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1. Sex-Specific Association of Apolipoprotein E With Cerebrospinal Fluid Levels of Tau

Author

Hohman, Timothy J, Dumitrescu, Logan, Barnes, Lisa L, Thambisetty, Madhav, Beecham, Gary, Kunkle, Brian, Gifford, Katherine A, Bush, William S, Chibnik, Lori B, Mukherjee, Shubhabrata, De Jager, Philip L, Kukull, Walter, Crane, Paul K, Resnick, Susan M, Keene, C Dirk, Montine, Thomas J, Schellenberg, Gerard D, Haines, Jonathan L, Zetterberg, Henrik, Blennow, Kaj, Larson, Eric B, Johnson, Sterling C, Albert, Marilyn, Bennett, David A, Schneider, Julie A, and Jefferson, Angela L

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Acquired Cognitive Impairment, Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Neurodegenerative, Aging, Alzheimer's Disease, Genetics, Clinical Research, Dementia, Detection, screening and diagnosis, 4.2 Evaluation of markers and technologies, 2.1 Biological and endogenous factors, Aetiology, 4.1 Discovery and preclinical testing of markers and technologies, Neurological, Aged, 80 and over, Alzheimer Disease, Amyloid beta-Peptides, Apolipoproteins E, Cohort Studies, Female, Genotype, Humans, Male, Neurofibrillary Tangles, Peptide Fragments, Phosphoproteins, Plaque, Amyloid, Sex Factors, tau Proteins, Alzheimer’s Disease Genetics Consortium and the Alzheimer’s Disease Neuroimaging Initiative
Abstract

ImportanceThe strongest genetic risk factor for Alzheimer disease (AD), the apolipoprotein E (APOE) gene, has a stronger association among women compared with men. Yet limited work has evaluated the association between APOE alleles and markers of AD neuropathology in a sex-specific manner.ObjectiveTo evaluate sex differences in the association between APOE and markers of AD neuropathology measured in cerebrospinal fluid (CSF) during life or in brain tissue at autopsy.Design, setting, and participantsThis multicohort study selected data from 10 longitudinal cohort studies of normal aging and AD. Cohorts had variable recruitment criteria and follow-up intervals and included population-based and clinic-based samples. Inclusion in our analysis required APOE genotype data and either CSF data available for analysis. Analyses began on November 6, 2017, and were completed on December 20, 2017.Main outcomes and measuresBiomarker analyses included levels of β-amyloid 42, total tau, and phosphorylated tau measured in CSF. Autopsy analyses included Consortium to Establish a Registry for Alzheimer's Disease staging for neuritic plaques and Braak staging for neurofibrillary tangles.ResultsOf the 1798 patients in the CSF biomarker cohort, 862 were women, 226 had AD, 1690 were white, and the mean (SD) age was 70 [9] years. Of the 5109 patients in the autopsy cohort, 2813 were women, 4953 were white, and the mean (SD) age was 84 (9) years. After correcting for multiple comparisons using the Bonferroni procedure, we observed a statistically significant interaction between APOE-ε4 and sex on CSF total tau (β = 0.41; 95% CI, 0.27-0.55; P

Published
2018

2. Association of GBA Mutations and the E326K Polymorphism With Motor and Cognitive Progression in Parkinson Disease

Author

Davis, Marie Y, Johnson, Catherine O, Leverenz, James B, Weintraub, Daniel, Trojanowski, John Q, Chen-Plotkin, Alice, Van Deerlin, Vivianna M, Quinn, Joseph F, Chung, Kathryn A, Peterson-Hiller, Amie L, Rosenthal, Liana S, Dawson, Ted M, Albert, Marilyn S, Goldman, Jennifer G, Stebbins, Glenn T, Bernard, Bryan, Wszolek, Zbigniew K, Ross, Owen A, Dickson, Dennis W, Eidelberg, David, Mattis, Paul J, Niethammer, Martin, Yearout, Dora, Hu, Shu-Ching, Cholerton, Brenna A, Smith, Megan, Mata, Ignacio F, Montine, Thomas J, Edwards, Karen L, and Zabetian, Cyrus P

