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1. Disease-modifying therapies for Parkinson disease: lessons from multiple sclerosis

Author

Kalia, Lorraine V., Asis, Angelica, Arbour, Nathalie, Bar-Or, Amit, Bove, Riley, Di Luca, Daniel G., Fon, Edward A., Fox, Susan, Gan-Or, Ziv, Gommerman, Jennifer L., Kang, Un Jung, Klawiter, Eric C., Koch, Marcus, Kolind, Shannon, Lang, Anthony E., Lee, Karen K., Lincoln, Matthew R., MacDonald, Penny A., McKeown, Martin J., Mestre, Tiago A., Miron, Veronique E., Ontaneda, Daniel, Rousseaux, Maxime W. C., Schlossmacher, Michael G., Schneider, Raphael, Stoessl, A. Jon, and Oh, Jiwon

Published
2024
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4. Genetic and pharmacological reduction of CDK14 mitigates synucleinopathy

Author

Parmasad, Jean-Louis A., Ricke, Konrad M., Nguyen, Benjamin, Stykel, Morgan G., Buchner-Duby, Brodie, Bruce, Amanda, Geertsma, Haley M., Lian, Eric, Lengacher, Nathalie A., Callaghan, Steve M., Joselin, Alvin, Tomlinson, Julianna J., Schlossmacher, Michael G., Stanford, William L., Ma, Jiyan, Brundin, Patrik, Ryan, Scott D., and Rousseaux, Maxime W. C.

Published
2024
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5. Parkin coregulates glutathione metabolism in adult mammalian brain

Author

El Kodsi, Daniel N., Tokarew, Jacqueline M., Sengupta, Rajib, Lengacher, Nathalie A., Chatterji, Ajanta, Nguyen, Angela P., Boston, Heather, Jiang, Qiubo, Palmberg, Carina, Pileggi, Chantal, Holterman, Chet E., Shutinoski, Bojan, Li, Juan, Fehr, Travis K., LaVoie, Matthew J., Ratan, Rajiv R., Shaw, Gary S., Takanashi, Masashi, Hattori, Nobutaka, Kennedy, Christopher R., Harper, Mary-Ellen, Holmgren, Arne, Tomlinson, Julianna J., and Schlossmacher, Michael G.

Published
2023
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7. Advancing Parkinson's Disease Research in Canada: The Canadian Open Parkinson Network (C-OPN) Cohort.

Author

Cressatti, Marisa, Pinilla-Monsalve, Gabriel D., Blais, Mathieu, Normandeau, Catherine P., Degroot, Clotilde, Kathol, Iris, Bogard, Sarah, Bendas, Anna, Camicioli, Richard, Dupré, Nicolas, Gan-Or, Ziv, Grimes, David A., Kalia, Lorraine V., MacDonald, Penny A., McKeown, Martin J., Martino, Davide, Miyasaki, Janis M., Schlossmacher, Michael G., Stoessl, A. Jon, and Strafella, Antonio P.

Subjects
MONONUCLEAR leukocytes, PARKINSON'S disease, MEDICAL personnel, SYMPTOMS, DISEASE management
Abstract

