Jump to main content
Jump to site search
Access to RSC content Close the message box

Continue to access RSC content when you are not at your institution. Follow our step-by-step guide.


Issue 9, 2008
Previous Article Next Article

Small molecule enhancers of autophagy for neurodegenerative diseases

Author affiliations

Abstract

Neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, prion diseases and polyglutamine disorders, including Huntington’s disease and various spinocerebellar ataxias, are associated with the formation of protein aggregates. These aggregates and/or their precursors are thought to be toxic disease-causing species. Autophagy is a major degradation pathway for intracytosolic aggregate-prone proteins, including those associated with neurodegeneration. It is a constitutive self-degradative process involved both in the basal turnover of cellular components and in response to nutrient starvation in eukaryotes. Enhancing autophagy may be a possible therapeutic strategy for neurodegenerative disorders where the mutant proteins are autophagy substrates. In cell and animal models, chemical induction of autophagy protects against the toxic insults of these mutant aggregate-prone proteins by enhancing their clearance. We will discuss various autophagy-inducing small molecules that have emerged in the past few years that may be leads towards the treatment of such devastating diseases.

Graphical abstract: Small molecule enhancers of autophagy for neurodegenerative diseases

Back to tab navigation

Article information


First published
04 Jul 2008

Mol. BioSyst., 2008,4, 895-901
Article type
Highlight

Small molecule enhancers of autophagy for neurodegenerative diseases

S. Sarkar and D. C. Rubinsztein, Mol. BioSyst., 2008, 4, 895
DOI: 10.1039/B804606A

Search articles by author

Spotlight

Advertisements