Autophagy in neuroprotection and neurodegeneration: A question of balance

Salvatore J. Cherra, Charleen T. Chu

Research output: Contribution to journalReview articlepeer-review

163 Scopus citations


A central issue in developing therapies for neurodegenerative diseases involves understanding why adaptive responses to stress or injury fail to prevent synaptic dysfunction and neuronal cell death. Macroaufophagy is a major, evolutionarily conserved response to nutrient and bioenergetic stresses, which has the capacity to remove aggregated proteins and damaged organelles such as mitochondria. This has prompted intense interest in autophagy-related therapies for Huntington's, Alzheimer's, Parkinson's, stroke and other neurological diseases. However, excessive or imbalanced induction of autophagic recycling can actively contribute to neuronal atrophy, neurite degeneration and cell death. xidative-, aging- and disease-related increases in demand for autophagy, coupled with declining axonal trafficking, lysosomal degradation or biosynthetic efficiencies promote increased susceptibility to a harmful state of autophagic stress. A more complete understanding of dysfunction along the entire spectrum of autophagic recycling, from autophagosome formation through clearance and regeneration of new cellular components, is necessary to restore balance to the system, promote neuronal health and maximize therapeutic potentials.

Original languageEnglish
Pages (from-to)309-323
Number of pages15
JournalFuture Neurology
Issue number3
StatePublished - May 2008


  • Aging
  • Alzheimer's disease
  • Autophagy
  • Huntington's disease
  • Hypoxic-ischemic brain injury
  • Lysosomal storage disease
  • Neurite degeneration
  • Neuronal cell death
  • Parkinson's disease
  • Protein aggregation

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology


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