Background: Enhancing the interactions between study participants, clinicians, and investigators is imperative for advancing Parkinson's disease (PD) research. The Canadian Open Parkinson Network (C-OPN) stands as a nationwide endeavor, connecting the PD community with ten accredited universities and movement disorders research centers spanning, at the time of this analysis, British Columbia, Alberta, Ontario, and Quebec. Objective: Our aim is to showcase C-OPN as a paradigm for bolstering national collaboration to accelerate PD research and to provide an initial overview of already collected data sets. Methods: The C-OPN database comprises de-identified data concerning demographics, symptoms and signs, treatment approaches, and standardized assessments. Additionally, it collects venous blood-derived biomaterials, such as for analyses of DNA, peripheral blood mononuclear cells (PBMC), and serum. Accessible to researchers, C-OPN resources are available through web-based data management systems for multi-center studies, including REDCap. Results: As of November 2023, the C-OPN had enrolled 1,505 PD participants. The male-to-female ratio was 1.77:1, with 83% (n = 1098) residing in urban areas and 82% (n = 1084) having pursued post-secondary education. The average age at diagnosis was 60.2±10.3 years. Herein, our analysis of the C-OPN PD cohort encompasses environmental factors, motor and non-motor symptoms, disease management, and regional differences among provinces. As of April 2024, 32 research projects have utilized C-OPN resources. Conclusions: C-OPN represents a national platform promoting multidisciplinary and multisite research that focuses on PD to promote innovation, exploration of care models, and collaboration among Canadian scientists. Plain Language Summary: Teamwork and communication between people living with Parkinson's disease (PD), physicians, health professionals, and research scientists is important for improving the lives of those living with this condition. The Canadian Open Parkinson Network (C-OPN) is a Canada-wide initiative, connecting the PD community with ten accredited universities and movement disorders research centers located in – at the time of this analysis–British Columbia, Alberta, Ontario, and Quebec. The aim of this paper is to showcase C-OPN as a useful resource for physician and research scientists studying PD in Canada and around the world, and to provide snapshot of already collected data. The C-OPN database comprises de-identified (meaning removal of any identifying information, such as name or date of birth) data concerning lifestyle, disease symptoms, treatments, and results from standardized tests. It also collects blood samples for further analysis. As of November 2023, C-OPN had enrolled 1,505 PD participants across Canada. Most of the participants were male (64%), living in urban areas (83%), and completed post-secondary education (82%). The average age at diagnosis was 60.2±10.3 years. In this paper, we look at environmental factors, motor and non-motor symptoms, different disease management strategies, and regional differences between provinces. In conclusion, C-OPN represents a national platform that encourages multidisciplinary and multisite research focusing on PD to promote innovation and collaboration among Canadian scientists. [ABSTRACT FROM AUTHOR]

Published
2024
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9. Advancing Parkinson's Disease Research in Canada: The Canadian Open Parkinson Network (C-OPN) Cohort

Author

Cressatti, Marisa, primary, Pinilla-Monsalve, Gabriel D, additional, Blais, Mathieu, additional, Normandeau, Catherine P, additional, Degroot, Clotilde, additional, Kathol, Iris, additional, Bogard, Sarah, additional, Bendas, Anna, additional, Camicioli, Richard, additional, Dupre, Nicolas, additional, Gan-Or, Ziv, additional, Grimes, David A, additional, Kalia, Lorraine V, additional, MacDonald, Penny A, additional, McKeown, Martin J, additional, Martino, Davide, additional, Miyasaki, Janis M, additional, Schlossmacher, Michael G, additional, Stoessl, A Jon, additional, Strafella, Antonio P, additional, Fon, Edward A, additional, and Monchi, Oury, additional

Published
2024
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11. Age-associated insolubility of parkin in human midbrain is linked to redox balance and sequestration of reactive dopamine metabolites

Author

Tokarew, Jacqueline M., El-Kodsi, Daniel N., Lengacher, Nathalie A., Fehr, Travis K., Nguyen, Angela P., Shutinoski, Bojan, O’Nuallain, Brian, Jin, Ming, Khan, Jasmine M., Ng, Andy C. H., Li, Juan, Jiang, Qiubo, Zhang, Mei, Wang, Liqun, Sengupta, Rajib, Barber, Kathryn R., Tran, An, Im, Doo Soon, Callaghan, Steve, Park, David S., Zandee, Stephanie, Dong, Xiajun, Scherzer, Clemens R., Prat, Alexandre, Tsai, Eve C., Takanashi, Masashi, Hattori, Nobutaka, Chan, Jennifer A., Zecca, Luigi, West, Andrew B., Holmgren, Arne, Puente, Lawrence, Shaw, Gary S., Toth, Gergely, Woulfe, John M., Taylor, Peggy, Tomlinson, Julianna J., and Schlossmacher, Michael G.

Published
2021
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12. Unraveling the assembloid: Real-time monitoring of dopaminergic neurites in an inter-organoid pathway connecting midbrain and striatal regions

Author

Ozgun, Alp, primary, Lomboni, David J., additional, Aylsworth, Amy, additional, Macdonald, Allison, additional, Staines, William A., additional, Martina, Marzia, additional, Schlossmacher, Michael G., additional, Tauskela, Joseph S., additional, Woulfe, John, additional, and Variola, Fabio, additional

Published
2024
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16. Expansion of the Parkinson disease-associated SNCA- Rep1 allele upregulates human α-synuclein in transgenic mouse brain

Author

Cronin, Kenneth D, Ge, Dongliang, Manninger, Paul, Linnertz, Colton, Rossoshek, Anna, Orrison, Bonnie M, Bernard, David J, El-Agnaf, Omar MA, Schlossmacher, Michael G, Nussbaum, Robert L, and Chiba-Falek, Ornit

