extant precedent upholding the limited use of race-conscious admissions policies on the view that '[e]liminating racial discrimination means eliminating all of it.' Viewing the Roberts Court's approach to stare decisis through a remedial lens is clarifying. It helps us to understand--and better anticipate--the Court's treatment of earlier decisions. Understanding the Court's approach to stare decisis as a form of remedy renders more legible the Court's conception of legal injuries--and, in particular, racialized injuries. As this Essay explains, the Roberts Court's remedial approach to stare decisis is often deployed to correct what a majority of the Court views as a racial injustice. In some cases, like Ramos v. Louisiana, this remedial impulse focuses on correcting historic injustices wrought by white supremacy and historic acts of racism. But critically, a remedial lens may also render visible a reparative logic that unites a series of recent cases involving religious freedom, gun rights, and affirmative action. Although these cases focus on distinct doctrinal questions, they share a unifying impulse: the Court's apparent desire to remedy injuries done to Christian conservatives, working-class whites, and, more generally, white people. In this regard, viewing the Court's decisions through a remedial lens may provide a more coherent account--across legal doctrines--of the Roberts Court's understanding of discrimination, the injuries it produces, and its apparent victims., TABLE OF CONTENTS Introduction 1503 I. Stare Decisis--In Principle 1507 II. Stare Decisis and the Roberts Court 1511 III. Stare Decisis and Remedy 1517 A. Remedial Stare Decisis in Theory [...]
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- 2024
6. Synthesis and preliminary evaluation of novel PET probes for GSK-3 imaging
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Gundam, Surendra Reddy, Bansal, Aditya, Kethamreddy, Manasa, Ghatamaneni, Sujala, Lowe, Val J., Murray, Melissa E., and Pandey, Mukesh K.
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- 2024
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7. Gliovascular transcriptional perturbations in Alzheimer’s disease reveal molecular mechanisms of blood brain barrier dysfunction
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İş, Özkan, Wang, Xue, Reddy, Joseph S., Min, Yuhao, Yilmaz, Elanur, Bhattarai, Prabesh, Patel, Tulsi, Bergman, Jeremiah, Quicksall, Zachary, Heckman, Michael G., Tutor-New, Frederick Q., Can Demirdogen, Birsen, White, Launia, Koga, Shunsuke, Krause, Vincent, Inoue, Yasuteru, Kanekiyo, Takahisa, Cosacak, Mehmet Ilyas, Nelson, Nastasia, Lee, Annie J., Vardarajan, Badri, Mayeux, Richard, Kouri, Naomi, Deniz, Kaancan, Carnwath, Troy, Oatman, Stephanie R., Lewis-Tuffin, Laura J., Nguyen, Thuy, Carrasquillo, Minerva M., Graff-Radford, Jonathan, Petersen, Ronald C., Jr Jack, Clifford R., Kantarci, Kejal, Murray, Melissa E., Nho, Kwangsik, Saykin, Andrew J., Dickson, Dennis W., Kizil, Caghan, Allen, Mariet, and Ertekin-Taner, Nilüfer
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- 2024
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8. Impact of APOE on amyloid and tau accumulation in argyrophilic grain disease and Alzheimer’s disease
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Raulin, Ana-Caroline, Doss, Sydney V., Heckman, Michael G., Craver, Emily C., Li, Zonghua, Ikezu, Tadafumi C., Sekiya, Hiroaki, Liu, Chia-Chen, Martens, Yuka A., Rosenberg, Cassandra L., Kuchenbecker, Lindsey A., DeTure, Michael, Reichard, R. Ross, Nguyen, Aivi T., Constantopoulos, Eleni, Larsen, Rachel A., Kounaves, Emmaline K., Murray, Melissa E., Dickson, Dennis W., Petersen, Ronald C., Bu, Guojun, and Kanekiyo, Takahisa
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- 2024
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9. Role of GBA variants in Lewy body disease neuropathology
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Walton, Ronald L., Koga, Shunsuke, Beasley, Alexandra I., White, Launia J., Griesacker, Teresa, Murray, Melissa E., Kasanuki, Koji, Hou, Xu, Fiesel, Fabienne C., Springer, Wolfdieter, Uitti, Ryan J., Fields, Julie A., Botha, Hugo, Ramanan, Vijay K., Kantarci, Kejal, Lowe, Val J., Jack, Clifford R., Ertekin-Taner, Nilufer, Savica, Rodolfo, Graff-Radford, Jonathan, Petersen, Ronald C., Parisi, Joseph E., Reichard, R. Ross, Graff-Radford, Neill R., Ferman, Tanis J., Boeve, Bradley F., Wszolek, Zbigniew K., Dickson, Dennis W., Ross, Owen A., and Heckman, Michael G.
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- 2024
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10. Dobbs, Democracy, and Distortion
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LITTLEJOHN, KRYSTALE E., primary and MURRAY, MELISSA, additional
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- 2024
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11. Pandemics, Privatization, and Public Education
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Murray, Melissa, primary and Millat, Caitlin, additional
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- 2024
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12. DOBBS AND DEMOCRACY
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Murray, Melissa and Shaw, Katherine
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Supreme Court justices -- Political activity ,Affirmative action -- Laws, regulations and rules ,Sex discrimination -- Laws, regulations and rules ,Voter turnout -- Demographic aspects ,Political questions and judicial power -- Analysis ,Stare decisis -- Analysis ,Abortion -- Access control -- Political aspects -- Laws, regulations and rules ,Deliberative democracy -- Analysis ,Political participation -- Demographic aspects ,Government regulation ,Law ,Dobbs v. Jackson Women's Health Organization (142 S. Ct. 2228 (2022)) ,Planned Parenthood v. Casey (505 U.S. 833 (1992)) ,Roe v. Wade (410 U.S. 113 (1973)) - Abstract
In Dobbs v. Jackson Women's Health Organization, Justice Alito justified the decision to overrule Roe v. Wade and Planned Parenthood of Southeastern Pennsylvania v. Casey with an appeal to democracy. He insisted that it was 'time to heed the Constitution and return the issue of abortion to the people's elected representatives.' This invocation of democracy had undeniable rhetorical power: it allowed the Dobbs majority to lay waste to decades' worth of precedent, while rebutting charges of judicial imperialism and purporting to restore the people's voices. This Article interrogates Dobbs's claim to vindicate principles of democracy, examining both the intellectual pedigree of this claim and its substantive vision of democracy. In grounding its decision in democracy, the Dobbs majority relied on a well-worn but dubious narrative: that Roe, and later Casey, disrupted ongoing democratic deliberation on the abortion issue, wresting this contested question from the people and imposing the Court's own will. The majority insisted that this critique had always attended Roe. However, in tracing the provenance of the democratic deliberation argument, this Article finds more complicated intellectual origins. In fact, the argument did not surface in Roe's immediate aftermath, but rather emerged years later. And it did so not organically, but through a series of interconnected legal, movement, and political efforts designed to undermine and ultimately topple Roe and Casey. The product of these efforts, the Dobbs majority's claim that democracy demanded overruling Roe and Casey, was deployed to overcome the force of stare decisis in Dobbs--and may ultimately reshape the scope and substance of the Court's stare decisis analysis in future cases. Having identified the intellectual origins of the democratic deliberation argument and its contemporary consequences, this Article examines the contours of the Dobbs majority's vision of democratic deliberation. We show that although Dobbs trafficked in the rhetoric of democracy, its conception of democracy was both internally inconsistent and extraordinarily limited, even myopic. The opinion misapprehended the processes and institutions that are constitutive of democracy, focusing on state legislatures while overlooking a range of other federal, state, and local constitutional actors. As troublingly, it reflected a distorted understanding of political power and representation-- one that makes political power reducible to voting, entirely overlooking metrics like representation in electoral office and in the ecosystem of campaign finance. The opinion was also willfully blind to the antidemocratic implications of its 'history and tradition' interpretive method, which binds the recognition of constitutional rights to a past in which very few Americans were meaningful participants in the production of law and legal meaning. The deficits of the Dobbs majority's conception of democracy appear even more pronounced when considered alongside the Court's recent and active interventions to distort and disrupt the functioning of the electoral process. Indeed, Dobbs purported to 'return' the abortion question to the people and to democratic deliberation at the precise moment when the Court's own actions have ensured that the extant system is unlikely either to produce genuine deliberation or to yield widely desired outcomes. Ultimately, a close examination of the Dobbs majority's invocation of democracy suggests that the majority may have employed the values and vernacular of democracy as a means to a different end. As we explain, the majority's embrace of democracy and democratic deliberation allowed it to shield its actions from claims of judicial activism and overreach. More profoundly, and perhaps paradoxically, the opinion may lay the groundwork for the eventual vindication and protection of particular minority interests--those of the fetus. With this in mind, the Dobbs majority's settlement of the abortion question is unlikely to be a lasting one. Indeed, aspects of the opinion suggest that this settlement is merely a way station en route to a more permanent resolution--the recognition of fetal personhood and the total abolition of legal abortion in the United States., CONTENTS INTRODUCTION I. THE EVOLUTION OF AN ARGUMENT A. Roe's Immediate Aftermath B. The Emergence of the Democratic Deliberation Argument II. DEMOCRACY AND STARE DECISIS A. A New Stare Decisis [...]
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- 2024
13. The status of digital pathology and associated infrastructure within Alzheimer’s Disease Centers
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Scalco, Rebeca, Hamsafar, Yamah, White, Charles L, Schneider, Julie A, Reichard, Robert Ross, Prokop, Stefan, Perrin, Richard J, Nelson, Peter T, Mooney, Sean, Lieberman, Andrew P, Kukull, Walter A, Kofler, Julia, Keene, Christopher Dirk, Kapasi, Alifiya, Irwin, David J, Gutman, David A, Flanagan, Margaret E, Crary, John F, Chan, Kwun C, Murray, Melissa E, and Dugger, Brittany N
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Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Neurodegenerative ,Alzheimer's Disease ,Aging ,Acquired Cognitive Impairment ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Dementia ,Brain Disorders ,Industry ,Innovation and Infrastructure ,Humans ,Alzheimer Disease ,Workflow ,Machine Learning ,Surveys and Questionnaires ,Alzheimer disease ,Computational pathology ,Deep Learning ,Digital pathology ,Quantitative pathology ,Slide scanner ,Neurology & Neurosurgery ,Clinical sciences - Abstract
Digital pathology (DP) has transformative potential, especially for Alzheimer disease and related disorders. However, infrastructure barriers may limit adoption. To provide benchmarks and insights into implementation barriers, a survey was conducted in 2019 within National Institutes of Health's Alzheimer's Disease Centers (ADCs). Questions covered infrastructure, funding sources, and data management related to digital pathology. Of the 35 ADCs to which the survey was sent, 33 responded. Most respondents (81%) stated that their ADC had digital slide scanner access, with the most frequent brand being Aperio/Leica (62.9%). Approximately a third of respondents stated there were fees to utilize the scanner. For DP and machine learning (ML) resources, 41% of respondents stated none was supported by their ADC. For scanner purchasing and operations, 50% of respondents stated they received institutional support. Some were unsure of the file size of scanned digital images (37%) and total amount of storage space files occupied (50%). Most (76%) were aware of other departments at their institution working with ML; a similar (76%) percentage were unaware of multiuniversity or industry partnerships. These results demonstrate many ADCs have access to a digital slide scanner; additional investigations are needed to further understand hurdles to implement DP and ML workflows.
