Results 121 to 130 of about 67,783 (305)

Equine models in translational medicine: A comparative approach to human health

Animal Models and Experimental Medicine, EarlyView.
This diagram summarizes and contrasts rodent and equine models, outlining their strengths, limitations, and applications. Horses offer naturally occurring diseases, genetic and physiological similarities to humans, and suitability for longitudinal and clinical‐scale studies.
Shayan Boozarjomehri Amnieh, Katarzyna Ropka‐Molik   +1 more
wiley   +1 more source

Association between Plasma P‐tau217 and Alzheimer's Copathology and Cognitive Decline in Parkinson's Disease

Annals of Neurology, EarlyView.
Objective Clinically relevant Alzheimer's disease co‐pathology is common in Lewy body disorders. Plasma P‐tau217 is a sensitive biomarker for amyloid and tau pathology in Alzheimer's disease. The objective was to determine if plasma P‐tau217 associates with Alzheimer's disease co‐pathology and cognition in Lewy body disorders. Methods Participants had (
Thomas F. Tropea, Patricia Aldea Stevenson, Matthew Flitter, David Meehan, Amanda Morris, Ming Lu, Leonardo Iaccarino, Emily C. Collins, Michael E. Hodsdon, David Irwin, Meredith Spindler, Andres Deik, Nabila Dahodwala, Katheryn A.Q. Cousins, David A. Wolk, Leslie Shaw, Daniel Weintraub, Edward B. Lee, Alice Chen‐Plotkin, Mark Mintun, Andrew Siderowf   +20 more
wiley   +1 more source

Alpha-synuclein inclusions reduced by PIKfyve inhibition in Parkinson disease cell models

Neurobiology of Disease
Objective: Parkinson's disease (PD) pathophysiology is associated with a progressive loss of dopaminergic neurons in the substantia nigra and accumulation of insoluble inclusions of misfolded alpha-synuclein.
Sara Lucas-Del-Pozo, Giuseppe Uras, Federico Fierli, Veronica Lentini, Sofia Koletsi, Carlos Lazaro-Hernandez, Kai-Yin Chau, Derralynn A. Hughes, Anthony H.V. Schapira   +8 more
doaj   +1 more source

Structures of fibrils formed by α-synuclein hereditary disease mutant H50Q reveal new polymorphs. [PDF]

, 2019
Deposits of amyloid fibrils of α-synuclein are the histological hallmarks of Parkinson's disease, dementia with Lewy bodies and multiple system atrophy, with hereditary mutations in α-synuclein linked to the first two of these conditions.
Boyer, David R, Eisenberg, David S, Fan, Weijia, Jiang, Lin, Li, Binsen, Sawaya, Michael R, Sun, Chuanqi   +6 more
core  

Predominance of Ferroptotic Cell Death Mechanisms in Substantia Nigra Neurodegeneration in Parkinson's Disease

Annals of Neurology, EarlyView.
Objective The extent of neuronal loss in Parkinson's disease (PD) and the pathogenic processes underlying neuronal dysfunction and loss remain poorly understood. Here, we analyzed the expression of key molecules representing different cell death signaling pathways and their association with Lewy pathology, dopaminergic (DA) neuron loss and stage of PD ...
Yue Jing Heng, Anusha Jayaraman, Richard Reynolds, Jia Nee Foo   +3 more
wiley   +1 more source

Acetylated α-Tubulin and α-Synuclein: Physiological Interplay and Contribution to α-Synuclein Oligomerization

International Journal of Molecular Sciences; Volume 24; Issue 15; Pages: 12287, 2023
Emerging evidence supports that altered α-tubulin acetylation occurs in Parkinson’s disease (PD), a neurodegenerative disorder characterized by the deposition of α-synuclein fibrillary aggregates within Lewy bodies and nigrostriatal neuron degeneration. Nevertheless, studies addressing the interplay between α-tubulin acetylation
openaire   +1 more source