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Dementia, Neurodegenerative, Acquired Cognitive Impairment, Clinical Research, Genetics, Aging, Brain Disorders, Parkinson's Disease, Aetiology, 2.1 Biological and endogenous factors, Neurological, Aged, Cognitive Dysfunction, Disease Progression, Female, Glucosylceramidase, Humans, Longitudinal Studies, Male, Middle Aged, Mutation, Parkinson Disease, Polymorphism, Genetic
Abstract

ImportanceParkinson disease (PD) is heterogeneous in symptom manifestation and rate of progression. Identifying factors that influence disease progression could provide mechanistic insight, improve prognostic accuracy, and elucidate novel therapeutic targets.ObjectiveTo determine whether GBA mutations and the E326K polymorphism modify PD symptom progression.Design, setting, and participantsThe entire GBA coding region was screened for mutations and E326K in 740 patients with PD enrolled at 7 sites from the PD Cognitive Genetics Consortium. Detailed longitudinal motor and cognitive assessments were performed with patients in the on state.Main outcomes and measuresLinear regression was used to test for an association between GBA genotype and motor progression, with the Movement Disorder Society-sponsored version of the Unified Parkinson's Disease Rating Scale Part III (MDS-UPDRS III) score at the last assessment as the outcome and GBA genotype as the independent variable, with adjustment for levodopa equivalent dose, sex, age, disease duration, MDS-UPDRS III score at the first assessment, duration of follow-up, and site. Similar methods were used to examine the association between genotype and tremor and postural instability and gait difficulty (PIGD) scores. To examine the effect of GBA genotype on cognitive progression, patients were classified into those with conversion to mild cognitive impairment or dementia during the study (progression) and those without progression. The association between GBA genotype and progression status was then tested using logistic regression, adjusting for sex, age, disease duration, duration of follow-up, years of education, and site.ResultsOf the total sample of 733 patients who underwent successful genotyping, 226 (30.8%) were women and 507 (69.2%) were men (mean [SD] age, 68.1 [8.8] years). The mean (SD) duration of follow-up was 3.0 (1.7) years. GBA mutations (β = 4.65; 95% CI, 1.72-7.58; P = .002), E326K (β = 3.42; 95% CI, 0.66-6.17; P = .02), and GBA variants combined as a single group (β = 4.01; 95% CI, 1.95-6.07; P = 1.5 × 10-4) were associated with a more rapid decline in MDS-UPDRS III score. Combined GBA variants (β = 0.38; 95% CI, 0.23-0.53; P = .01) and E326K (β = 0.64; 95% CI, 0.43-0.86; P = .002) were associated with faster progression in PIGD scores, but not in tremor scores. A significantly higher proportion of E326K carriers (10 of 21 [47.6%]; P = .01) and GBA variant carriers (15 of 39 [38.5%]; P = .04) progressed to mild cognitive impairment or dementia.Conclusions and relevanceGBA variants predict a more rapid progression of cognitive dysfunction and motor symptoms in patients with PD, with a greater effect on PIGD than tremor. Thus, GBA variants influence the heterogeneity in symptom progression observed in PD.

Published
2016

3. APOE, MAPT, and SNCA Genes and Cognitive Performance in Parkinson Disease

Author

Mata, Ignacio F, Leverenz, James B, Weintraub, Daniel, Trojanowski, John Q, Hurtig, Howard I, Van Deerlin, Vivianna M, Ritz, Beate, Rausch, Rebecca, Rhodes, Shannon L, Factor, Stewart A, Wood-Siverio, Cathy, Quinn, Joseph F, Chung, Kathryn A, Peterson, Amie L, Espay, Alberto J, Revilla, Fredy J, Devoto, Johnna, Hu, Shu-Ching, Cholerton, Brenna A, Wan, Jia Y, Montine, Thomas J, Edwards, Karen L, and Zabetian, Cyrus P

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Clinical Research, Parkinson's Disease, Brain Disorders, Aging, Neurodegenerative, Genetics, Dementia, Behavioral and Social Science, Acquired Cognitive Impairment, Aetiology, 2.1 Biological and endogenous factors, Neurological, Adult, Aged, Aged, 80 and over, Alzheimer Disease, Apolipoprotein E4, Cognition, Cognition Disorders, Female, Genetic Predisposition to Disease, Genotype, Humans, Male, Memory, Middle Aged, Neuropsychological Tests, Parkinson Disease, alpha-Synuclein, tau Proteins
Abstract

