Autophagy in neurodegenerative diseases and metal neurotoxicity

Ziyan Zhang, Mahfuzur Miah, Megan Culbreth, Michael Aschner

Research output: Contribution to journalArticle

40 Scopus citations

Abstract

Autophagy generally refers to cell catabolic and recycling process in which cytoplasmic components are delivered to lysosomes for degradation. During the last two decades, autophagy research has experienced a recent boom because of a newfound connection between this process and many human diseases. Autophagy plays a significant role in maintaining cellular homeostasis and protects cells from varying insults, including misfolded and aggregated proteins and damaged organelles, which is particularly crucial in neuronal survival. Mounting evidence has implicated autophagic dysfunction in the pathogenesis of several major neurodegenerative disorders, such as Parkinson’s disease, Alzheimer’s disease and Huntington’s disease, where deficient elimination of abnormal and toxic protein aggregates promotes cellular stress, failure and death. In addition, autophagy has also been found to affect neurotoxicity induced by exposure to essential metals, such as manganese, copper, and iron, and other heavy metals, such as cadmium, lead, and methylmercury. This review examines current literature on the role of autophagy in the mechanisms of disease pathogenesis amongst common neurodegenerative disorders and of metal-induced neurotoxicity.

Original languageEnglish (US)
Pages (from-to)409-422
Number of pages14
JournalNeurochemical Research
Volume41
Issue number1-2
DOIs
StatePublished - Feb 11 2016

Keywords

  • Autophagy
  • Metals
  • Neurodegeneration
  • Neurotoxicity

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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