Diffusion MRI and α‐Synuclein Seed Amplification Status in Parkinson's Disease

Annals of Neurology, EarlyView.
Objective Positive α‐synuclein seed amplification assay (SAA) is a biomarker found in most people with Parkinson's disease (PD). We explored if free‐water (FW) imaging detects microstructural differences in the brains of patients with early PD with SAA+ or SAA– status.
Shannon Y. Chiu, Wei‐en Wang, Robin Chen, Jesse C. DeSimone, Derek B. Archer, Charles H. Adler, Shyamal H. Mehta, Sara R. Dresler, Melissa J. Armstrong, Nikolaus McFarland, Michael Okun, David E. Vaillancourt, Parkinson's Progression Markers Initiative, Neha Prakash, Tanya Simuni, Nabila Dahodwala, Caroline Tanner, Lana Chahine, Brit Mollenhauer, Anat Mirelman, Roy Alcalay; Katherine Leaver, Marie Saint‐Hilaire, Ruth Schneider, Christopher Tarolli, Werner Poewe, Aleksandar Videnovic, David Standaert, Marissa Dean, Sonja Jonsdottir, Rejko Krueger, Claire Pauly, Stewart Factor, Penelope Hogarth, Robert Hauser, Amy Amara, Michelle Fullard, Cyrus Zabetian, Hubert Fernandez, Kathrin Brockmann, Isabel Wurster, Yen Tai, Paolo Barone, Marina Picillo, Stuart Isaacson, Alberto Espay, Eduardo Tolosa, Javier Ruiz Martinez, Leonidas Stefanis, Kelvin Chou, Lorraine Kalia, Connie Marras, David Grimes, Tiago Mestre, Rajesh Pahwa, Mark Lew, Holly Shill, Shyamal Mehta, Giulietta Riboldi, Nikolaus McFarland, Ron Postuma, Zoltan Mari, David Ledingham, Nicola Pavese, Michele Hu, Norbert Brueggemann, Christine Klein, Bastiaan Bloem, Cristina Simonet, Alastair Noyce, Anette Janzen, David Pedrosa, Wolfgang Oertel, Njideka Okubadejo, David Shprecher, Arjun Tarakad, Emile Moukheiber, Joy Antala, Carla Aranda, Karen Williams, Sophia Melton, Karina Benson, Ashwini Ramachandran, Danielle Potts, Grace LaMoure, Ritikha Vengadesh, Ryan Manzler, Jaime Heller, Primi Ranola, Farah Kausar, Sherri Mosovsky, Diana Willeke, Elizabeth Kalinkara Gomez, Janelle Rodriguez, Nobuko Kemmotsu, May Eshel, Deborah Raymond, Abigail Desrosiers, Raymond James, Lauren Jackson, Iris Egner, Wesley Schlett, Courtney Blair, Lauren Ruffrage, Berenice Sevilla, Barbara Sommerfeld, Dustin Le, Erica Botting, Gabriella Mazur, Daniele Derlein, Ying Liu, Ciera Cobb, Olivia Masiewicz, Jennifer Mule, Michael Morsillo, Ella Hilt, Lisbeth Pennente, Bobbie Stubbeman, Alicia Garrido, Valeria Ravasi, Ioana Croitoru, Christos Koros, Nikolas Papagiannakis, Frank Ferrari, Mengyu Zheng, Shawna Reddie, Alicia Alejandra, Andrea Gray, Alejandra Valenzuela, Caitlin Goodman, Sara Dresler, Neil Santos, Fahrial Esha, Kyle Rizer, Nadine Zablith, Liliana Dumitrescu, Debra Galley, Victoria Kate Foster, Jamil Razzaque, Madita Grümmer, Yara Krasowski, Elisabeth Sittig, Oluwadamilola Ojo, Kelly Clark, Rory Mahabir, Kori Ribb, Shamera Willoughby   +145 more
wiley   +1 more source

Rab1A Over-Expression Prevents Golgi Apparatus Fragmentation and Partially Corrects Motor Deficits in an Alpha-Synuclein Based Rat Model of Parkinson's Disease

Journal of Parkinson’s Disease, 2011
Although the overabundance of human alpha-synuclein in nigral dopaminergic neurons is considered to play a pathogenic role in Parkinson's disease (PD), it remains unclear how alpha-synuclein leads to neuronal degeneration and motor symptoms.
P.G. Coune, J.C. Bensadoun, P. Aebischer, B.L. Schneider   +3 more
doaj   +1 more source

Exosomal cell-to-cell transmission of alpha synuclein oligomers

Molecular Neurodegeneration, 2012
Background Aggregation of alpha-synuclein (αsyn) and resulting cytotoxicity is a hallmark of sporadic and familial Parkinson’s disease (PD) as well as dementia with Lewy bodies, with recent evidence implicating oligomeric and pre-fibrillar forms of αsyn ...
Danzer Karin M, Kranich Lisa R, Ruf Wolfgang P, Cagsal-Getkin Ozge, Winslow Ashley R, Zhu Liya, Vanderburg Charles R, McLean Pamela J   +7 more
doaj   +1 more source

Analysis of Single Particles of Amyloid Beta and α‐Synuclein With Seeded Amplification for the Diagnosis of Alzheimer's and Parkinson's Disease

Biotechnology and Applied Biochemistry, EarlyView.
ABSTRACT Neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD), are characterized by the pathological aggregation of specific proteins such as amyloid beta (Aβ) and α‐synuclein, respectively. Early detection of these protein aggregates in biological fluids could facilitate timely diagnosis and therapeutic ...
Alexandra Dybala, Marlene Pils, Oliver Bannach, Gültekin Tamgüney, Detlev Riesner   +4 more
wiley   +1 more source