ImportanceCognitive impairment is a common and disabling problem in Parkinson disease (PD) that is not well understood and is difficult to treat. Identification of genetic variants that influence the rate of cognitive decline or pattern of early cognitive deficits in PD might provide a clearer understanding of the etiopathogenesis of this important nonmotor feature.ObjectiveTo determine whether common variation in the APOE, MAPT, and SNCA genes is associated with cognitive performance in patients with PD.Design, setting, and participantsWe studied 1079 PD patients from 6 academic centers in the United States who underwent assessments of memory (Hopkins Verbal Learning Test-Revised [HVLT-R]), attention and executive function (Letter-Number Sequencing Test and Trail Making Test), language processing (semantic and phonemic verbal fluency tests), visuospatial skills (Benton Judgment of Line Orientation test), and global cognitive function (Montreal Cognitive Assessment). Participants underwent genotyping for the APOE ε2/ε3/ε4 alleles, MAPT H1/H2 haplotypes, and SNCA rs356219. We used linear regression to test for association between genotype and baseline cognitive performance with adjustment for age, sex, years of education, disease duration, and site. We used a Bonferroni correction to adjust for the 9 comparisons that were performed for each gene.Main outcomes and measuresNine variables derived from 7 psychometric tests.ResultsThe APOE ε4 allele was associated with lower performance on the HVLT-R Total Recall (P = 6.7 × 10(-6); corrected P [Pc] = 6.0 × 10(-5)), Delayed Recall (P = .001; Pc = .009), and Recognition Discrimination Index (P = .004; Pc = .04); a semantic verbal fluency test (P = .002; Pc = .02); the Letter-Number Sequencing Test (P = 1 × 10(-5); Pc = 9 × 10(-5)); and Trail Making Test B minus Trail Making Test A (P = .002; Pc = .02). In a subset of 645 patients without dementia, the APOE ε4 allele was associated with lower scores on the HVLT-R Total Recall (P = .005; Pc = .045) and the semantic verbal fluency (P = .005; Pc = .045) measures. Variants of MAPT and SNCA were not associated with scores on any tests.Conclusions and relevanceOur data indicate that the APOE ε4 allele is an important predictor of cognitive function in PD across multiple domains. Among PD patients without dementia, the APOE ε4 allele was only associated with lower performance on word list learning and semantic verbal fluency, a pattern more typical of the cognitive deficits seen in early Alzheimer disease than PD.

Published
2014

4. Effects of Multiple Genetic Loci on Age at Onset in Late-Onset Alzheimer Disease

Author

Naj, Adam C, Jun, Gyungah, Reitz, Christiane, Kunkle, Brian W, Perry, William, Park, Yo Son, Beecham, Gary W, Rajbhandary, Ruchita A, Hamilton-Nelson, Kara L, Wang, Li-San, Kauwe, John S. K, Huentelman, Matthew J, Myers, Amanda J, Bird, Thomas D, Boeve, Bradley F, Baldwin, Clinton T, Jarvik, Gail P, Crane, Paul K, Rogaeva, Ekaterina, Barmada, M. Michael, Demirci, F. Yesim, Cruchaga, Carlos, Kramer, Patricia L, Ertekin-Taner, Nilufer, Hardy, John, Graff-Radford, Neill R, Green, Robert C, Larson, Eric B, St. George-Hyslop, Peter H, Buxbaum, Joseph D, Evans, Denis A, Schneider, Julie A, Lunetta, Kathryn L, Kamboh, M. Ilyas, Saykin, Andrew J, Reiman, Eric M, De Jager, Philip L, Bennett, David A, Morris, John C, Montine, Thomas J, Goate, Alison M, Blacker, Deborah, Tsuang, Debby W, Hakonarson, Hakon, Kukull, Walter A, Foroud, Tatiana M, Martin, Eden R, Haines, Jonathan L, Mayeux, Richard P, Farrer, Lindsay A, Schellenberg, Gerard D, Pericak-Vance, Margaret A, Albert, Marilyn S, Albin, Roger L, Apostolova, Liana G, Arnold, Steven E, Barber, Robert, Barnes, Lisa L, Beach, Thomas G, Becker, James T, Beekly, Duane, Bigio, Eileen H, Bowen, James D, Boxer, Adam, Burke, James R, Cairns, Nigel J, Cantwell, Laura B, Cao, Chuanhai, Carlson, Chris S, Carney, Regina M, Carrasquillo, Minerva M, Carroll, Steven L, Chui, Helena C, Clark, David G, Corneveaux, Jason, Cribbs, David H, Crocco, Elizabeth A, DeCarli, Charles, DeKosky, Steven T, Dick, Malcolm, Dickson, Dennis W, Duara, Ranjan, Faber, Kelley M, Fallon, Kenneth B, Farlow, Martin R, Ferris, Steven, Frosch, Matthew P, Galasko, Douglas R, Ganguli, Mary, Gearing, Marla, Geschwind, Daniel H, Ghetti, Bernardino, Gilbert, John R, Glass, Jonathan D, Growdon, John H, Hamilton, Ronald L, Harrell, Lindy E, Head, Elizabeth, Honig, Lawrence S, and Hulette, Christine M

