Therapeutic induction of autophagy to modulate neurodegenerative disease progression
Abstract
Warren E HOCHFELD, Shirley LEE, David C RUBINSZTEIN*
Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, CB2 0XY, United Kingdom
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.
Keywords: autophagy; neurodegenerative disease; Alzheimer disease; Huntington’s disease; Parkinson’s disease; amyotropic lateral sclerosis; mTOR; rapamycin; IP3; lithium
DCR is funded by a Wellcome Trust Principal Fellowship, a Wellcome Trust/MRC Strategic Grant on Alzheimer’s disease, the Tau Consortium, and the Biomedical Research Unit in Dementia at Addenbrooke’s Hospital. We are grateful to HM’s Government of Brunei Darussalam (SHFL), The Oppenheimer Memorial Trust, The Cambridge Commonwealth Trust and The Higher Education Funding Council for England (WEH).
* To whom correspondence should be addressed.
E-mail dcr1000@cam.ac.uk
Received 2012-11-09 Accepted 2012-12-20
Keywords:
Department of Medical Genetics, University of Cambridge, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, CB2 0XY, United Kingdom
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.
Keywords: autophagy; neurodegenerative disease; Alzheimer disease; Huntington’s disease; Parkinson’s disease; amyotropic lateral sclerosis; mTOR; rapamycin; IP3; lithium
DCR is funded by a Wellcome Trust Principal Fellowship, a Wellcome Trust/MRC Strategic Grant on Alzheimer’s disease, the Tau Consortium, and the Biomedical Research Unit in Dementia at Addenbrooke’s Hospital. We are grateful to HM’s Government of Brunei Darussalam (SHFL), The Oppenheimer Memorial Trust, The Cambridge Commonwealth Trust and The Higher Education Funding Council for England (WEH).
* To whom correspondence should be addressed.
E-mail dcr1000@cam.ac.uk
Received 2012-11-09 Accepted 2012-12-20