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- 2023
14. LATE-NC staging in routine neuropathologic diagnosis: an update
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Nelson, Peter T, Lee, Edward B, Cykowski, Matthew D, Alafuzoff, Irina, Arfanakis, Konstantinos, Attems, Johannes, Brayne, Carol, Corrada, Maria M, Dugger, Brittany N, Flanagan, Margaret E, Ghetti, Bernardino, Grinberg, Lea T, Grossman, Murray, Grothe, Michel J, Halliday, Glenda M, Hasegawa, Masato, Hokkanen, Suvi RK, Hunter, Sally, Jellinger, Kurt, Kawas, Claudia H, Keene, C Dirk, Kouri, Naomi, Kovacs, Gabor G, Leverenz, James B, Latimer, Caitlin S, Mackenzie, Ian R, Mao, Qinwen, McAleese, Kirsty E, Merrick, Richard, Montine, Thomas J, Murray, Melissa E, Myllykangas, Liisa, Nag, Sukriti, Neltner, Janna H, Newell, Kathy L, Rissman, Robert A, Saito, Yuko, Sajjadi, S Ahmad, Schwetye, Katherine E, Teich, Andrew F, Thal, Dietmar R, Tomé, Sandra O, Troncoso, Juan C, Wang, Shih-Hsiu J, White, Charles L, Wisniewski, Thomas, Yang, Hyun-Sik, Schneider, Julie A, Dickson, Dennis W, and Neumann, Manuela
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Biomedical and Clinical Sciences ,Clinical Sciences ,Neurosciences ,Genetics ,Acquired Cognitive Impairment ,Neurodegenerative ,Brain Disorders ,Dementia ,Rare Diseases ,Neurological ,Humans ,Alzheimer Disease ,Frontotemporal Dementia ,Amyotrophic Lateral Sclerosis ,DNA-Binding Proteins ,Processes ,NCI ,TDP-43 ,FTD ,Stages ,Hippocampal sclerosis ,Neuroanatomy ,Aging ,Neurology & Neurosurgery - Abstract
An international consensus report in 2019 recommended a classification system for limbic-predominant age-related TDP-43 encephalopathy neuropathologic changes (LATE-NC). The suggested neuropathologic staging system and nomenclature have proven useful for autopsy practice and dementia research. However, some issues remain unresolved, such as cases with unusual features that do not fit with current diagnostic categories. The goal of this report is to update the neuropathologic criteria for the diagnosis and staging of LATE-NC, based primarily on published data. We provide practical suggestions about how to integrate available genetic information and comorbid pathologies [e.g., Alzheimer's disease neuropathologic changes (ADNC) and Lewy body disease]. We also describe recent research findings that have enabled more precise guidance on how to differentiate LATE-NC from other subtypes of TDP-43 pathology [e.g., frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS)], and how to render diagnoses in unusual situations in which TDP-43 pathology does not follow the staging scheme proposed in 2019. Specific recommendations are also made on when not to apply this diagnostic term based on current knowledge. Neuroanatomical regions of interest in LATE-NC are described in detail and the implications for TDP-43 immunohistochemical results are specified more precisely. We also highlight questions that remain unresolved and areas needing additional study. In summary, the current work lays out a number of recommendations to improve the precision of LATE-NC staging based on published reports and diagnostic experience.
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- 2023
15. Demographic, clinical, biomarker, and neuropathological correlates of posterior cortical atrophy: an international cohort study and individual participant data meta-analysis
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Abdi, Zeinab, Agosta, Federica, Ahmed, Samrah, Alcolea, Daniel, Allen, Isabel Elaine, Allinson, Kieren S.J., Apostolova, Liana G., Arighi, Andrea, Balasa, Mircea, Barkhof, Frederik, Best, John, Boon, Baayla D., Brandt, Katherine D., Brosch, Jared, Burrell, James, Butler, Christopher R., Calandri, Ismael, Caminiti, Silvia Paola, Canu, Elisa, Carrillo, Maria C., Caso, Francesca, Chapleau, Marianne, Chrem Mendez, Patricio, Chu, Min, Crutch, Sebastian, Cordato, Nicholas, Costa, Ana Sofia, Cui, Yue, Dickerson, Bradford, Dickson, Dennis W., Duara, Ranjan, Dubois, Bruno, Eldaief, Mark, Farlow, Martin, Fenoglio, Chiara, Filippi, Massimo, Fliessbach, Klaus, Formaglio, Maïté, Fortea, Juan, Fox, Nick, Foxe, David, Tilikete, Caroline Froment, Frosch, Matthew P., Fumagalli, Giorgio Giulio, Galasko, Douglas, Galimberti, Daniela, Garat, Oscar, Giardinieri, Giulia, Graff-Radford, Jonathan, Graff-Radford, Neill R., Grinberg, Lea, Groot, Colin, Hake, Ann Marie, Hansson, Oskar, Headley, Alison, Hernandez, Micaela, Hochberg, Daisy, Hodges, John R., Hof, Patrick R., Holton, Janice, Hromas, Gabrielle, Gala, Ignacio Illán, Irwin, David J., Jaunmuktane, Zane, Jing, Donglai, Josephs, Keith, Kagerer, Sonja M., Kasuga, Kensaku, Kong, Yu, Kövari, Enikö, Lacombe-Thibault, Mégane, Lleó, Alberto, Laforce, Robert, La Joie, Renaud, Lashley, Tammaryn, Leger, Gabriel, Levin, Netta, Levy, Richard, Liu, Yang, Liu, Li, Lladó Plarrumaní, Albert, Lucente, Diane E., Machulda, Mary M., Magnani, Giuseppe, Magnin, Eloi, Malpetti, Maura, Matthews, Brandy, McGinnis, Scott, Mendez, Mario F., Mesulam, Marsel, Migliaccio, Raffaella, Miklitz, Carolin, Miller, Zachary A., Montembeault, Maxime, Murray, Melissa E., Mundada, Nidhi, Nemes, Sara, Nestor, Peter J., Ocal, Dilek, Ossenkoppele, Rik, Paterson, Ross, Pelak, Victoria, Perani, Daniela, Phillips, Jeffrey, Piguet, Olivier, Pijnenburg, Yolande, Putcha, Deepti, Quimby, Megan, Rabinovici, Gil D., Reetz, Kathrin, Rein, Netaniel, Revesz, Tamas, Rezaii, Neguine, Rodriguez-Porcel, Federico, Rogalski, Emily, Rowe, James B., Ryan, Natalie, Sanchez-Valle, Raquel, Sacchi, Luca, Santos-Santos, Miguel Ángel, Schott, Jonathan M., Seeley, William, Sherman, Janet, Spina, Salvatore, Stomrud, Erik, Sullivan, A. Campbell, Tanner, Jeremy, Tideman, Pontus, Tokutake, Takayoshi, Tondo, Giacomo, Touroutoglou, Alexandra, Tousi, Babak, Vandenberghe, Rik, van der Flier, Wiesje, Walker, Jamie M., Weintraub, Sandra, Whitwell, Jennifer L., Wolk, David A., Wong, Bonnie, Wu, Liyong, Xie, Kexin, Yong, Keir, Apostolova, Liana, Boon, Baayla D C, Grinberg, Lea T, Irwin, David J, Josephs, Keith A, Mendez, Mario F, Mendez, Patricio Chrem, Miller, Zachary A, Murray, Melissa E, Nemes, Sára, Schott, Jonathan M, Sullivan, A Campbell, Walker, Jamie, Whitwell, Jennifer L, Wolk, David A, and Rabinovici, Gil D
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- 2024
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16. Differential Vulnerability of Hippocampal Subfields in Primary Age-Related Tauopathy and Chronic Traumatic Encephalopathy.
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Farrell, Kurt, Iida, Megan A, Cherry, Jonathan D, Casella, Alicia, Stein, Thor D, Bieniek, Kevin F, Walker, Jamie M, Richardson, Timothy E, White, Charles L, Alvarez, Victor E, Huber, Bertrand R, Dickson, Dennis W, Insausti, Ricardo, Dams-O'Connor, Kristen, Vonsattel, Jean-Paul, Teich, Andy F, Gearing, Marla, Glass, Jonathan, Troncoso, Juan C, Frosch, Matthew P, Hyman, Bradley T, Murray, Melissa E, Attems, Johannes, Flanagan, Margaret E, Mao, Qinwen, Mesulam, M-Marsel, Weintraub, Sandra, Woltjer, Randy L, Pham, Thao, Kofler, Julia, Schneider, Julie A, Yu, Lei, Purohit, Dushyant P, Haroutunian, Vahram, Hof, Patrick R, Gandy, Sam, Sano, Mary, Beach, Thomas G, Poon, Wayne, Kawas, Claudia H, Corrada, María M, Rissman, Robert A, Metcalf, Jeff, Shuldberg, Sara, Salehi, Bahar, Nelson, Peter T, Trojanowski, John Q, Lee, Edward B, Wolk, David A, McMillan, Corey T, Keene, C Dirk, Latimer, Caitlin S, Montine, Thomas J, Kovacs, Gabor G, Lutz, Mirjam I, Fischer, Peter, Perrin, Richard J, Cairns, Nigel J, McKee, Ann C, and Crary, John F
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Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Frontotemporal Dementia (FTD) ,Acquired Cognitive Impairment ,Aging ,Brain Disorders ,Dementia ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Alzheimer's Disease ,Neurodegenerative ,Aetiology ,2.1 Biological and endogenous factors ,Chronic Traumatic Encephalopathy ,Hippocampus ,Humans ,Neurofibrillary Tangles ,Tauopathies ,tau Proteins ,Chronic traumatic encephalopathy ,Primary age-related tauopathy ,Repetitive head impacts ,Tauopathy ,Part Working Group ,Neurology & Neurosurgery ,Clinical sciences - Abstract
Chronic traumatic encephalopathy (CTE) is a tauopathy associated with repetitive mild head impacts characterized by perivascular hyperphosphorylated tau (p-tau) in neurofibrillary tangles (NFTs) and neurites in the depths of the neocortical sulci. In moderate to advanced CTE, NFTs accumulate in the hippocampus, potentially overlapping neuroanatomically with primary age-related tauopathy (PART), an age-related tauopathy characterized by Alzheimer disease-like tau pathology in the hippocampus devoid of amyloid plaques. We measured p-tau burden using positive-pixel counts on immunohistochemically stained and neuroanatomically segmented hippocampal tissue. Subjects with CTE had a higher total p-tau burden than PART subjects in all sectors (p = 0.005). Within groups, PART had significantly higher total p-tau burden in CA1/subiculum compared to CA3 (p = 0.02) and CA4 (p = 0.01) and total p-tau burden in CA2 trended higher than CA4 (p = 0.06). In CTE, total p-tau burden in CA1/subiculum was significantly higher than in the dentate gyrus; and CA2 also trended higher than dentate gyrus (p = 0.01, p = 0.06). When controlling for p-tau burden across the entire hippocampus, CA3 and CA4 had significantly higher p-tau burden in CTE than PART (p
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- 2022
17. Frequency of LATE neuropathologic change across the spectrum of Alzheimer’s disease neuropathology: combined data from 13 community-based or population-based autopsy cohorts