Subjects
Biological Sciences, Genetics, Acquired Cognitive Impairment, Neurodegenerative, Parkinson's Disease, Neurosciences, Aging, Dementia, Prevention, Brain Disorders, 2.1 Biological and endogenous factors, Aetiology, Neurological, Alleles, Animals, Brain, Female, Humans, Male, Mice, Mice, Transgenic, Microsatellite Repeats, Parkinson Disease, Polymorphism, Genetic, Up-Regulation, alpha-Synuclein, Medical and Health Sciences, Genetics & Heredity
Abstract

Alpha-synuclein (SNCA) gene has been implicated in the development of rare forms of familial Parkinson disease (PD). Recently, it was shown that an increase in SNCA copy numbers leads to elevated levels of wild-type SNCA-mRNA and protein and is sufficient to cause early-onset, familial PD. A critical question concerning the molecular pathogenesis of PD is what contributory role, if any, is played by the SNCA gene in sporadic PD. The expansion of SNCA-Rep1, an upstream, polymorphic microsatellite of the SNCA gene, is associated with elevated risk for sporadic PD. However, whether SNCA-Rep1 is the causal variant and the underlying mechanism with which its effect is mediated by remained elusive. We report here the effects of three distinct SNCA-Rep1 variants in the brains of 72 mice transgenic for the entire human SNCA locus. Human SNCA-mRNA and protein levels were increased 1.7- and 1.25-fold, respectively, in homozygotes for the expanded, PD risk-conferring allele compared with homozygotes for the shorter, protective allele. When adjusting for the total SNCA-protein concentration (endogenous mouse and transgenic human) expressed in each brain, the expanded risk allele contributed 2.6-fold more to the SNCA steady-state than the shorter allele. Furthermore, targeted deletion of Rep1 resulted in the lowest human SNCA-mRNA and protein concentrations in murine brain. In contrast, the Rep1 effect was not observed in blood lysates from the same mice. These results demonstrate that Rep1 regulates human SNCA expression by enhancing its transcription in the adult nervous system and suggest that homozygosity for the expanded Rep1 allele may mimic locus multiplication, thereby elevating PD risk.

Published
2009

17. Expansion of the Parkinson disease-associated SNCA-Rep1 allele upregulates human alpha-synuclein in transgenic mouse brain.

Author

Cronin, Kenneth D, Ge, Dongliang, Manninger, Paul, Linnertz, Colton, Rossoshek, Anna, Orrison, Bonnie M, Bernard, David J, El-Agnaf, Omar MA, Schlossmacher, Michael G, Nussbaum, Robert L, and Chiba-Falek, Ornit

Subjects
Brain, Animals, Mice, Transgenic, Humans, Mice, Parkinson Disease, Up-Regulation, Microsatellite Repeats, Polymorphism, Genetic, Alleles, Female, Male, alpha-Synuclein, Transgenic, Polymorphism, Genetic, Biological Sciences, Medical and Health Sciences, Genetics & Heredity
Abstract

Alpha-synuclein (SNCA) gene has been implicated in the development of rare forms of familial Parkinson disease (PD). Recently, it was shown that an increase in SNCA copy numbers leads to elevated levels of wild-type SNCA-mRNA and protein and is sufficient to cause early-onset, familial PD. A critical question concerning the molecular pathogenesis of PD is what contributory role, if any, is played by the SNCA gene in sporadic PD. The expansion of SNCA-Rep1, an upstream, polymorphic microsatellite of the SNCA gene, is associated with elevated risk for sporadic PD. However, whether SNCA-Rep1 is the causal variant and the underlying mechanism with which its effect is mediated by remained elusive. We report here the effects of three distinct SNCA-Rep1 variants in the brains of 72 mice transgenic for the entire human SNCA locus. Human SNCA-mRNA and protein levels were increased 1.7- and 1.25-fold, respectively, in homozygotes for the expanded, PD risk-conferring allele compared with homozygotes for the shorter, protective allele. When adjusting for the total SNCA-protein concentration (endogenous mouse and transgenic human) expressed in each brain, the expanded risk allele contributed 2.6-fold more to the SNCA steady-state than the shorter allele. Furthermore, targeted deletion of Rep1 resulted in the lowest human SNCA-mRNA and protein concentrations in murine brain. In contrast, the Rep1 effect was not observed in blood lysates from the same mice. These results demonstrate that Rep1 regulates human SNCA expression by enhancing its transcription in the adult nervous system and suggest that homozygosity for the expanded Rep1 allele may mimic locus multiplication, thereby elevating PD risk.