Published
2014

6. Rarity of the Alzheimer Disease–Protective APP A673T Variant in the United States

Author

Wang, Li-San, Naj, Adam C., Graham, Robert R., Crane, Paul K., Kunkle, Brian W., Cruchaga, Carlos, Murcia, Josue D. Gonzalez, Cannon-Albright, Lisa, Baldwin, Clinton T., Zetterberg, Henrik, Blennow, Kaj, Kukull, Walter A., Faber, Kelley M., Schupf, Nicole, Norton, Maria C., Tschanz, JoAnn T., Munger, Ronald G., Corcoran, Christopher D., Rogaeva, Ekaterina, Lin, Chiao-Feng, Dombroski, Beth A., Cantwell, Laura B., Partch, Amanda, Valladares, Otto, Hakonarson, Hakon, St George-Hyslop, Peter, Green, Robert C., Goate, Alison M., Foroud, Tatiana M., Carney, Regina M., Larson, Eric B., Behrens, Timothy W., Kauwe, John S. K., Haines, Jonathan L., Farrer, Lindsay A., Pericak-Vance, Margaret A., Mayeux, Richard, Schellenberg, Gerard D., Albert, Marilyn S., Albin, Roger L., Apostolova, Liana G., Arnold, Steven E., Barber, Robert, Barmada, M. Michael, Barnes, Lisa L., Beach, Thomas G., Becker, James T., Beecham, Gary W., Beekly, Duane, Bennett, David A., Bigio, Eileen H., Bird, Thomas D., Blacker, Deborah, Boeve, Bradley F., Bowen, James D., Boxer, Adam, Burke, James R., Buxbaum, Joseph D., Cairns, Nigel J., Cao, Chuanhai, Carlson, Chris S., Carroll, Steven L., Chui, Helena C., Clark, David G., Cribbs, David H., Crocco, Elizabeth A., DeCarli, Charles, DeKosky, Steven T., Demirci, F. Yesim, Dick, Malcolm, Dickson, Dennis W., Duara, Ranjan, Ertekin-Taner, Nilufer, Fallon, Kenneth B., Farlow, Martin R., Ferris, Steven, Frosch, Matthew P., Galasko, Douglas R., Ganguli, Mary, Gearing, Marla, Geschwind, Daniel H., Ghetti, Bernardino, Gilbert, John R., Glass, Jonathan D., Graff-Radford, Neill R., Growdon, John H., Hamilton, Ronald L., Hamilton-Nelson, Kara L., Harrell, Lindy E., Head, Elizabeth, Honig, Lawrence S., Hulette, Christine M., Hyman, Bradley T., Jarvik, Gail P., Jicha, Gregory A., Jin, Lee-Way, Jun, Gyungah, Kamboh, M. Ilyas, Karydas, Anna, Kaye, Jeffrey A., Kim, Ronald, Koo, Edward H., Kowall, Neil W., Kramer, Joel H., Kramer, Patricia, LaFerla, Frank M., Lah, James J., Leverenz, James B., Levey, Allan I., Li, Ge, Lieberman, Andrew P., Lopez, Oscar L., Lunetta, Kathryn L., Lyketsos, Constantine G., Mack, Wendy J., Marson, Daniel C., Martin, Eden R., Martiniuk, Frank, Mash, Deborah C., Masliah, Eliezer, McCormick, Wayne C., McCurry, Susan M., McDavid, Andrew N., McKee, Ann C., Mesulam, M. Marsel, Miller, Bruce L., Miller, Carol A., Miller, Joshua W., Montine, Thomas J., Morris, John C., Murrell, Jill R., Olichney, John M., Parisi, Joseph E., Perry, William, Peskind, Elaine, Petersen, Ronald C., Pierce, Aimee, Poon, Wayne W., Potter, Huntington, Quinn, Joseph F., Raj, Ashok, Raskind, Murray, Reiman, Eric M., Reisberg, Barry, Reitz, Christiane, Ringman, John M., Roberson, Erik D., Rosen, Howard J., Rosenberg, Roger N., Sano, Mary, Saykin, Andrew J., Schneider, Julie A., Schneider, Lon S., Seeley, William W., Smith, Amanda G., Sonnen, Joshua A., Spina, Salvatore, Stern, Robert A., Tanzi, Rudolph E., Thornton-Wells, Tricia A., Trojanowski, John Q., Troncoso, Juan C., Tsuang, Debby W., Van Deerlin, Vivianna M., Van Eldik, Linda J., Vardarajan, Badri N., Vinters, Harry V., Vonsattel, Jean Paul, Weintraub, Sandra, Welsh-Bohmer, Kathleen A., Williamson, Jennifer, Wishnek, Sarah, Woltjer, Randall L., Wright, Clinton B., Younkin, Steven G., Yu, Chang-En, and Yu, Lei

