Autophagic/lysosomal dysfunction in Alzheimer's disease

Miranda E. Orr, Salvatore Oddo

Research output: Contribution to journalReview article

66 Scopus citations

Abstract

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.

Original languageEnglish (US)
Article number53
JournalAlzheimer's Research and Therapy
Volume5
Issue number5
DOIs
StatePublished - Nov 25 2013

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cognitive Neuroscience

Fingerprint Dive into the research topics of 'Autophagic/lysosomal dysfunction in Alzheimer's disease'. Together they form a unique fingerprint.

  • Cite this