Published
2009

18. Prediction of cognition in Parkinson's disease with a clinical–genetic score: a longitudinal analysis of nine cohorts

Author

Scherzer, Clemens R., Hyman, Bradley T., Ivinson, Adrian J., Trisini-Lipsanopoulos, Ana, Franco, Daly, Burke, Kyle, Sudarsky, Lewis R., Hayes, Michael T., Umeh, Chizoba C., Sperling, Reisa, Growdon, John H., Schwarzschild, Michael A., Hung, Albert Y., Flaherty, Alice W., Blacker, Deborah, Wills, Anne-Marie, Sohur, U. Shivraj, Mejia, Nicte I., Viswanathan, Anand, Gomperts, Stephen N., Khurana, Vikram, Albers, Mark W., Alora-Palli, Maria, McGinnis, Scott, Sharma, Nutan, Dickerson, Bradford, Frosch, Matthew, Gomez-Isla, Teresa, Greenberg, Steven, Gusella, James, Hedden, Trey, Hedley-Whyte, E Tessa, Koenig, Aaron, Marquis-Sayagues, Marta, Marshall, Gad, Okereke, Olivia, Stemmer-Rachaminov, Anat, Kloppenburg, Jessica, Schlossmacher, Michael G., Selkoe, Dennis J., Yi, Thomas, Locascio, Joseph J., Li, Haining, Stalberg, Gabriel, Liao, Zhixiang, Barker, Roger, Foltynie, Tom, Williams-Gray, Caroline, Robbins, Trevor, Brayne, Carol, Mason, Sarah, Winder-Rhodes, Sophie, Breen, David P, Cummins, Gemma, Evans, Jonathan, van Hilten, Jacobus J., Marinus, Johan, Corvol, Jean-Christophe, Brice, Alexis, Elbaz, Alexis, Mallet, Alain, Vidailhet, Marie, Bonnet, Anne-Marie, Bonnet, Cecilia, Grabli, David, Hartmann, Andreas, Klebe, Stephan, Lacomblez, Lucette, Mangone, Graziella, Bourdain, Frédéric, Brandel, Jean-Philippe, Derkinderen, Pascal, Durif, Franck, Mesnage, Valérie, Pico, Fernando, Rascol, Olivier, Brefel-Courbon, Christine, Ory-Magne, Fabienne, Forlani, Sylvie, Lesage, Suzanne, Tahiri, Khadija, Albin, Roger, Alcalay, Roy, Ascherio, Alberto, Bowman, Dubois, Chen-Plotkin, Alice, Dawson, Ted, Dewey, Richard, German, Dwight, Saunders-Pullman, Rachel, Scherzer, Clemens, Vaillancourt, David, Petyuk, Vladislav, West, Andy, Zhang, Jing, Liu, Ganqiang, Locascio, Joseph J, Boot, Brendon, Page, Kara, Jansen, Iris E, Tanner, Caroline M, Lang, Anthony E, Eberly, Shirley, Ravina, Bernard, Shoulson, Ira, Cormier-Dequaire, Florence, Heutink, Peter, van Hilten, Jacobus J, Barker, Roger A, Williams-Gray, Caroline H, and Scherzer, Clemens R

Published
2017
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21. Defining the Riddle in Order to Solve It: There Is More Than One “Parkinson's Disease”

Author

Outeiro, Tiago F., primary, Alcalay, Roy N., additional, Antonini, Angelo, additional, Attems, Johannes, additional, Bonifati, Vincenzo, additional, Cardoso, Francisco, additional, Chesselet, Marie‐Françoise, additional, Hardy, John, additional, Madeo, Graziella, additional, McKeith, Ian, additional, Mollenhauer, Brit, additional, Moore, Darren J., additional, Rascol, Olivier, additional, Schlossmacher, Michael G., additional, Soreq, Hermona, additional, Stefanis, Leonidas, additional, and Ferreira, Joaquim J., additional

Published
2023
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22. Defining the Riddle in Order to Solve It: There Is More Than One “Parkinson's Disease”

