Journal
BRAIN
Volume 140, Issue -, Pages 266-278Publisher
OXFORD UNIV PRESS
DOI: 10.1093/brain/aww230
Keywords
Alzheimer's disease; alpha-synuclein; Parkinson's disease; prion-like; tau
Categories
Funding
- UK Medical Research Council [MC_U105184291]
- EU Joint Programme - Neurodegenerative Disease Research
- MRC [MC_U105184291, MC_EX_MR/N027892/1] Funding Source: UKRI
- Medical Research Council [MC_U105184291, MC_EX_MR/N027892/1] Funding Source: researchfish
Ask authors/readers for more resources
The abnormal aggregation of a small number of known proteins underlies the most common human neurodegenerative diseases. In tauopathies and synucleinopathies, the normally soluble intracellular proteins tau and alpha-synuclein become insoluble and filamentous. In recent years, non-cell autonomous mechanisms of aggregate formation have come to the fore, suggesting that nucleation-dependent aggregation may occur in a localized fashion in human tauopathies and synucleinopathies, followed by seed-dependent propagation. There is a long prodromal phase between the formation of protein aggregates and the appearance of the first clinical symptoms, which manifest only after extensive propagation, opening novel therapeutic avenues.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available