Therapeutic induction of autophagy to modulate neurodegenerative disease progression

There is accumulating evidence that aggregating, misfolded proteins may have an impact on autophagic function, suggesting that this could be a secondary pathological mechanism in many diseases. In this review, we focus on the role of autophagy in four major neurodegenerative diseases: Alzheimer disease (AD), Huntington's disease (HD), Parkinson's disease (PD) and amyotropic lateral sclerosis.

• Publication year

  2013

• Venue

  Acta Pharmacologica Sinica

• Publication date

  2013-02-04

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1038/aps.2012.189PMID 23377551PMCID 3647215
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• α-Synuclein Is Degraded by Both Autophagy and the Proteasome*

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• Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy.

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• Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease.

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• Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

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• Antibody to an abnormal protein in amyotrophic lateral sclerosis identifies Lewy body-like inclusions in ALS and Lewy bodies in Parkinson's disease.

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• Bunina bodies in amyotrophic lateral sclerosis immunostained with rabbit anti-cystatin C serum.

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• Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increases beta-protein production.

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