Autophagy serves as the sole catabolic mechanism for degrading organelles and protein aggregates. Increasing evidence implicates autophagic dysfunction in Alzheimer’s disease (AD) and other neurodegenerative diseases associated with protein misprocessing and accumulation. Under physiologic conditions, the autophagic/lysosomal system efficiently recycles organelles and substrate proteins. However, reduced autophagy function leads to the accumulation of proteins and autophagic and lysosomal vesicles. These vesicles contain toxic lysosomal hydrolases as well as the proper cellular machinery to generate amyloid-beta, the major component of AD plaques. Here, we provide an overview of current research focused on the relevance of autophagic/lysosomal dysfunction in AD pathogenesis as well as potential therapeutic targets aimed at restoring autophagic/lysosomal pathway function.
Autophagic/lysosomal dysfunction in Alzheimer’s disease
Published 2013 in Alzheimer's Research & Therapy
ABSTRACT
PUBLICATION RECORD
- Publication year
2013
- Venue
Alzheimer's Research & Therapy
- Publication date
2013-10-29
- Fields of study
Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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