Published
2015
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10. APOE ε4 Increases Risk for Dementia in Pure Synucleinopathies

Author

Tsuang, Debby, Leverenz, James B., Lopez, Oscar L., Hamilton, Ronald L., Bennett, David A., Schneider, Julie A., Buchman, Aron S., Larson, Eric B., Crane, Paul K., Kaye, Jeffrey A., Kramer, Patricia, Woltjer, Randy, Trojanowski, John Q., Weintraub, Daniel, Chen-Plotkin, Alice S., Irwin, David J., Rick, Jacqueline, Schellenberg, Gerard D., Watson, G. Stennis, Kukull, Walter, Nelson, Peter T., Jicha, Gregory A., Neltner, Janna H., Galasko, Doug, Masliah, Eliezer, Quinn, Joseph F., Chung, Kathryn A., Yearout, Dora, Mata, Ignacio F., Wan, Jia Y., Edwards, Karen L., Montine, Thomas J., and Zabetian, Cyrus P.

Published
2013
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11. Positron Emission Tomography Imaging With [18F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes.

Author

Fleisher, Adam S., Pontecorvo, Michael J., Devous, Michael D., Lu, Ming, Arora, Anupa K., Truocchio, Stephen P., Aldea, Patricia, Flitter, Matthew, Locascio, Tricia, Devine, Marybeth, Siderowf, Andrew, Beach, Thomas G., Montine, Thomas J., Serrano, Geidy E., Curtis, Craig, Perrin, Allison, Salloway, Stephen, Daniel, Misty, Wellman, Charles, and Joshi, Abhinay D.

Published
2020
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12. Positron Emission Tomography Imaging With [18F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes

Author

Fleisher, Adam S., Pontecorvo, Michael J., Devous, Michael D., Lu, Ming, Arora, Anupa K., Truocchio, Stephen P., Aldea, Patricia, Flitter, Matthew, Locascio, Tricia, Devine, Marybeth, Siderowf, Andrew, Beach, Thomas G., Montine, Thomas J., Serrano, Geidy E., Curtis, Craig, Perrin, Allison, Salloway, Stephen, Daniel, Misty, Wellman, Charles, Joshi, Abhinay D., Irwin, David J., Lowe, Val J., Seeley, William W., Ikonomovic, Milos D., Masdeu, Joseph C., Kennedy, Ian, Harris, Thomas, Navitsky, Michael, Southekal, Sudeepti, and Mintun, Mark A.