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Nelson, Peter T, Brayne, Carol, Flanagan, Margaret E, Abner, Erin L, Agrawal, Sonal, Attems, Johannes, Castellani, Rudolph J, Corrada, Maria M, Cykowski, Matthew D, Di, Jing, Dickson, Dennis W, Dugger, Brittany N, Ervin, John F, Fleming, Jane, Graff-Radford, Jonathan, Grinberg, Lea T, Hokkanen, Suvi RK, Hunter, Sally, Kapasi, Alifiya, Kawas, Claudia H, Keage, Hannah AD, Keene, C Dirk, Kero, Mia, Knopman, David S, Kouri, Naomi, Kovacs, Gabor G, Labuzan, Sydney A, Larson, Eric B, Latimer, Caitlin S, Leite, Renata EP, Matchett, Billie J, Matthews, Fiona E, Merrick, Richard, Montine, Thomas J, Murray, Melissa E, Myllykangas, Liisa, Nag, Sukriti, Nelson, Ruth S, Neltner, Janna H, Nguyen, Aivi T, Petersen, Ronald C, Polvikoski, Tuomo, Reichard, R Ross, Rodriguez, Roberta D, Suemoto, Claudia K, Wang, Shih-Hsiu J, Wharton, Stephen B, White, Lon, and Schneider, Julie A
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Biomedical and Clinical Sciences ,Neurosciences ,Clinical Research ,Alzheimer's Disease ,Acquired Cognitive Impairment ,Aging ,Brain Disorders ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Neurodegenerative ,Alzheimer's Disease Related Dementias (ADRD) ,Dementia ,Behavioral and Social Science ,2.1 Biological and endogenous factors ,Aetiology ,Neurological ,Aged ,80 and over ,Alzheimer Disease ,Amyloid ,Autopsy ,DNA-Binding Proteins ,Frontotemporal Dementia ,Humans ,Male ,Nervous System Diseases ,Plaque ,Amyloid ,ADRD ,Tau ,NFT ,Nondemented ,Oldest-old ,Epidemiology ,APOE ,ROS-MAP ,Vantaa 85+ ,HAAS ,CFAS ,CC75C ,The 90+study ,ACT ,VITA ,Nun study ,Biobank for aging studies ,Mayo clinic study of aging ,The 90 + study ,Vantaa 85 + ,Clinical Sciences ,Neurology & Neurosurgery - Abstract
Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) and Alzheimer's disease neuropathologic change (ADNC) are each associated with substantial cognitive impairment in aging populations. However, the prevalence of LATE-NC across the full range of ADNC remains uncertain. To address this knowledge gap, neuropathologic, genetic, and clinical data were compiled from 13 high-quality community- and population-based longitudinal studies. Participants were recruited from United States (8 cohorts, including one focusing on Japanese-American men), United Kingdom (2 cohorts), Brazil, Austria, and Finland. The total number of participants included was 6196, and the average age of death was 88.1 years. Not all data were available on each individual and there were differences between the cohorts in study designs and the amount of missing data. Among those with known cognitive status before death (n = 5665), 43.0% were cognitively normal, 14.9% had MCI, and 42.4% had dementia-broadly consistent with epidemiologic data in this age group. Approximately 99% of participants (n = 6125) had available CERAD neuritic amyloid plaque score data. In this subsample, 39.4% had autopsy-confirmed LATE-NC of any stage. Among brains with "frequent" neuritic amyloid plaques, 54.9% had comorbid LATE-NC, whereas in brains with no detected neuritic amyloid plaques, 27.0% had LATE-NC. Data on LATE-NC stages were available for 3803 participants, of which 25% had LATE-NC stage > 1 (associated with cognitive impairment). In the subset of individuals with Thal Aβ phase = 0 (lacking detectable Aβ plaques), the brains with LATE-NC had relatively more severe primary age-related tauopathy (PART). A total of 3267 participants had available clinical data relevant to frontotemporal dementia (FTD), and none were given the clinical diagnosis of definite FTD nor the pathological diagnosis of frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). In the 10 cohorts with detailed neurocognitive assessments proximal to death, cognition tended to be worse with LATE-NC across the full spectrum of ADNC severity. This study provided a credible estimate of the current prevalence of LATE-NC in advanced age. LATE-NC was seen in almost 40% of participants and often, but not always, coexisted with Alzheimer's disease neuropathology.
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- 2022
18. Plasma biomarkers for prediction of Alzheimer’s disease neuropathologic change
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Bermudez, Camilo, Graff-Radford, Jonathan, Syrjanen, Jeremy A., Stricker, Nikki H., Algeciras-Schimnich, Alicia, Kouri, Naomi, Kremers, Walter K., Petersen, Ronald C., Jack, Jr, Clifford R., Knopman, David S., Dickson, Dennis W., Nguyen, Aivi T., Reichard, R. Ross, Murray, Melissa E., Mielke, Michelle M., and Vemuri, Prashanthi
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- 2023
- Full Text
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19. MAPT H2 haplotype and risk of Pick's disease in the Pick's disease International Consortium: a genetic association study
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Warner, Thomas T, Jaunmuktane, Zane, Boeve, Bradley F, Duara, Ranjan, Graff-Radford, Neill R, Josephs, Keith A, Knopman, David S, Koga, Shunsuke, Murray, Melissa E, Lyons, Kelly E, Pahwa, Rajesh, Petersen, Ronald C, Whitwell, Jennifer L, Grinberg, Lea T, Miller, Bruce, Schlereth, Athena, Spina, Salvatore, Grossman, Murray, Irwin, David J, Suh, EunRan, Trojanowski, John Q, Van Deerlin, Vivianna M, Wolk, David A, Connors, Theresa R, Dooley, Patrick M, Oakley, Derek H, Aldecoa, Iban, Balasa, Mircea, Gelpi, Ellen, Borrego-Écija, Sergi, Gascon-Bayarri, Jordi, Sánchez-Valle, Raquel, Sanz-Cartagena, Pilar, Piñol-Ripoll, Gerard, Bigio, Eileen H, Flanagan, Margaret E, Rogalski, Emily J, Weintraub, Sandra, Schneider, Julie A, Peng, Lihua, Zhu, Xiongwei, Chang, Koping, Troncoso, Juan C, Prokop, Stefan, Newell, Kathy L, Jones, Matthew, Richardson, Anna, Roncaroli, Federico, Snowden, Julie, Allinson, Kieren, Singh, Poonam, Serrano, Geidy E, Flowers, Xena E, Goldman, James E, Heaps, Allison C, Leskinen, Sandra P, Black, Sandra E, Masellis, Mario, King, Andrew, Al-Sarraj, Safa, Troakes, Claire, Hodges, John R, Kril, Jillian J, Kwok, John B, Piguet, Olivier, Roeber, Sigrun, Attems, Johannes, Thomas, Alan J, Evers, Bret M., Bieniek, Kevin F, Sieben, Anne A, Cras, Patrick P, De Vil, Bart B, Bird, Thomas, Castellani, Rudolph J, Chaffee, Ann, Franklin, Erin, Haroutunian, Vahram, Jacobsen, Max, Keene, Dirk, Latimer, Caitlin S, Metcalf, Jeff, Perrin, Richard J, Purohit, Dushyant P, Rissman, Robert A, Schantz, Aimee, Walker, Jamie, De Deyn, Peter P, Duyckaerts, Charles, Le Ber, Isabelle, Seilhean, Danielle, Turbant-Leclere, Sabrina, Ervin, John F, Nennesmo, Inger, Riehl, James, Nacmias, Benedetta, Finger, Elizabeth C, Blauwendraat, Cornelis, Nalls, Mike A, Singleton, Andrew B, Vitale, Dan, Cunha, Cristina, Wszolek, Zbigniew K, Valentino, Rebecca R, Scotton, William J, Roemer, Shanu F, Lashley, Tammaryn, Heckman, Michael G, Shoai, Maryam, Martinez-Carrasco, Alejandro, Tamvaka, Nicole, Walton, Ronald L, Baker, Matthew C, Macpherson, Hannah L, Real, Raquel, Soto-Beasley, Alexandra I, Mok, Kin, Revesz, Tamas, Christopher, Elizabeth A, DeTure, Michael, Seeley, William W, Lee, Edward B, Frosch, Matthew P, Molina-Porcel, Laura, Gefen, Tamar, Redding-Ochoa, Javier, Ghetti, Bernardino, Robinson, Andrew C, Kobylecki, Christopher, Rowe, James B, Beach, Thomas G, Teich, Andrew F, Keith, Julia L, Bodi, Istvan, Halliday, Glenda M, Gearing, Marla, Arzberger, Thomas, Morris, Christopher M, White, Charles L, 3rd, Mechawar, Naguib, Boluda, Susana, MacKenzie, Ian R, McLean, Catriona, Cykowski, Matthew D, Wang, Shih-Hsiu J, Graff, Caroline, Nagra, Rashed M, Kovacs, Gabor G, Giaccone, Giorgio, Neumann, Manuela, Ang, Lee-Cyn, Carvalho, Agostinho, Morris, Huw R, Rademakers, Rosa, Hardy, John A, Dickson, Dennis W, Rohrer, Jonathan D, and Ross, Owen A
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- 2024
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20. Single-cell dissection of the human motor and prefrontal cortices in ALS and FTLD
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Pineda, S. Sebastian, Lee, Hyeseung, Ulloa-Navas, Maria J., Linville, Raleigh M., Garcia, Francisco J., Galani, Kyriakitsa, Engelberg-Cook, Erica, Castanedes, Monica C., Fitzwalter, Brent E., Pregent, Luc J., Gardashli, Mahammad E., DeTure, Michael, Vera-Garcia, Diana V., Hucke, Andre T.S., Oskarsson, Bjorn E., Murray, Melissa E., Dickson, Dennis W., Heiman, Myriam, Belzil, Veronique V., and Kellis, Manolis
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- 2024
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21. Genome-wide association study of brain biochemical phenotypes reveals distinct genetic architecture of Alzheimer’s disease related proteins
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Oatman, Stephanie R., Reddy, Joseph S., Quicksall, Zachary, Carrasquillo, Minerva M., Wang, Xue, Liu, Chia-Chen, Yamazaki, Yu, Nguyen, Thuy T., Malphrus, Kimberly, Heckman, Michael, Biswas, Kristi, Nho, Kwangsik, Baker, Matthew, Martens, Yuka A., Zhao, Na, Kim, Jun Pyo, Risacher, Shannon L., Rademakers, Rosa, Saykin, Andrew J., DeTure, Michael, Murray, Melissa E., Kanekiyo, Takahisa, Dickson, Dennis W., Bu, Guojun, Allen, Mariet, and Ertekin-Taner, Nilüfer
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- 2023
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22. Genome-wide association study and functional validation implicates JADE1 in tauopathy
