Autophagy in aging and neurodegenerative diseases: implications for pathogenesis and therapy

Neurobiol Aging. 2014 May;35(5):941-57. doi: 10.1016/j.neurobiolaging.2013.11.019. Epub 2013 Nov 28.

Abstract

Neurodegenerative diseases, such as Alzheimer's disease Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis, share a common cellular and molecular pathogenetic mechanism involving aberrant misfolded protein or peptide aggregation and deposition. Autophagy represents a major route for degradation of aggregated cellular proteins and dysfunctional organelles. Emerging studies have demonstrated that up-regulation of autophagy can lead to decreased levels of these toxic aggregate-prone proteins, and is beneficial in the context of aging and various models of neurodegenerative diseases. Understanding the signaling pathways involved in the regulation of autophagy is crucial to the development of strategies for therapy. This review will discuss the cellular and molecular mechanisms of autophagy and its important role in the pathogenesis of aging and neurodegenerative diseases, and the ongoing drug discovery strategies for therapeutic modulation.

Keywords: Aging; Alzheimer's disease; Amyotrophic lateral sclerosis; Autophagy; Huntington's disease; Lysosomal storage disorders; Parkinson's disease; Therapy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging / genetics*
  • Aging / pathology*
  • Autophagy* / genetics
  • Autophagy* / physiology
  • Molecular Targeted Therapy
  • Neurodegenerative Diseases / genetics*
  • Neurodegenerative Diseases / pathology*
  • Neurodegenerative Diseases / therapy
  • Neurons / pathology*
  • Neurons / physiology*
  • Signal Transduction / genetics
  • Signal Transduction / physiology
  • TOR Serine-Threonine Kinases / physiology

Substances

  • TOR Serine-Threonine Kinases