Author

Outeiro, Tiago F., Alcalay, Roy N., Antonini, Angelo, Attems, Johannes, Bonifati, Vincenzo, Cardoso, Francisco, Chesselet, Marie-Françoise, Hardy, John, Madeo, Graziella, McKeith, Ian, Mollenhauer, Brit, Moore, Darren J., Rascol, Olivier, Schlossmacher, Michael G., Soreq, Hermona, Stefanis, Leonidas, Ferreira, Joaquim J., Outeiro, Tiago F., Alcalay, Roy N., Antonini, Angelo, Attems, Johannes, Bonifati, Vincenzo, Cardoso, Francisco, Chesselet, Marie-Françoise, Hardy, John, Madeo, Graziella, McKeith, Ian, Mollenhauer, Brit, Moore, Darren J., Rascol, Olivier, Schlossmacher, Michael G., Soreq, Hermona, Stefanis, Leonidas, and Ferreira, Joaquim J.

Abstract

Background: More than 200 years after James Parkinsondescribed a clinical syndrome based on his astute observations, Parkinson's disease (PD) has evolved into a complex entity, akin to the heterogeneity of other complex human syndromes of the central nervous system such as dementia, motor neuron disease, multiple sclerosis, and epilepsy. Clinicians, pathologists, and basic science researchers evolved arrange of concepts andcriteria for the clinical, genetic, mechanistic, and neuropathological characterization of what, in their best judgment, constitutes PD. However, these specialists have generated and used criteria that are not necessarily aligned between their different operational definitions, which may hinder progress in solving the riddle of the distinct forms of PD and ultimately how to treat them. Objective: This task force has identified current in consistencies between the definitions of PD and its diverse variants in different domains: clinical criteria, neuropathological classification, genetic subtyping, biomarker signatures, and mechanisms of disease. This initial effort for “defining the riddle” will lay the foundation for future attempts to better define the range of PD and its variants, as has been done and implemented for other heterogeneous neurological syndromes, such as stroke and peripheral neuropathy. We strongly advocate for a more systematic and evidence-based integration of our diverse disciplines by looking at well-defined variants of the syndrome of PD. Conclusion: Accuracy in defining endophenotypes of “typical PD” across these different but interrelated disciplines will enable better definition of variants and their stratification in therapeutic trials, a prerequisite for breakthroughs in the era of precision medicine. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on beh

Published
2023

23. Defining the Riddle in Order to Solve It:There Is More Than One “Parkinson's Disease”

Author

Outeiro, Tiago F., Alcalay, Roy N., Antonini, Angelo, Attems, Johannes, Bonifati, Vincenzo, Cardoso, Francisco, Chesselet, Marie Françoise, Hardy, John, Madeo, Graziella, McKeith, Ian, Mollenhauer, Brit, Moore, Darren J., Rascol, Olivier, Schlossmacher, Michael G., Soreq, Hermona, Stefanis, Leonidas, Ferreira, Joaquim J., Outeiro, Tiago F., Alcalay, Roy N., Antonini, Angelo, Attems, Johannes, Bonifati, Vincenzo, Cardoso, Francisco, Chesselet, Marie Françoise, Hardy, John, Madeo, Graziella, McKeith, Ian, Mollenhauer, Brit, Moore, Darren J., Rascol, Olivier, Schlossmacher, Michael G., Soreq, Hermona, Stefanis, Leonidas, and Ferreira, Joaquim J.

Abstract

Background: More than 200 years after James Parkinsondescribed a clinical syndrome based on his astute observations, Parkinson's disease (PD) has evolved into a complex entity, akin to the heterogeneity of other complex human syndromes of the central nervous system such as dementia, motor neuron disease, multiple sclerosis, and epilepsy. Clinicians, pathologists, and basic science researchers evolved arrange of concepts andcriteria for the clinical, genetic, mechanistic, and neuropathological characterization of what, in their best judgment, constitutes PD. However, these specialists have generated and used criteria that are not necessarily aligned between their different operational definitions, which may hinder progress in solving the riddle of the distinct forms of PD and ultimately how to treat them. Objective: This task force has identified current in consistencies between the definitions of PD and its diverse variants in different domains: clinical criteria, neuropathological classification, genetic subtyping, biomarker signatures, and mechanisms of disease. This initial effort for “defining the riddle” will lay the foundation for future attempts to better define the range of PD and its variants, as has been done and implemented for other heterogeneous neurological syndromes, such as stroke and peripheral neuropathy. We strongly advocate for a more systematic and evidence-based integration of our diverse disciplines by looking at well-defined variants of the syndrome of PD. Conclusion: Accuracy in defining endophenotypes of “typical PD” across these different but interrelated disciplines will enable better definition of variants and their stratification in therapeutic trials, a prerequisite for breakthroughs in the era of precision medicine.