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Farrell, Kurt, Kim, SoongHo, Han, Natalia, Iida, Megan A, Gonzalez, Elias M, Otero-Garcia, Marcos, Walker, Jamie M, Richardson, Timothy E, Renton, Alan E, Andrews, Shea J, Fulton-Howard, Brian, Humphrey, Jack, Vialle, Ricardo A, Bowles, Kathryn R, de Paiva Lopes, Katia, Whitney, Kristen, Dangoor, Diana K, Walsh, Hadley, Marcora, Edoardo, Hefti, Marco M, Casella, Alicia, Sissoko, Cheick T, Kapoor, Manav, Novikova, Gloriia, Udine, Evan, Wong, Garrett, Tang, Weijing, Bhangale, Tushar, Hunkapiller, Julie, Ayalon, Gai, Graham, Robert R, Cherry, Jonathan D, Cortes, Etty P, Borukov, Valeriy Y, McKee, Ann C, Stein, Thor D, Vonsattel, Jean-Paul, Teich, Andy F, Gearing, Marla, Glass, Jonathan, Troncoso, Juan C, Frosch, Matthew P, Hyman, Bradley T, Dickson, Dennis W, Murray, Melissa E, Attems, Johannes, Flanagan, Margaret E, Mao, Qinwen, Mesulam, M-Marsel, Weintraub, Sandra, Woltjer, Randy L, Pham, Thao, Kofler, Julia, Schneider, Julie A, Yu, Lei, Purohit, Dushyant P, Haroutunian, Vahram, Hof, Patrick R, Gandy, Sam, Sano, Mary, Beach, Thomas G, Poon, Wayne, Kawas, Claudia H, Corrada, María M, Rissman, Robert A, Metcalf, Jeff, Shuldberg, Sara, Salehi, Bahar, Nelson, Peter T, Trojanowski, John Q, Lee, Edward B, Wolk, David A, McMillan, Corey T, Keene, C Dirk, Latimer, Caitlin S, Montine, Thomas J, Kovacs, Gabor G, Lutz, Mirjam I, Fischer, Peter, Perrin, Richard J, Cairns, Nigel J, Franklin, Erin E, Cohen, Herbert T, Raj, Towfique, Cobos, Inma, Frost, Bess, Goate, Alison, White III, Charles L, and Crary, John F
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Biomedical and Clinical Sciences ,Neurosciences ,Neurodegenerative ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Brain Disorders ,Genetics ,Dementia ,Acquired Cognitive Impairment ,Frontotemporal Dementia (FTD) ,Aging ,Alzheimer's Disease ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Aged ,Aged ,80 and over ,Animals ,Cohort Studies ,Drosophila ,Female ,Genome-Wide Association Study ,Homeodomain Proteins ,Humans ,Male ,Middle Aged ,Polymorphism ,Single Nucleotide ,Tauopathies ,Tumor Suppressor Proteins ,Clinical Sciences ,Neurology & Neurosurgery - Abstract
Primary age-related tauopathy (PART) is a neurodegenerative pathology with features distinct from but also overlapping with Alzheimer disease (AD). While both exhibit Alzheimer-type temporal lobe neurofibrillary degeneration alongside amnestic cognitive impairment, PART develops independently of amyloid-β (Aβ) plaques. The pathogenesis of PART is not known, but evidence suggests an association with genes that promote tau pathology and others that protect from Aβ toxicity. Here, we performed a genetic association study in an autopsy cohort of individuals with PART (n = 647) using Braak neurofibrillary tangle stage as a quantitative trait. We found some significant associations with candidate loci associated with AD (SLC24A4, MS4A6A, HS3ST1) and progressive supranuclear palsy (MAPT and EIF2AK3). Genome-wide association analysis revealed a novel significant association with a single nucleotide polymorphism on chromosome 4 (rs56405341) in a locus containing three genes, including JADE1 which was significantly upregulated in tangle-bearing neurons by single-soma RNA-seq. Immunohistochemical studies using antisera targeting JADE1 protein revealed localization within tau aggregates in autopsy brains with four microtubule-binding domain repeats (4R) isoforms and mixed 3R/4R, but not with 3R exclusively. Co-immunoprecipitation in post-mortem human PART brain tissue revealed a specific binding of JADE1 protein to four repeat tau lacking N-terminal inserts (0N4R). Finally, knockdown of the Drosophila JADE1 homolog rhinoceros (rno) enhanced tau-induced toxicity and apoptosis in vivo in a humanized 0N4R mutant tau knock-in model, as quantified by rough eye phenotype and terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) in the fly brain. Together, these findings indicate that PART has a genetic architecture that partially overlaps with AD and other tauopathies and suggests a novel role for JADE1 as a modifier of neurofibrillary degeneration.
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- 2022
23. EDUCATION AS CHILDCARE
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Millat, Caitlin and Murray, Melissa
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Social service -- Laws, regulations and rules -- Research ,Education law -- Evaluation -- Comparative analysis -- Research ,Child welfare -- Laws, regulations and rules -- Research ,Child care -- Laws, regulations and rules -- Comparative analysis -- Research ,Duty of care (Law) -- Laws, regulations and rules -- Research ,Government regulation ,Law - Abstract
American parents have their feet in two camps: one, the vast, state-sponsored project of education, and another, the highly privatized world of childcare. Much has been made of the fact that there are few public supports for families and childcare. But what often goes unstated is that the provision of public education effectively serves as a significant 'care' subsidy. To be sure, most are loath to frame public education in this way, but as the recent COVID-19 pandemic lays bare, in fact, the provision of public education does serve as critical childcare scaffolding for families, enabling workplace participation and productivity. The crisis of caregiving that resulted when families lost access to in-person education--for many their sole state subsidy for the provision of care--revealed the ways in which education and childcare are necessary bedfellows. Although education and childcare, two sides of the childrearing coin, share deep roots in American society, they have, since the early twentieth century, been disaggregated. Though education and childcare occupy separate spheres, the pandemic has challenged us to reevaluate the ways in which education and care interact both with one another and with the state. Drawing on a history in which education and childcare were understood as unified, this Article considers how these two core aspects of childrearing might again be brought together as part of a system of public provision for families. More particularly, it suggests that the time is right to reconsider not only the role of education and childcare vis-a-vis the state, but also the ways in which education and childcare comprise dual parts of a spectrum of care., INTRODUCTION 1464 I. MAKING CARE 'PRIVATE' 1467 A. Models of Dependency 1467 B. The Family as Childcare 1469 C. Subsidizing Care and Facilitating Work 1471 1. The Founding and the [...]
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- 2023
24. The colorectal cancer patients' journey : the Auckland region
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Murray, Melissa
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- 2011
25. The Longitudinal Early‐onset Alzheimer's Disease Study (LEADS): Framework and methodology
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Apostolova, Liana G, Aisen, Paul, Eloyan, Ani, Fagan, Anne, Fargo, Keith N, Foroud, Tatiana, Gatsonis, Constantine, Grinberg, Lea T, Jack, Clifford R, Kramer, Joel, Koeppe, Robert, Kukull, Walter A, Murray, Melissa E, Nudelman, Kelly, Rumbaugh, Malia, Toga, Arthur, Vemuri, Prashanthi, Trullinger, Amy, Iaccarino, Leonardo, Day, Gregory S, Graff‐Radford, Neill R, Honig, Lawrence S, Jones, David T, Masdeu, Joseph, Mendez, Mario, Musiek, Erik, Onyike, Chiadi U, Rogalski, Emily, Salloway, Steve, Wolk, David A, Wingo, Thomas S, Carrillo, Maria C, Dickerson, Bradford C, Rabinovici, Gil D, and Consortium, the LEADS
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Biomedical and Clinical Sciences ,Clinical Sciences ,Brain Disorders ,Alzheimer's Disease ,Clinical Research ,Neurosciences ,Dementia ,Neurodegenerative ,Acquired Cognitive Impairment ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Aging ,Biomedical Imaging ,4.1 Discovery and preclinical testing of markers and technologies ,2.1 Biological and endogenous factors ,4.2 Evaluation of markers and technologies ,Detection ,screening and diagnosis ,Aetiology ,Neurological ,Alzheimer Disease ,Aniline Compounds ,Autopsy ,Biomarkers ,Brain ,Cognitive Dysfunction ,Early Diagnosis ,Female ,Humans ,Longitudinal Studies ,Magnetic Resonance Imaging ,Male ,Middle Aged ,National Institute on Aging (U.S.) ,Positron-Emission Tomography ,Stilbenes ,United States ,Alzheimer&apos ,s disease ,early‐ ,onset ,EOAD ,LEADS ,YOAD ,young onset ,LEADS Consortium ,Alzheimer's disease ,early-onset ,Geriatrics ,Clinical sciences ,Biological psychology - Abstract
Patients with early-onset Alzheimer's disease (EOAD) are commonly excluded from large-scale observational and therapeutic studies due to their young age, atypical presentation, or absence of pathogenic mutations. The goals of the Longitudinal EOAD Study (LEADS) are to (1) define the clinical, imaging, and fluid biomarker characteristics of EOAD; (2) develop sensitive cognitive and biomarker measures for future clinical and research use; and (3) establish a trial-ready network. LEADS will follow 400 amyloid beta (Aβ)-positive EOAD, 200 Aβ-negative EOnonAD that meet National Institute on Aging-Alzheimer's Association (NIA-AA) criteria for mild cognitive impairment (MCI) or AD dementia, and 100 age-matched controls. Participants will undergo clinical and cognitive assessments, magnetic resonance imaging (MRI), [18 F]Florbetaben and [18 F]Flortaucipir positron emission tomography (PET), lumbar puncture, and blood draw for DNA, RNA, plasma, serum and peripheral blood mononuclear cells, and post-mortem assessment. To develop more effective AD treatments, scientists need to understand the genetic, biological, and clinical processes involved in EOAD. LEADS will develop a public resource that will enable future planning and implementation of EOAD clinical trials.
