Small molecule enhancers of autophagy for neurodegenerative diseases.

@article{citeulike:3134609, 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.}, address = {Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Road, Cambridge, UK. ss457@cam.ac.uk}, author = {Sarkar, S. and Rubinsztein, D. C. }, citeulike-article-id = {3134609}, doi = {http://dx.doi.org/10.1039/b804606a}, issn = {1742-2051}, journal = {Molecular bioSystems}, keywords = {autophagy, neurodegeneration}, month = {September}, number = {9}, pages = {895--901}, posted-at = {2008-08-19 01:42:04}, priority = {2}, title = {Small molecule enhancers of autophagy for neurodegenerative diseases.}, url = {http://dx.doi.org/10.1039/b804606a}, volume = {4}, year = {2008} }

TY - JOUR ID - citeulike:3134609 L3 - citeulike-article-id:3134609 N2 - 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. IS - 9 JF - Molecular bioSystems SN - 1742-2051 AD - Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Road, Cambridge, UK. ss457@cam.ac.uk EP - 901 TI - Small molecule enhancers of autophagy for neurodegenerative diseases. VL - 4 SP - 895 KW - autophagy KW - neurodegeneration AU - Sarkar, S AU - Rubinsztein, DC PY - 2008/09// UR - http://dx.doi.org/10.1039/b804606a ER -