Abstract

IMPORTANCE: Positron emission tomography (PET) may increase the diagnostic accuracy and confirm the underlying neuropathologic changes of Alzheimer disease (AD). OBJECTIVE: To determine the accuracy of antemortem [18F]flortaucipir PET images for predicting the presence of AD-type tau pathology at autopsy. DESIGN, SETTING, AND PARTICIPANTS: This diagnostic study (A16 primary cohort) was conducted from October 2015 to June 2018 at 28 study sites (27 in US sites and 1 in Australia). Individuals with a terminal illness who were older than 50 years and had a projected life expectancy of less than 6 months were enrolled. All participants underwent [18F]flortaucipir PET imaging, and scans were interpreted by 5 independent nuclear medicine physicians or radiologists. Supplemental autopsy [18F]flortaucipir images and pathological samples were also collected from 16 historically collected cases. A second study (FR01 validation study) was conducted from March 26 to April 26, 2019, in which 5 new readers assessed the original PET images for comparison to autopsy. MAIN OUTCOMES AND MEASURES: [18F]flortaucipir PET images were visually assessed and compared with immunohistochemical tau pathology. An AD tau pattern of flortaucipir retention was assessed for correspondence with a postmortem B3-level (Braak stage V or VI) pathological pattern of tau accumulation and to the presence of amyloid-β plaques sufficient to meet the criteria for high levels of AD neuropathological change. Success was defined as having at least 3 of the 5 readers above the lower bounds of the 95% CI for both sensitivity and specificity of 50% or greater. RESULTS: A total of 156 patients were enrolled in the A16 study and underwent [18F]flortaucipir PET imaging. Of these, 73 died during the study, and valid autopsies were performed for 67 of these patients. Three autopsies were evaluated as test cases and removed from the primary cohort (n = 64). Of the 64 primary cohort patients, 34 (53%) were women and 62 (97%) were white; mean (SD) age was 82.5 (9.6) years; and 49 (77%) had dementia, 1 (2%) had mild cognitive impairment, and 14 (22%) had normal cognition. Prespecified success criteria were met for the A16 primary cohort. The flortaucipir PET scans predicted a B3 level of tau pathology, with sensitivity ranging from 92.3% (95% CI, 79.7%-97.3%) to 100.0% (95% CI, 91.0%-100.0%) and specificity ranging from 52.0% (95% CI, 33.5%-70.0%) to 92.0% (95% CI, 75.0%-97.8%). A high level of AD neuropathological change was predicted with sensitivity of 94.7% (95% CI, 82.7%-98.5%) to 100.0% (95% CI, 90.8%-100.0%) and specificity of 50.0% (95% CI, 32.1%-67.9%) to 92.3% (95% CI, 75.9%-97.9%). The FR01 validation study also met prespecified success criteria. Addition of the supplemental autopsy data set and 3 test cases, which comprised a total of 82 patients and autopsies for both the A16 and FR01 studies, resulted in improved specificity and comparable overall accuracy. Among the 156 enrolled participants, 14 (9%) experienced at least 1 treatment-emergent adverse event. CONCLUSIONS AND RELEVANCE: This study’s findings suggest that PET imaging with [18F]flortaucipir could be used to identify the density and distribution of AD-type tau pathology and the presence of high levels of AD neuropathological change, supporting a neuropathological diagnosis of AD.