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- 2021
26. Constitutionalizing Reproductive Rights (and Justice)
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Murray, Melissa, Meyers, Hilarie, Brake, Deborah, book editor, Chamallas, Martha, book editor, and Williams, Verna, book editor
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- 2023
- Full Text
- View/download PDF
27. Genome-wide association study and functional validation implicates JADE1 in tauopathy
- Author
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Farrell, Kurt, Kim, SoongHo, Han, Natalia, Iida, Megan A, Gonzalez, Elias, Otero-Garcia, Marcos, Walker, Jamie, Richardson, Tim, Renton, Alan E, Andrews, Shea J, Fulton-Howard, Brian, Humphrey, Jack, Vialle, Ricardo A, Bowles, Kathryn R, Whitney, Kristen, Dangoor, Diana K, Marcora, Edoardo, Hefti, Marco M, Casella, Alicia, Sissoko, Cheick, Kapoor, Manav, Novikova, Gloriia, Udine, Evan, Wong, Garrett, Tang, Weijing, Bhangale, Tushar, Hunkapiller, Julie, Ayalon, Gai, Graham, Rob, Cherry, Jonathan D, Cortes, Etty, Borukov, Valeriy, McKee, Ann C, Stein, Thor D, Vonsattel, Jean-Paul, Teich, Andy F, Gearing, Marla, Glass, Jonathan, Troncoso, Juan C, Frosch, Matthew P, Hyman, Bradley T, Dickson, Dennis W, Murray, Melissa E, Attems, Johannes, Flanagan, Margaret E, Mao, Qinwen, Mesulam, M-Marsel, Weintraub, Sandra, Woltjer, Randy, Pham, Thao, Kofler, Julia, Schneider, Julie A, Yu, Lei, Purohit, Dushyant P, Haroutunian, Vahram, Hof, Patrick R, Gandy, Sam, Sano, Mary, Beach, Thomas G, Poon, Wayne, Kawas, Claudia, Corrada, María, Rissman, Robert A, Metcalf, Jeff, Shuldberg, Sara, Salehi, Bahar, Nelson, Peter T, Trojanowski, John Q, Lee, Edward B, Wolk, David A, McMillan, Corey T, Keene, Dirk C, Montine, Thomas J, Kovacs, Gabor G, Lutz, Mirjam I, Fischer, Peter, Perrin, Richard J, Cairns, Nigel, Franklin, Erin E, Cohen, Herbert T, Sillero, Maria Inmaculada Cobos, Frost, Bess, Raj, Towfique, Goate, Alison, White, Charles L, and Crary, John F
- Subjects
Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Genetics ,Dementia ,Alzheimer's Disease ,Frontotemporal Dementia (FTD) ,Brain Disorders ,Neurosciences ,Biotechnology ,Neurodegenerative ,Aging ,Acquired Cognitive Impairment ,Aetiology ,2.1 Biological and endogenous factors ,Neurological - Abstract
AbstractPrimary age-related tauopathy (PART) is a neurodegenerative tauopathy with features distinct from but also overlapping with Alzheimer disease (AD). While both exhibit Alzheimer-type temporal lobe neurofibrillary degeneration alongside amnestic cognitive impairment, PART develops independently of amyloid-β (Aβ) deposition in plaques. The pathogenesis of PART is unknown, but evidence suggests it is associated with genes that promote tau pathology as well as others that protect from Aβ toxicity. Here, we performed a genetic association study in an autopsy cohort of individuals with PART (n=647) using Braak neurofibrillary tangle stage as a quantitative trait adjusting for sex, age, genotyping platform, and principal components. We found significant associations with some candidate loci associated with AD and progressive supranuclear palsy, a primary tauopathy (SLC24A4, MS4A6A, HS3ST1, MAPT and EIF2AK3). Genome-wide association analysis revealed a novel significant association with a single nucleotide polymorphism on chromosome 4 (rs56405341) in a locus containing three genes, including JADE1 which was significantly upregulated in tangle-bearing neurons by single-soma RNA-seq. Immunohistochemical studies using antisera targeting JADE1 protein revealed localization within tau aggregates in autopsy brain from tauopathies containing isoforms with four microtubule-binding domain repeats (4R) and mixed 3R/4R, but not with 3R exclusively. Co-immunoprecipitation revealed a direct and specific binding of JADE1 protein to tau containing four (4R) and no N-terminal inserts (0N4R) in post-mortem human PART brain tissue. Finally, knockdown of the Drosophila JADE1 homolog rhinoceros (rno) enhanced tau-induced toxicity and apoptosis in vivo in a humanized 0N4R mutant tau knock-in model as quantified by rough eye phenotype and terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) in the fly brain. Together, these findings indicate that PART has a genetic architecture that partially overlaps with AD and other tauopathies and suggests a novel role for JADE1 as a mediator of neurofibrillary degeneration.
- Published
- 2021
28. The mechanistic link between selective vulnerability of the locus coeruleus and neurodegeneration in Alzheimer’s disease
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Matchett, Billie J, Grinberg, Lea T, Theofilas, Panos, and Murray, Melissa E
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Biomedical and Clinical Sciences ,Neurosciences ,Dementia ,Acquired Cognitive Impairment ,Aging ,Brain Disorders ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Alzheimer's Disease ,Neurodegenerative ,2.1 Biological and endogenous factors ,Aetiology ,Neurological ,Alzheimer Disease ,Animals ,Humans ,Locus Coeruleus ,Nerve Degeneration ,Locus coeruleus ,Alzheimer's disease ,Tau ,Norepinephrine ,Selective vulnerability ,Alzheimer’s disease ,Clinical Sciences ,Neurology & Neurosurgery - Abstract
Alzheimer's disease (AD) is neuropathologically characterized by the intracellular accumulation of hyperphosphorylated tau and the extracellular deposition of amyloid-β plaques, which affect certain brain regions in a progressive manner. The locus coeruleus (LC), a small nucleus in the pons of the brainstem, is widely recognized as one of the earliest sites of neurofibrillary tangle formation in AD. Patients with AD exhibit significant neuronal loss in the LC, resulting in a marked reduction of its size and function. The LC, which vastly innervates several regions of the brain, is the primary source of the neurotransmitter norepinephrine (NE) in the central nervous system. Considering that NE is a major modulator of behavior, contributing to neuroprotection and suppression of neuroinflammation, degeneration of the LC in AD and the ultimate dysregulation of the LC-NE system has detrimental effects in the brain. In this review, we detail the neuroanatomy and function of the LC, its essential role in neuroprotection, and how this is dysregulated in AD. We discuss AD-related neuropathologic changes in the LC and mechanisms by which LC neurons are selectively vulnerable to insult. Further, we elucidate the neurotoxic effects of LC de-innervation both locally and at projection sites, and how this augments disease pathology, progression and severity. We summarize how preservation of the LC-NE system could be used in the treatment of AD and other neurodegenerative diseases affected by LC degeneration.
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- 2021
29. Early Selective Vulnerability of the CA2 Hippocampal Subfield in Primary Age-Related Tauopathy (vol 80, nlaa153, 2021)
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Walker, Jamie M, Richardson, Timothy E, Farrell, Kurt, Iida, Megan A, Foong, Chan, Shang, Ping, Attems, Johannes, Ayalon, Gai, Beach, Thomas G, Bigio, Eileen H, Budson, Andrew, Cairns, Nigel J, Corrada, Maria, Cortes, Etty, Dickson, Dennis W, Fischer, Peter, Flanagan, Margaret E, Franklin, Erin, Gearing, Marla, Glass, Jonathan, Hansen, Lawrence A, Haroutunian, Vahram, Hof, Patrick R, Honig, Lawrence, Kawas, Claudia, Keene, C Dirk, Kofler, Julia, Kovacs, Gabor G, Lee, Edward B, Lutz, Mirjam I, Mao, Qinwen, Masliah, Eliezer, McKee, Ann C, McMillan, Corey T, Mesulam, M Marsel, Murray, Melissa, Nelson, Peter T, Perrin, Richard, Pham, Thao, Poon, Wayne, Dushyant, P Purohit, Rissman, Robert A, Sakai, Kenji, Sano, Mary, Schneider, Julie A, Stein, Thor D, Teich, Andrew F, Trojanowski, John Q, Troncoso, Juan C, Vonsattel, Jean-Paul, Weintraub, Sandra, Wolk, David A, Woltjer, Randall L, Yamada, Masahito, Yu, Lei, White, Charles L, and Crary, John F
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Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Neurology & Neurosurgery ,Clinical sciences - Published
- 2021
30. Analysis of hypervelocity-impacted thin films for space applications
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Murray, Melissa A., Anz - Meador, Phillip D., and Cowardin, Heather M.
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- 2023
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31. New insights into atypical Alzheimer's disease in the era of biomarkers
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Graff-Radford, Jonathan, Yong, Keir XX, Apostolova, Liana G, Bouwman, Femke H, Carrillo, Maria, Dickerson, Bradford C, Rabinovici, Gil D, Schott, Jonathan M, Jones, David T, and Murray, Melissa E
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Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Aging ,Brain Disorders ,Dementia ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Neurodegenerative ,Alzheimer's Disease ,Acquired Cognitive Impairment ,Detection ,screening and diagnosis ,4.1 Discovery and preclinical testing of markers and technologies ,2.1 Biological and endogenous factors ,Aetiology ,Neurological ,Good Health and Well Being ,Age of Onset ,Aged ,Aged ,80 and over ,Alzheimer Disease ,Biomarkers ,Female ,Humans ,Male ,Middle Aged ,Neuroimaging ,Neurology & Neurosurgery ,Clinical sciences - Abstract
Most patients with Alzheimer's disease present with amnestic problems; however, a substantial proportion, over-represented in young-onset cases, have atypical phenotypes including predominant visual, language, executive, behavioural, or motor dysfunction. In the past, these individuals often received a late diagnosis; however, availability of CSF and PET biomarkers of Alzheimer's disease pathologies and incorporation of atypical forms of Alzheimer's disease into new diagnostic criteria increasingly allows them to be more confidently diagnosed early in their illness. This early diagnosis in turn allows patients to be offered tailored information, appropriate care and support, and individualised treatment plans. These advances will provide improved access to clinical trials, which often exclude atypical phenotypes. Research into atypical Alzheimer's disease has revealed previously unrecognised neuropathological heterogeneity across the Alzheimer's disease spectrum. Neuroimaging, genetic, biomarker, and basic science studies are providing key insights into the factors that might drive selective vulnerability of differing brain networks, with potential mechanistic implications for understanding typical late-onset Alzheimer's disease.
- Published
- 2021
32. The Sexual Subject
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Murray, Melissa, primary
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- 2023
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33. Neuropathologic scales of cerebrovascular disease associated with diffusion changes on MRI
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Nguyen, Aivi T., Kouri, Naomi, Labuzan, Sydney A., Przybelski, Scott A., Lesnick, Timothy G., Raghavan, Sheelakumari, Reid, Robert I., Reichard, R. Ross, Knopman, David S., Petersen, Ronald C., Jack, Jr., Clifford R., Mielke, Michelle M., Dickson, Dennis W., Graff-Radford, Jonathan, Murray, Melissa E., and Vemuri, Prashanthi
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- 2022
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- View/download PDF
34. Clinical and pathologic features of cognitive-predominant corticobasal degeneration
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Sakae, Nobutaka, Santos, Octavio A, Pedraza, Otto, Litvan, Irene, Murray, Melissa E, Duara, Ranjan, Uitti, Ryan J, Wszolek, Zbigniew K, Graff-Radford, Neill R, Josephs, Keith A, and Dickson, Dennis W
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Acquired Cognitive Impairment ,Frontotemporal Dementia (FTD) ,Brain Disorders ,Neurosciences ,Alzheimer's Disease ,Dementia ,Alzheimer's Disease Related Dementias (ADRD) ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Aging ,Rare Diseases ,Neurodegenerative ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Aged ,Alzheimer Disease ,Cognition Disorders ,Diagnosis ,Differential ,Female ,Frontotemporal Dementia ,Humans ,Male ,Middle Aged ,Tauopathies ,Clinical Sciences ,Cognitive Sciences ,Neurology & Neurosurgery - Abstract
ObjectiveTo describe clinical and pathologic characteristics of corticobasal degeneration (CBD) with cognitive predominant problems during the disease course.MethodsIn a series of autopsy-confirmed cases of CBD, we identified patients with cognitive rather than motor predominant features (CBD-Cog), including 5 patients thought to have Alzheimer disease (AD) and 10 patients thought to have behavioral variant frontotemporal dementia (FTD). We compared clinical and pathologic features of CBD-Cog with those from a series of 31 patients with corticobasal syndrome (CBD-CBS). For pathologic comparisons between CBD-Cog and CBD-CBS, we used semiquantitative scoring of neuronal and glial lesion types in multiple brain regions and quantitative assessments of tau burden from image analysis.ResultsFive of 15 patients with CBD-Cog never had significant motor problems during their disease course. The most common cognitive abnormalities in CBD-Cog were executive and visuospatial dysfunction. The frequency of language problems did not differ between CBD-Cog and CBD-CBS. Argyrophilic grain disease, which is a medial temporal tauopathy associated with mild cognitive impairment, was more frequent in CBD-Cog. Apathy was also more frequent in CBD-Cog. Tau pathology in CBD-Cog was greater in the temporal and less in perirolandic cortices than in CBD-CBS.ConclusionA subset of patients with CBD has a cognitive predominant syndrome than can be mistaken for AD or FTD. Our findings suggest that distribution of tau cortical pathology (greater in temporal and less in perirolandic cortices) may be the basis of this uncommon clinical variant of CBD.