Published
2023

25. Holocranohistochemistry enables the visualization of α-synuclein expression in the murine olfactory system and discovery of its systemic anti-microbial effects

Author

Tomlinson, Julianna J., Shutinoski, Bojan, Dong, Li, Meng, Fanyi, Elleithy, Dina, Lengacher, Nathalie A., Nguyen, Angela P., Cron, Greg O., Jiang, Qiubo, Roberson, Erik D., Nussbaum, Robert L., Majbour, Nour K., El-Agnaf, Omar M., Bennett, Steffany A., Lagace, Diane C., Woulfe, John M., Sad, Subash, Brown, Earl G., and Schlossmacher, Michael G.

Published
2017
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28. Ubiquitination of a Novel form of α-Synuclein by Parkin

Author

Shimura, Hideki, Schlossmacher, Michael G., Hattori, Nobutaka, Frosch, Matthew P., Trockenbacher, Alexander, Schneider, Rainer, Mizuno, Yoshikuni, Kosik, Kenneth S., Selkoe, Dennis J., Mizuno, Yoshikuni, editor, Fisher, Abraham, editor, and Hanin, Israel, editor

Published
2002
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34. Genetic and pharmacological reduction of CDK14 mitigates synucleinopathy

Author

Parmasad, Jean-Louis A, primary, Ricke, Konrad M, additional, Stykel, Morgan G, additional, Buchner-Duby, Brodie, additional, Lian, Eric, additional, Nguyen, Benjamin, additional, Lengacher, Nathalie A, additional, Geertsma, Haley M, additional, Bruce, Amanda, additional, Callaghan, Steve M, additional, Joselin, Alvin, additional, Tomlinson, Julianna J, additional, Schlossmacher, Michael G, additional, Stanford, William L, additional, Brundin, Patrik, additional, Ryan, Scott D, additional, and Rousseaux, Maxime W.C., additional

Published
2022
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39. BATL: Bayesian annotations for targeted lipidomics

Author

Chitpin, Justin G, primary, Surendra, Anuradha, additional, Nguyen, Thao T, additional, Taylor, Graeme P, additional, Xu, Hongbin, additional, Alecu, Irina, additional, Ortega, Roberto, additional, Tomlinson, Julianna J, additional, Crawley, Angela M, additional, McGuinty, Michaeline, additional, Schlossmacher, Michael G, additional, Saunders-Pullman, Rachel, additional, Cuperlovic-Culf, Miroslava, additional, Bennett, Steffany A L, additional, and Perkins, Theodore J, additional

Published
2021
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41. Association between α-synuclein blood transcripts and early, neuroimaging-supported Parkinson’s disease

Author

Locascio, Joseph J., Eberly, Shirley, Liao, Zhixiang, Liu, Ganqiang, Hoesing, Ashley N., Duong, Karen, Trisini-Lipsanopoulos, Ana, Dhima, Kaltra, Hung, Albert Y., Flaherty, Alice W., Schwarzschild, Michael A., Hayes, Michael T., Wills, Anne-Marie, Shivraj Sohur, U., Mejia, Nicte I., Selkoe, Dennis J., Oakes, David, Shoulson, Ira, Dong, Xianjun, Marek, Ken, Zheng, Bin, Ivinson, Adrian, Hyman, Bradley T., Growdon, John H., Sudarsky, Lewis R., Schlossmacher, Michael G., Ravina, Bernard, and Scherzer, Clemens R.

Published
2015
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45. Parkinson’s disease-linked LRRK2 is expressed in circulating and tissue immune cells and upregulated following recognition of microbial structures

Author

Hakimi, Mansoureh, Selvanantham, Thirumahal, Swinton, Erika, Padmore, Ruth F., Tong, Youren, Kabbach, Ghassan, Venderova, Katerina, Girardin, Stephen E., Bulman, Dennis E., Scherzer, Clemens R., LaVoie, Matthew J., Gris, Denis, Park, David S., Angel, Jonathan B., Shen, Jie, Philpott, Dana J., and Schlossmacher, Michael G.

