Biases inα-synuclein immuno-quantitation:a core problem for basic and ancillary studies of Parkinson’s disease and multiple system atrophy  

作　　者：Florent Laferrière Ludivine Sabatier Stéphane Claverol Francesca De Giorgi François Ichas 

机构地区：[1]Univ.Bordeaux,CNRS,IMN,UMR 5293,33000 Bordeaux,France [2]Bordeaux Proteome,Univ.Bordeaux,Bordeaux,France [3]DiSTeBA,Univ.Salento,Anatomia Umana,Lecce,Italy

出　　处：《Translational Neurodegeneration》2024年第1期874-878,共5页转化神经变性病(英文)

基　　金：support from the French Agence Nationale de la Recherche(ANR),under grant ANR-22-CE16-0002(project ASAPS);supported by the Center of Excellence in Neurodegeneration(CoEN)Bordeaux Initiative for Neurodegenerative Disorders(BIND)reference CHUBX 2022/07,by the MSA Coalition Global Seed Grant reference MSAC-2022-12-005(project FibrilloScreen).

摘　　要：Parkinson’s disease(PD)and multiple system atrophy(MSA)are distinct neurodegenerative disorders sharing the accumulation of pathological alpha-synuclein(α-syn)amyloids in neurons or glial cells.Amyloidogenesis arises with the nucleation ofβ-sheet foldedα-syn assemblies serving as conformational templates in the amyloid buildup at the expense of monomericα-syn(for review see[1]).This pathological aggregation process can be experimentally mimicked in test tubes with recombinantα-syn[2],or by treatment with brain-derivedα-syn amy-loids or syntheticα-syn pre-formed fibrils(PFFs)in bio-logical systems[3-5].Noteworthy,scoring pathological aggregation in biological samples and qualifying the spe-cific seeding propensity of extracts for comparing them both depend on the capability of identifying and quanti-fying the amyloid share of totalα-syn.

关 键 词：ATROPHY AMYLOID aggregation 

分 类 号：R74[医药卫生—神经病学与精神病学]