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- 2020
35. EQUAL PROTECTION IN DOBBS AND BEYOND: HOW STATES PROTECT LIFE INSIDE AND OUTSIDE OF THE ABORTION CONTEXT
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Siegel, Reva B., Mayeri, Serena, and Murray, Melissa
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Motherhood -- Laws, regulations and rules -- Political aspects -- Ethical aspects ,Equality before the law -- Laws, regulations and rules -- Usage -- Analysis ,Paternalism -- Laws, regulations and rules -- Political aspects -- Ethical aspects ,Abortion -- Laws, regulations and rules -- Access control ,Government regulation ,Law ,Women's issues/gender studies ,Dobbs v. Jackson Women's Health Organization (142 S. Ct. 2228 (2022)) ,Geduldig v. Aiello (417 U.S. 484 (1974)) ,Nevada Department of Human Resources v. Hibbs (538 U.S. 721 (2003)) ,Pregnancy Discrimination Act of 1978 ,United States Constitution (U.S. Const. amend. 14) - Abstract
Abstract In two paragraphs at the beginning o/Dobbs v. Jackson Women's Health Organization, the Supreme Court rejected the Equal Protection Clause as an alternative groundfor the abortion right. As the [...]
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- 2022
36. LEGITIMIZING ILLEGITIMACY IN CONSTITUTIONAL LAW
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Murray, Melissa
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Law -- Study and teaching ,Illegitimacy -- Laws, regulations and rules -- Remedies ,Sociological jurisprudence -- Research -- Study and teaching ,Constitutional law -- Political aspects -- Social aspects -- Study and teaching ,Government regulation ,Law - Abstract
ABSTRACT The traditional constitutional law course is a staple of the first-year law school curriculum and a gateway to more advanced public law courses. In constitutional law, students are introduced [...]
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- 2022
37. Neuropathologic basis of frontotemporal dementia in progressive supranuclear palsy
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Sakae, Nobutaka, Josephs, Keith A, Litvan, Irene, Murray, Melissa E, Duara, Ranjan, Uitti, Ryan J, Wszolek, Zbigniew K, Graff‐Radford, Neil R, and Dickson, Dennis W
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Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Dementia ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Acquired Cognitive Impairment ,Rare Diseases ,Clinical Research ,Frontotemporal Dementia (FTD) ,Alzheimer's Disease ,Aging ,Alzheimer's Disease Related Dementias (ADRD) ,Brain Disorders ,Neurodegenerative ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Aged ,Brain ,Female ,Frontotemporal Dementia ,Humans ,Male ,Middle Aged ,Movement Disorders ,Parkinsonian Disorders ,Supranuclear Palsy ,Progressive ,Tauopathies ,tau Proteins ,behavioral variant frontotemporal dementia ,immunohistochemistry ,image analysis ,progressive supranuclear palsy ,tau ,immunohistochemistry ,image analysis ,Human Movement and Sports Sciences ,Neurology & Neurosurgery ,Clinical sciences - Abstract
BackgroundProgressive supranuclear palsy (PSP) is a neurodegenerative disorder characterized by neuronal loss in the extrapyramidal system with pathologic accumulation of tau in neurons and glia. The most common clinical presentation of PSP, referred to as Richardson syndrome, is that of atypical parkinsonism with vertical gaze palsy, axial rigidity, and frequent falls. Although cognitive deficits in PSP are often ascribed to subcortical dysfunction, a subset of patients has dementia with behavioral features similar to the behavioral variant of frontotemporal dementia. In this study we aimed to identify the clinical and pathological characteristics of PSP presenting with frontotemporal dementia.MethodsIn this study, we compared clinical and pathologic characteristics of 31 patients with PSP with Richardson syndrome with 15 patients with PSP with frontotemporal dementia. For pathological analysis, we used semiquantitative methods to assess neuronal and glial lesions with tau immunohistochemistry, as well image analysis of tau burden using digital microscopic methods.ResultsWe found greater frontal and temporal neocortical neuronal tau pathology in PSP with frontotemporal dementia compared with PSP with Richardson syndrome. White matter tau pathology was also greater in PSP with frontotemporal dementia than PSP with Richardson syndrome. Genetic and demographic factors were not associated with atypical distribution of tau pathology in PSP with frontotemporal dementia.ConclusionsThe results confirm the subset of cognitive-predominant PSP mimicking frontotemporal dementia in PSP. PSP with frontotemporal dementia has distinct clinical features that differ from PSP with Richardson syndrome, as well as differences in distribution and density of tau pathology. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
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- 2019
38. ABORTION, STERILIZATION, AND THE UNIVERSE OF REPRODUCTIVE RIGHTS
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Murray, Melissa
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Eugenics -- Demographic aspects -- Laws, regulations and rules -- Political aspects ,Sterilization of women -- Demographic aspects -- Ethical aspects -- Laws, regulations and rules ,Poor women -- Demographic aspects -- Economic aspects -- Family ,White women -- Economic aspects -- Family -- Laws, regulations and rules ,Sterilization, Eugenic -- Laws, regulations and rules -- Demographic aspects ,Abortion -- Demographic aspects -- Laws, regulations and rules ,Contraception -- Demographic aspects -- Laws, regulations and rules -- Access control ,Race discrimination -- Health aspects -- Laws, regulations and rules ,Minority women -- Laws, regulations and rules -- Economic aspects -- Family ,Government regulation ,Law ,Cox v. Stanton (529 F.2d 47 (4th Cir. 1975)) ,Skinner v. Oklahoma ex rel. Williamson (316 U.S. 535 (1942)) ,Box v. Planned Parenthood (139 S. Ct. 1780 (2019)) ,Buck v. Bell (274 U.S. 200 (1927)) - Abstract
In recent years, a new narrative associating reproductive rights with the eugenics movement of the 1920s has taken root. As this narrative maintains, in the 1920s, Margaret Sanger, a pioneer of the modern birth control movement, joined forces with the eugenics movement to market family planning measures to marginalized minority communities. Although the history undergirding this narrative is incomplete and misleading, the narrative itself has flourished as the debate over the continued vitality of reproductive rights has unfolded in the United States. Indeed, in just the last three years, a member of the United States Supreme Court and a number of lower federal court judges have referenced the alleged links between abortion, contraception, and eugenics in their defense of abortion restrictions. The effort to link abortion and contraception to the racialized logic of the eugenics movement is interesting on a number of fronts. As I have written elsewhere, this narrative is at once a potent defense of abortion restrictions and a more calculated effort to recast the social meaning of reproductive rights from a question of gender equality to one of racial inequality. But equally noteworthy is the narrative's utter neglect of the eugenics movement's investment in coercive sterilization--not abortion or contraception--as its preferred vehicle of reproductive control and social engineering. With all of this in mind, this Article seeks to reframe the interest in reproductive rights, racism, and eugenics to include a more robust discussion of sterilization practices. To do so, the Article supplements the historical narrative to clarify that the eugenics movement's interest in racial betterment was primarily directed at improving and purifying the white race. To the extent the eugenics movement focused on abortion and contraception, it was in limiting middle-and upper-class white women's access to these vehicles of reproductive freedom on the ground that the reproduction of these constituencies was vital to the future of the white race. Insofar as eugenicists were interested in limiting reproduction, their interest was directed toward those individuals who possessed traits deemed unsuitable for the propagation of the white race--and meaningfully, their preferred vehicle for limiting reproduction among the 'unfit' was not contraception or abortion, but rather, sterilization. And even as popular interest in eugenics waned in the 1940s, the state's interest in sterilization as a means of reproductive control did not abate. Indeed, as the Civil Rights Movement and the welfare rights movement dawned, many states repurposed sterilization to limit the reproductive capacities of those deemed sexually immoral or unduly dependent on the public fisc, usually poor women of color. To underscore the relationship between race, class, dependence, and state-endorsed sterilization, the Article highlights Cox v. Stanton, a challenge to North Carolina's sterilization program litigated by Ruth Bader Ginsburg, Brenda Feigen Fasteau, and the ACLU's Women's Rights Project in the 1970s. Although Cox did not result in the invalidation of state sterilization programs, it--and other contemporary challenges to sterilization abuse--made clear the centrality of sterilization as a technology of reproductive control, as well as sterilization abuse's racialized impact. In this regard, the nascent effort to associate abortion and contraception with eugenic racism not only equates state-sponsored reproductive abuses with an individual's decision to terminate or avoid pregnancy, but also overlooks--and indeed, further obscures--the significant history of racialized sterilization abuse in the United States., Table of Contents Introduction 1602 I. Race, Sterilization, and the Eugenics Movement 1610 A. Buck v. Bell and the Racial Politics of the Eugenics Movement 1613 B. Race, Dependence, and [...]