Published
2020
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13. Association ofGBAMutations and the E326K Polymorphism With Motor and Cognitive Progression in Parkinson Disease

Author

Davis, Marie Y., primary, Johnson, Catherine O., additional, Leverenz, James B., additional, Weintraub, Daniel, additional, Trojanowski, John Q., additional, Chen-Plotkin, Alice, additional, Van Deerlin, Vivianna M., additional, Quinn, Joseph F., additional, Chung, Kathryn A., additional, Peterson-Hiller, Amie L., additional, Rosenthal, Liana S., additional, Dawson, Ted M., additional, Albert, Marilyn S., additional, Goldman, Jennifer G., additional, Stebbins, Glenn T., additional, Bernard, Bryan, additional, Wszolek, Zbigniew K., additional, Ross, Owen A., additional, Dickson, Dennis W., additional, Eidelberg, David, additional, Mattis, Paul J., additional, Niethammer, Martin, additional, Yearout, Dora, additional, Hu, Shu-Ching, additional, Cholerton, Brenna A., additional, Smith, Megan, additional, Mata, Ignacio F., additional, Montine, Thomas J., additional, Edwards, Karen L., additional, and Zabetian, Cyrus P., additional

Published
2016
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14. Association of Traumatic Brain Injury With Late-Life Neurodegenerative Conditions and Neuropathologic Findings

Author

Crane, Paul K., primary, Gibbons, Laura E., additional, Dams-O’Connor, Kristen, additional, Trittschuh, Emily, additional, Leverenz, James B., additional, Keene, C. Dirk, additional, Sonnen, Joshua, additional, Montine, Thomas J., additional, Bennett, David A., additional, Leurgans, Sue, additional, Schneider, Julie A., additional, and Larson, Eric B., additional

Published
2016
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15. Rarity of the Alzheimer Disease–ProtectiveAPPA673T Variant in the United States