Published
2011
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47. GATA transcription factors directly regulate the Parkinson's disease-linked gene [alpha]-synuclein

Author

Scherzer, Clemens R., Grass, Jeffrey A., Liao, Zhixiang, Pepivani, Imelda, Zheng, Bin, Eklund, Aron C., Ney, Paul A., Ng, Juliana, McGoldrick, Meghan, Mollenhauer, Brit, Bresnick, Emery H., and Schlossmacher, Michael G.

Subjects
DNA binding proteins -- Properties, Parkinson's disease -- Development and progression, Parkinson's disease -- Genetic aspects, Gene expression -- Research, DNA microarrays -- Usage, Genetic regulation -- Research, Science and technology
Abstract

Increased [alpha]-synuclein gene (SNCA) dosage due to locus multiplication causes autosomal dominant Parkinson's disease (PD). Variation in SNCA expression may be critical in common, genetically complex PD but the underlying regulatory mechanism is unknown. We show that SNCA and the heme metabolism genes ALAS2, FECH, and BLVRB form a block of tightly correlated gene expression in 113 samples of human blood, where SNCA naturally abounds (validated P = 1.6 x [10.sup.-11], 1.8 x [10.sup.-10], and 6.6 x [10.sup.-5]). Genetic complementation analysis revealed that these four genes are co-induced by the transcription factor GATA-1. GATA-1 specifically occupies a conserved region within SNCA intron-1 and directly induces a 6.9-fold increase in [alpha]-synuclein. Endogenous GATA-2 is highly expressed in substantia nigra vulnerable to PD, occupies intron-1, and modulates SNCA expression in dopaminergic cells. This critical link between GATA factors and SNCA may enable therapies designed to lower [alpha]-synuclein production. [alpha]-synuclein dosage | GATA-1 | GATA-2 | gene expression | microarray

Published
2008

48. Conversations With Dr. Oleh Hornykiewicz, Founding Father of the Dopamine Era in Parkinson's: How Do You Wish to Be Remembered?

Author

McGovern Institute for Brain Research at MIT, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Schlossmacher, Michael G., Graybiel, Ann M, McGovern Institute for Brain Research at MIT, Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Schlossmacher, Michael G., and Graybiel, Ann M

Abstract

On May 26, 2020, Dr. Oleh Hornykiewicz died at the age of 93 years. His twin discoveries in the early 1960s of dopamine deficiency in the brains of subjects with Parkinson's disease and the amelioration of patients' symptoms by levodopa therapy represent milestone events in the history of medicine. These breakthroughs enabled much-needed relief for millions of patients suffering from neurological disorders every year and have given rise to the field of dopamine signaling in the regulation of complex behaviors in primates. What did Dr. Hornykiewicz, who was actively engaged in research until shortly before his 91st birthday, wish to pass on to younger scientists? What were his thoughts regarding the elusive cause of Parkinson's disease? How did he wish to be remembered? Here, the authors, one a former student and the other an admired colleague, recall messages conveyed by Dr. Hornykiewicz in public lectures; they also share the content of conversations and letters exchanged with him since 2004, as he began to reflect on his legacy. Through Dr. Hornykiewicz's own words and writings, the picture emerges of an extraordinarily committed scientist, who was exemplary in his professional integrity, who knew how to deploy a gallous sense of humor, who displayed little patience for physicians offering advice, and who kept any sense of pride over his monumental contributions private. When asked at the age of 91 years about the secrets of his long and fulfilled career in neuroscience, he identified himself as “a mad scientist.…I am someone who continuously fantasizes. I am someone who chases fantastical ideas and who keeps on dreaming…”, and as a man who was supported by the loving companionship of his wife, Christine. © 2020 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Published
2021

50. BATL: Bayesian annotations for targeted lipidomics

Author

Chitpin, Justin G., primary, Surendra, Anuradha, additional, Nguyen, Thao T., additional, Taylor, Graeme P., additional, Xu, Hongbin, additional, Alecu, Irina, additional, Ortega, Roberto, additional, Tomlinson, Julianna J., additional, Crawley, Angela M., additional, McGuinty, Michaeline, additional, Schlossmacher, Michael G., additional, Saunders-Pullman, Rachel, additional, Cuperlovic-Culf, Miroslava, additional, Bennett, Steffany A.L., additional, and Perkins, Theodore J., additional

Published
2021
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