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- 2022
39. The UFMylation pathway is impaired in Alzheimer's disease
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Yan, Tingxiang, primary, Heckman, Michael G., additional, Craver, Emily C., additional, Liu, Chia-Chen, additional, Rawlinson, Bailey D., additional, Wang, Xue, additional, Murray, Melissa E., additional, Dickson, Dennis W., additional, Ertekin-Taner, Nilufer, additional, Lou, Zhenkun, additional, Bu, Guojun, additional, Springer, Wolfdieter, additional, and Fiesel, Fabienne C., additional
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- 2024
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40. MAPT H2 haplotype and risk of Pick's disease in the Pick's disease International Consortium: a genetic association study
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Valentino, Rebecca R, primary, Scotton, William J, additional, Roemer, Shanu F, additional, Lashley, Tammaryn, additional, Heckman, Michael G, additional, Shoai, Maryam, additional, Martinez-Carrasco, Alejandro, additional, Tamvaka, Nicole, additional, Walton, Ronald L, additional, Baker, Matthew C, additional, Macpherson, Hannah L, additional, Real, Raquel, additional, Soto-Beasley, Alexandra I, additional, Mok, Kin, additional, Revesz, Tamas, additional, Christopher, Elizabeth A, additional, DeTure, Michael, additional, Seeley, William W, additional, Lee, Edward B, additional, Frosch, Matthew P, additional, Molina-Porcel, Laura, additional, Gefen, Tamar, additional, Redding-Ochoa, Javier, additional, Ghetti, Bernardino, additional, Robinson, Andrew C, additional, Kobylecki, Christopher, additional, Rowe, James B, additional, Beach, Thomas G, additional, Teich, Andrew F, additional, Keith, Julia L, additional, Bodi, Istvan, additional, Halliday, Glenda M, additional, Gearing, Marla, additional, Arzberger, Thomas, additional, Morris, Christopher M, additional, White, Charles L, additional, Mechawar, Naguib, additional, Boluda, Susana, additional, MacKenzie, Ian R, additional, McLean, Catriona, additional, Cykowski, Matthew D, additional, Wang, Shih-Hsiu J, additional, Graff, Caroline, additional, Nagra, Rashed M, additional, Kovacs, Gabor G, additional, Giaccone, Giorgio, additional, Neumann, Manuela, additional, Ang, Lee-Cyn, additional, Carvalho, Agostinho, additional, Morris, Huw R, additional, Rademakers, Rosa, additional, Hardy, John A, additional, Dickson, Dennis W, additional, Rohrer, Jonathan D, additional, Ross, Owen A, additional, Warner, Thomas T, additional, Jaunmuktane, Zane, additional, Boeve, Bradley F, additional, Duara, Ranjan, additional, Graff-Radford, Neill R, additional, Josephs, Keith A, additional, Knopman, David S, additional, Koga, Shunsuke, additional, Murray, Melissa E, additional, Lyons, Kelly E, additional, Pahwa, Rajesh, additional, Petersen, Ronald C, additional, Whitwell, Jennifer L, additional, Grinberg, Lea T, additional, Miller, Bruce, additional, Schlereth, Athena, additional, Spina, Salvatore, additional, Grossman, Murray, additional, Irwin, David J, additional, Suh, EunRan, additional, Trojanowski, John Q, additional, Van Deerlin, Vivianna M, additional, Wolk, David A, additional, Connors, Theresa R, additional, Dooley, Patrick M, additional, Oakley, Derek H, additional, Aldecoa, Iban, additional, Balasa, Mircea, additional, Gelpi, Ellen, additional, Borrego-Écija, Sergi, additional, Gascon-Bayarri, Jordi, additional, Sánchez-Valle, Raquel, additional, Sanz-Cartagena, Pilar, additional, Piñol-Ripoll, Gerard, additional, Bigio, Eileen H, additional, Flanagan, Margaret E, additional, Rogalski, Emily J, additional, Weintraub, Sandra, additional, Schneider, Julie A, additional, Peng, Lihua, additional, Zhu, Xiongwei, additional, Chang, Koping, additional, Troncoso, Juan C, additional, Prokop, Stefan, additional, Newell, Kathy L, additional, Jones, Matthew, additional, Richardson, Anna, additional, Roncaroli, Federico, additional, Snowden, Julie, additional, Allinson, Kieren, additional, Singh, Poonam, additional, Serrano, Geidy E, additional, Flowers, Xena E, additional, Goldman, James E, additional, Heaps, Allison C, additional, Leskinen, Sandra P, additional, Black, Sandra E, additional, Masellis, Mario, additional, King, Andrew, additional, Al-Sarraj, Safa, additional, Troakes, Claire, additional, Hodges, John R, additional, Kril, Jillian J, additional, Kwok, John B, additional, Piguet, Olivier, additional, Roeber, Sigrun, additional, Attems, Johannes, additional, Thomas, Alan J, additional, Evers, Bret M., additional, Bieniek, Kevin F, additional, Sieben, Anne A, additional, Cras, Patrick P, additional, De Vil, Bart B, additional, Bird, Thomas, additional, Castellani, Rudolph J, additional, Chaffee, Ann, additional, Franklin, Erin, additional, Haroutunian, Vahram, additional, Jacobsen, Max, additional, Keene, Dirk, additional, Latimer, Caitlin S, additional, Metcalf, Jeff, additional, Perrin, Richard J, additional, Purohit, Dushyant P, additional, Rissman, Robert A, additional, Schantz, Aimee, additional, Walker, Jamie, additional, De Deyn, Peter P, additional, Duyckaerts, Charles, additional, Le Ber, Isabelle, additional, Seilhean, Danielle, additional, Turbant-Leclere, Sabrina, additional, Ervin, John F, additional, Nennesmo, Inger, additional, Riehl, James, additional, Nacmias, Benedetta, additional, Finger, Elizabeth C, additional, Blauwendraat, Cornelis, additional, Nalls, Mike A, additional, Singleton, Andrew B, additional, Vitale, Dan, additional, Cunha, Cristina, additional, and Wszolek, Zbigniew K, additional
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- 2024
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41. Clinicopathologic Heterogeneity and Glial Activation Patterns in Alzheimer Disease
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Kouri, Naomi, primary, Frankenhauser, Isabelle, additional, Peng, Zhongwei, additional, Labuzan, Sydney A., additional, Boon, Baayla D. C., additional, Moloney, Christina M., additional, Pottier, Cyril, additional, Wickland, Daniel P., additional, Caetano-Anolles, Kelsey, additional, Corriveau-Lecavalier, Nick, additional, Tranovich, Jessica F., additional, Wood, Ashley C., additional, Hinkle, Kelly M., additional, Lincoln, Sarah J., additional, Spychalla, A. J., additional, Senjem, Matthew L., additional, Przybelski, Scott A., additional, Engelberg-Cook, Erica, additional, Schwarz, Christopher G., additional, Kwan, Rain S., additional, Lesser, Elizabeth R., additional, Crook, Julia E., additional, Carter, Rickey E., additional, Ross, Owen A., additional, Lachner, Christian, additional, Ertekin-Taner, Nilüfer, additional, Ferman, Tanis J., additional, Fields, Julie A., additional, Machulda, Mary M., additional, Ramanan, Vijay K., additional, Nguyen, Aivi T., additional, Reichard, R. Ross, additional, Jones, David T., additional, Graff-Radford, Jonathan, additional, Boeve, Bradley F., additional, Knopman, David S., additional, Petersen, Ronald C., additional, Jack, Clifford R., additional, Kantarci, Kejal, additional, Day, Gregory S., additional, Duara, Ranjan, additional, Graff-Radford, Neill R., additional, Dickson, Dennis W., additional, Lowe, Val J., additional, Vemuri, Prashanthi, additional, and Murray, Melissa E., additional
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- 2024
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42. Effect of cerebrovascular risk factors on the prediction of Alzheimer’s disease neuropathologic change using plasma biomarkers (N4.003)
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Bermudez, Camilo, primary, Syrjanen, Jeremy, additional, Petersen, Ronald, additional, Knopman, David, additional, Ramanan, Vijay, additional, Jack, Clifford, additional, Nguyen, Aivi, additional, Reichard, Ross, additional, Kouri, Naomi, additional, Moloney, Christina, additional, Algeciras-Schimnich, Alicia, additional, Murray, Melissa, additional, Mielke, Michelle, additional, Vemuri, Prashanthi, additional, and Graff-Radford, Jonathan, additional
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- 2024
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43. 205 Microglia-Mediated Survival Outcomes in Preoperative Radiation for Glioblastoma: Insights From a Preclinical Model
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Otamendi-Lopez, Andrea, primary, Fernandez Gil, Beatriz Irene, additional, Vazquez-Ramo, Carla A, additional, Cherukuri, Yesesri, additional, Herchko, Steven, additional, Jentoft, Mark E., additional, Murray, Melissa, additional, Asmann, Yan, additional, Trifiletti, Daniel M., additional, Sarabia-Estrada, Rachel, additional, and Quinones-Hinojosa, Alfredo, additional
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- 2024
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44. Tau polygenic risk scoring: a cost-effective aid for prognostic counseling in Alzheimer’s disease
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Ramanan, Vijay K., Heckman, Michael G., Lesnick, Timothy G., Przybelski, Scott A., Cahn, Elliot J., Kosel, Matthew L., Murray, Melissa E., Mielke, Michelle M., Botha, Hugo, Graff-Radford, Jonathan, Jones, David T., Lowe, Val J., Machulda, Mary M., Jack Jr, Clifford R., Knopman, David S., Petersen, Ronald C., Ross, Owen A., and Vemuri, Prashanthi
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- 2022
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45. Association of plasma biomarkers of amyloid and neurodegeneration with cerebrovascular disease and Alzheimer's disease
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Graff-Radford, Jonathan, Mielke, Michelle M., Hofrenning, Ekaterina I., Kouri, Naomi, Lesnick, Timothy G., Moloney, Christina M., Rabinstein, Alejandro, Cabrera-Rodriguez, Janisse N., Rothberg, Darren M., Przybelski, Scott A., Petersen, Ronald C., Knopman, David S., Dickson, Dennis W., Jack, Clifford R., Algeciras-Schimnich, Alicia, Nguyen, Aivi T., Murray, Melissa E., and Vemuri, Prashanthi
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- 2022
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46. Clinicopathologic subtype of Alzheimer's disease presenting as corticobasal syndrome
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Sakae, Nobutaka, Josephs, Keith A, Litvan, Irene, Murray, Melissa E, Duara, Ranjan, Uitti, Ryan J, Wszolek, Zbigniew K, Gerpen, Jay, Graff‐Radford, Neil R, and Dickson, Dennis W
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Biological Psychology ,Cognitive and Computational Psychology ,Psychology ,Brain Disorders ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Dementia ,Mental Health ,Alzheimer's Disease ,Neurosciences ,Acquired Cognitive Impairment ,Aging ,Neurodegenerative ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Aged ,Alzheimer Disease ,Cerebral Cortex ,Female ,Gait Apraxia ,Humans ,Male ,Middle Aged ,Neurodegenerative Diseases ,Parkinsonian Disorders ,Temporal Lobe ,tau Proteins ,Alzheimer's disease ,Corticobasal syndrome ,Neuropathology ,Tau ,Neurodegeneration ,Clinical Sciences ,Geriatrics ,Clinical sciences ,Biological psychology - Abstract
IntroductionThe corticobasal syndrome (CBS) is associated with several neuropathologic disorders, including corticobasal degeneration and Alzheimer's disease (AD).MethodIn this report, we studied 43 AD patients with CBS (AD-CBS) and compared them with 42 AD patients with typical amnestic syndrome (AD-AS), as well as 15 cases of corticobasal degeneration and CBS pathology.ResultsUnlike AD-AS, AD-CBS had prominent motor problems, including limb apraxia (90%), myoclonus (81%), and gait disorders (70%). Alien limb phenomenon was reported in 26% and cortical sensory loss in 14%. Language problems were also more frequent in AD-CBS, and memory impairment was less frequent. AD-CBS had more tau pathology in perirolandic cortices but less in superior temporal cortex than AD-AS. In addition, AD-CBS had greater neuronal loss in the substantia nigra.DiscussionAD-CBS is a clinicopathological subtype of AD with an atypical distribution of Alzheimer-type tau pathology. Greater neuronal loss in the substantia nigra may contribute to Parkinsonism which is not a feature of typical AD.