Author

Wang, Li-San, primary, Naj, Adam C., additional, Graham, Robert R., additional, Crane, Paul K., additional, Kunkle, Brian W., additional, Cruchaga, Carlos, additional, Murcia, Josue D. Gonzalez, additional, Cannon-Albright, Lisa, additional, Baldwin, Clinton T., additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Kukull, Walter A., additional, Faber, Kelley M., additional, Schupf, Nicole, additional, Norton, Maria C., additional, Tschanz, JoAnn T., additional, Munger, Ronald G., additional, Corcoran, Christopher D., additional, Rogaeva, Ekaterina, additional, Lin, Chiao-Feng, additional, Dombroski, Beth A., additional, Cantwell, Laura B., additional, Partch, Amanda, additional, Valladares, Otto, additional, Hakonarson, Hakon, additional, St George-Hyslop, Peter, additional, Green, Robert C., additional, Goate, Alison M., additional, Foroud, Tatiana M., additional, Carney, Regina M., additional, Larson, Eric B., additional, Behrens, Timothy W., additional, Kauwe, John S. K., additional, Haines, Jonathan L., additional, Farrer, Lindsay A., additional, Pericak-Vance, Margaret A., additional, Mayeux, Richard, additional, Schellenberg, Gerard D., additional, Albert, Marilyn S., additional, Albin, Roger L., additional, Apostolova, Liana G., additional, Arnold, Steven E., additional, Barber, Robert, additional, Barmada, M. Michael, additional, Barnes, Lisa L., additional, Beach, Thomas G., additional, Becker, James T., additional, Beecham, Gary W., additional, Beekly, Duane, additional, Bennett, David A., additional, Bigio, Eileen H., additional, Bird, Thomas D., additional, Blacker, Deborah, additional, Boeve, Bradley F., additional, Bowen, James D., additional, Boxer, Adam, additional, Burke, James R., additional, Buxbaum, Joseph D., additional, Cairns, Nigel J., additional, Cao, Chuanhai, additional, Carlson, Chris S., additional, Carroll, Steven L., additional, Chui, Helena C., additional, Clark, David G., additional, Cribbs, David H., additional, Crocco, Elizabeth A., additional, DeCarli, Charles, additional, DeKosky, Steven T., additional, Demirci, F. Yesim, additional, Dick, Malcolm, additional, Dickson, Dennis W., additional, Duara, Ranjan, additional, Ertekin-Taner, Nilufer, additional, Fallon, Kenneth B., additional, Farlow, Martin R., additional, Ferris, Steven, additional, Frosch, Matthew P., additional, Galasko, Douglas R., additional, Ganguli, Mary, additional, Gearing, Marla, additional, Geschwind, Daniel H., additional, Ghetti, Bernardino, additional, Gilbert, John R., additional, Glass, Jonathan D., additional, Graff-Radford, Neill R., additional, Growdon, John H., additional, Hamilton, Ronald L., additional, Hamilton-Nelson, Kara L., additional, Harrell, Lindy E., additional, Head, Elizabeth, additional, Honig, Lawrence S., additional, Hulette, Christine M., additional, Hyman, Bradley T., additional, Jarvik, Gail P., additional, Jicha, Gregory A., additional, Jin, Lee-Way, additional, Jun, Gyungah, additional, Kamboh, M. Ilyas, additional, Karydas, Anna, additional, Kaye, Jeffrey A., additional, Kim, Ronald, additional, Koo, Edward H., additional, Kowall, Neil W., additional, Kramer, Joel H., additional, Kramer, Patricia, additional, LaFerla, Frank M., additional, Lah, James J., additional, Leverenz, James B., additional, Levey, Allan I., additional, Li, Ge, additional, Lieberman, Andrew P., additional, Lopez, Oscar L., additional, Lunetta, Kathryn L., additional, Lyketsos, Constantine G., additional, Mack, Wendy J., additional, Marson, Daniel C., additional, Martin, Eden R., additional, Martiniuk, Frank, additional, Mash, Deborah C., additional, Masliah, Eliezer, additional, McCormick, Wayne C., additional, McCurry, Susan M., additional, McDavid, Andrew N., additional, McKee, Ann C., additional, Mesulam, M. Marsel, additional, Miller, Bruce L., additional, Miller, Carol A., additional, Miller, Joshua W., additional, Montine, Thomas J., additional, Morris, John C., additional, Murrell, Jill R., additional, Olichney, John M., additional, Parisi, Joseph E., additional, Perry, William, additional, Peskind, Elaine, additional, Petersen, Ronald C., additional, Pierce, Aimee, additional, Poon, Wayne W., additional, Potter, Huntington, additional, Quinn, Joseph F., additional, Raj, Ashok, additional, Raskind, Murray, additional, Reiman, Eric M., additional, Reisberg, Barry, additional, Reitz, Christiane, additional, Ringman, John M., additional, Roberson, Erik D., additional, Rosen, Howard J., additional, Rosenberg, Roger N., additional, Sano, Mary, additional, Saykin, Andrew J., additional, Schneider, Julie A., additional, Schneider, Lon S., additional, Seeley, William W., additional, Smith, Amanda G., additional, Sonnen, Joshua A., additional, Spina, Salvatore, additional, Stern, Robert A., additional, Tanzi, Rudolph E., additional, Thornton-Wells, Tricia A., additional, Trojanowski, John Q., additional, Troncoso, Juan C., additional, Tsuang, Debby W., additional, Van Deerlin, Vivianna M., additional, Van Eldik, Linda J., additional, Vardarajan, Badri N., additional, Vinters, Harry V., additional, Vonsattel, Jean Paul, additional, Weintraub, Sandra, additional, Welsh-Bohmer, Kathleen A., additional, Williamson, Jennifer, additional, Wishnek, Sarah, additional, Woltjer, Randall L., additional, Wright, Clinton B., additional, Younkin, Steven G., additional, Yu, Chang-En, additional, and Yu, Lei, additional

Published
2015
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16. APOE,MAPT, andSNCAGenes and Cognitive Performance in Parkinson Disease

Author

Mata, Ignacio F., primary, Leverenz, James B., additional, Weintraub, Daniel, additional, Trojanowski, John Q., additional, Hurtig, Howard I., additional, Van Deerlin, Vivianna M., additional, Ritz, Beate, additional, Rausch, Rebecca, additional, Rhodes, Shannon L., additional, Factor, Stewart A., additional, Wood-Siverio, Cathy, additional, Quinn, Joseph F., additional, Chung, Kathryn A., additional, Peterson, Amie L., additional, Espay, Alberto J., additional, Revilla, Fredy J., additional, Devoto, Johnna, additional, Hu, Shu-Ching, additional, Cholerton, Brenna A., additional, Wan, Jia Y., additional, Montine, Thomas J., additional, Edwards, Karen L., additional, and Zabetian, Cyrus P., additional

Published
2014
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