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- 2019
47. Reply: LATE to the PART-y
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Nelson, Peter T, Dickson, Dennis W, Trojanowski, John Q, Jack, Clifford R, Boyle, Patricia A, Arfanakis, Konstantinos, Rademakers, Rosa, Alafuzoff, Irina, Attems, Johannes, Brayne, Carol, Coyle-Gilchrist, Ian TS, Fardo, David W, Flanagan, Margaret E, Halliday, Glenda, Hunter, Sally, Jicha, Gregory A, Katsumata, Yuriko, Kawas, Claudia H, Keene, C Dirk, Kovacs, Gabor G, Kukull, Walter A, Levey, Allan I, Makkinejad, Nazanin, Montine, Thomas J, Murray, Melissa E, Nag, Sukriti, Seeley, William W, Sperling, Reisa A, White, Charles L, and Schneider, Julie A
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Biomedical and Clinical Sciences ,Health Sciences ,Psychology ,Medical and Health Sciences ,Psychology and Cognitive Sciences ,Neurology & Neurosurgery ,Biomedical and clinical sciences ,Health sciences - Published
- 2019
48. Erratum
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Nelson, Peter T, Dickson, Dennis W, Trojanowski, John Q, Jack, Clifford R Jr, Boyle, Patricia A, Arfanakis, Konstantinos, Rademakers, Rosa, Alafuzoff, Irina, Attems, Johannes, Brayne, Carol, Coyle-Gilchrist, Ian TS, Chui, Helena C, Fardo, David W, Flanagan, Margaret E, Halliday, Glenda, Hokkanen, Suvi RK, Hunter, Sally, Jicha, Gregory A, Katsumata, Yuriko, Kawas, Claudia H, Keene, C Dirk, Kovacs, Gabor G, Kukull, Walter A, Levey, Allan I, Makkinejad, Nazanin, Montine, Thomas J, Murayama, Shigeo, Murray, Melissa E, Nag, Sukriti, Rissman, Robert A, Seeley, William W, Sperling, Reisa A, White, Charles LIII, Yu, Lei, and Schneider, Julie A
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Medical and Health Sciences ,Psychology and Cognitive Sciences ,Neurology & Neurosurgery - Abstract
The publisher apologizes for erroneously omitting part of the footnote for Table 2. This has now been corrected both online and in print.
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- 2019
49. Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD
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Pottier, Cyril, Ren, Yingxue, Perkerson, Ralph B, Baker, Matt, Jenkins, Gregory D, van Blitterswijk, Marka, DeJesus-Hernandez, Mariely, van Rooij, Jeroen GJ, Murray, Melissa E, Christopher, Elizabeth, McDonnell, Shannon K, Fogarty, Zachary, Batzler, Anthony, Tian, Shulan, Vicente, Cristina T, Matchett, Billie, Karydas, Anna M, Hsiung, Ging-Yuek Robin, Seelaar, Harro, Mol, Merel O, Finger, Elizabeth C, Graff, Caroline, Öijerstedt, Linn, Neumann, Manuela, Heutink, Peter, Synofzik, Matthis, Wilke, Carlo, Prudlo, Johannes, Rizzu, Patrizia, Simon-Sanchez, Javier, Edbauer, Dieter, Roeber, Sigrun, Diehl-Schmid, Janine, Evers, Bret M, King, Andrew, Mesulam, M Marsel, Weintraub, Sandra, Geula, Changiz, Bieniek, Kevin F, Petrucelli, Leonard, Ahern, Geoffrey L, Reiman, Eric M, Woodruff, Bryan K, Caselli, Richard J, Huey, Edward D, Farlow, Martin R, Grafman, Jordan, Mead, Simon, Grinberg, Lea T, Spina, Salvatore, Grossman, Murray, Irwin, David J, Lee, Edward B, Suh, EunRan, Snowden, Julie, Mann, David, Ertekin-Taner, Nilufer, Uitti, Ryan J, Wszolek, Zbigniew K, Josephs, Keith A, Parisi, Joseph E, Knopman, David S, Petersen, Ronald C, Hodges, John R, Piguet, Olivier, Geier, Ethan G, Yokoyama, Jennifer S, Rissman, Robert A, Rogaeva, Ekaterina, Keith, Julia, Zinman, Lorne, Tartaglia, Maria Carmela, Cairns, Nigel J, Cruchaga, Carlos, Ghetti, Bernardino, Kofler, Julia, Lopez, Oscar L, Beach, Thomas G, Arzberger, Thomas, Herms, Jochen, Honig, Lawrence S, Vonsattel, Jean Paul, Halliday, Glenda M, Kwok, John B, White, Charles L, Gearing, Marla, Glass, Jonathan, Rollinson, Sara, Pickering-Brown, Stuart, Rohrer, Jonathan D, Trojanowski, John Q, Van Deerlin, Vivianna, Bigio, Eileen H, Troakes, Claire, Al-Sarraj, Safa, Asmann, Yan, Miller, Bruce L, Graff-Radford, Neill R, Boeve, Bradley F, and Seeley, William W
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Biomedical and Clinical Sciences ,Neurosciences ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Clinical Research ,Brain Disorders ,Rare Diseases ,Human Genome ,Alzheimer's Disease Related Dementias (ADRD) ,Dementia ,Prevention ,Genetics ,Frontotemporal Dementia (FTD) ,Neurodegenerative ,Acquired Cognitive Impairment ,Biotechnology ,Aetiology ,2.1 Biological and endogenous factors ,Aged ,DNA Repeat Expansion ,Dipeptidyl-Peptidases and Tripeptidyl-Peptidases ,Female ,Frontal Lobe ,Frontotemporal Lobar Degeneration ,Genetic Predisposition to Disease ,Genome-Wide Association Study ,HLA-DQ Antigens ,Humans ,Intracellular Signaling Peptides and Proteins ,Loss of Function Mutation ,Male ,Middle Aged ,Nerve Tissue Proteins ,Potassium Channels ,Progranulins ,Protein Serine-Threonine Kinases ,Proteins ,RNA ,Messenger ,Risk Factors ,Sequence Analysis ,RNA ,Societies ,Scientific ,TDP-43 Proteinopathies ,White People ,Whole-genome sequencing FTLD-TDP ,TBK1 ,DPP6 ,UNC13A ,HLA ,Immunity ,Clinical Sciences ,Neurology & Neurosurgery - Abstract
Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) represents the most common pathological subtype of FTLD. We established the international FTLD-TDP whole-genome sequencing consortium to thoroughly characterize the known genetic causes of FTLD-TDP and identify novel genetic risk factors. Through the study of 1131 unrelated Caucasian patients, we estimated that C9orf72 repeat expansions and GRN loss-of-function mutations account for 25.5% and 13.9% of FTLD-TDP patients, respectively. Mutations in TBK1 (1.5%) and other known FTLD genes (1.4%) were rare, and the disease in 57.7% of FTLD-TDP patients was unexplained by the known FTLD genes. To unravel the contribution of common genetic factors to the FTLD-TDP etiology in these patients, we conducted a two-stage association study comprising the analysis of whole-genome sequencing data from 517 FTLD-TDP patients and 838 controls, followed by targeted genotyping of the most associated genomic loci in 119 additional FTLD-TDP patients and 1653 controls. We identified three genome-wide significant FTLD-TDP risk loci: one new locus at chromosome 7q36 within the DPP6 gene led by rs118113626 (p value = 4.82e - 08, OR = 2.12), and two known loci: UNC13A, led by rs1297319 (p value = 1.27e - 08, OR = 1.50) and HLA-DQA2 led by rs17219281 (p value = 3.22e - 08, OR = 1.98). While HLA represents a locus previously implicated in clinical FTLD and related neurodegenerative disorders, the association signal in our study is independent from previously reported associations. Through inspection of our whole-genome sequence data for genes with an excess of rare loss-of-function variants in FTLD-TDP patients (n ≥ 3) as compared to controls (n = 0), we further discovered a possible role for genes functioning within the TBK1-related immune pathway (e.g., DHX58, TRIM21, IRF7) in the genetic etiology of FTLD-TDP. Together, our study based on the largest cohort of unrelated FTLD-TDP patients assembled to date provides a comprehensive view of the genetic landscape of FTLD-TDP, nominates novel FTLD-TDP risk loci, and strongly implicates the immune pathway in FTLD-TDP pathogenesis.
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- 2019
50. Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report.
- Author
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Nelson, Peter T, Dickson, Dennis W, Trojanowski, John Q, Jack, Clifford R, Boyle, Patricia A, Arfanakis, Konstantinos, Rademakers, Rosa, Alafuzoff, Irina, Attems, Johannes, Brayne, Carol, Coyle-Gilchrist, Ian TS, Chui, Helena C, Fardo, David W, Flanagan, Margaret E, Halliday, Glenda, Hokkanen, Suvi RK, Hunter, Sally, Jicha, Gregory A, Katsumata, Yuriko, Kawas, Claudia H, Keene, C Dirk, Kovacs, Gabor G, Kukull, Walter A, Levey, Allan I, Makkinejad, Nazanin, Montine, Thomas J, Murayama, Shigeo, Murray, Melissa E, Nag, Sukriti, Rissman, Robert A, Seeley, William W, Sperling, Reisa A, White Iii, Charles L, Yu, Lei, and Schneider, Julie A
- Subjects
Brain ,Humans ,Brain Diseases ,Alzheimer Disease ,Retrospective Studies ,Aged ,Aged ,80 and over ,Middle Aged ,Female ,Male ,Frontotemporal Lobar Degeneration ,TDP-43 Proteinopathies ,Frontotemporal Dementia ,Neuroimaging ,FTLD ,MRI ,PET ,SNAP ,epidemiology ,and over ,Medical and Health Sciences ,Psychology and Cognitive Sciences ,Neurology & Neurosurgery - Abstract
We describe a recently recognized disease entity, limbic-predominant age-related TDP-43 encephalopathy (LATE). LATE neuropathological change (LATE-NC) is defined by a stereotypical TDP-43 proteinopathy in older adults, with or without coexisting hippocampal sclerosis pathology. LATE-NC is a common TDP-43 proteinopathy, associated with an amnestic dementia syndrome that mimicked Alzheimer's-type dementia in retrospective autopsy studies. LATE is distinguished from frontotemporal lobar degeneration with TDP-43 pathology based on its epidemiology (LATE generally affects older subjects), and relatively restricted neuroanatomical distribution of TDP-43 proteinopathy. In community-based autopsy cohorts, ∼25% of brains had sufficient burden of LATE-NC to be associated with discernible cognitive impairment. Many subjects with LATE-NC have comorbid brain pathologies, often including amyloid-β plaques and tauopathy. Given that the 'oldest-old' are at greatest risk for LATE-NC, and subjects of advanced age constitute a rapidly growing demographic group in many countries, LATE has an expanding but under-recognized impact on public health. For these reasons, a working group was convened to develop diagnostic criteria for LATE, aiming both to stimulate research and to promote awareness of this pathway to dementia. We report consensus-based recommendations including guidelines for diagnosis and staging of LATE-NC. For routine autopsy workup of LATE-NC, an anatomically-based preliminary staging scheme is proposed with TDP-43 immunohistochemistry on tissue from three brain areas, reflecting a hierarchical pattern of brain involvement: amygdala, hippocampus, and middle frontal gyrus. LATE-NC appears to affect the medial temporal lobe structures preferentially, but other areas also are impacted. Neuroimaging studies demonstrated that subjects with LATE-NC also had atrophy in the medial temporal lobes, frontal cortex, and other brain regions. Genetic studies have thus far indicated five genes with risk alleles for LATE-NC: GRN, TMEM106B, ABCC9, KCNMB2, and APOE. The discovery of these genetic risk variants indicate that LATE shares pathogenetic mechanisms with both frontotemporal lobar degeneration and Alzheimer's disease, but also suggests disease-specific underlying mechanisms. Large gaps remain in our understanding of LATE. For advances in prevention, diagnosis, and treatment, there is an urgent need for research focused on LATE, including in vitro and animal models. An obstacle to clinical progress is lack of diagnostic tools, such as biofluid or neuroimaging biomarkers, for ante-mortem detection of LATE. Development of a disease biomarker would augment observational studies seeking to further define the risk factors, natural history, and clinical features of LATE, as well as eventual subject recruitment for targeted therapies in clinical trials.
- Published
- 2019
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