SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis

By Dohoon Kim, Minh N. H. Nguyen, Matthew M. Dobbin, André Fischer, F. Sananbenesi, J. T. Rodgers, I. Delalle, Joseph A. Baur, Guangchao Sui, S. Armour and 3 more. EMBO Journal, 2007

1,067 citations recorded by the source corpus.

Subfields: Epidemiology, Geriatrics and Gerontology, Physiology

View Paper: https://www.semanticscholar.org/paper/4eae108847e7b2f667ed09397e17826838f95555

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In Epidemiology

In Geriatrics and Gerontology

In Physiology

Citations in the corpus

Neural mechanisms of ageing and cognitive decline (2010, background): “SIRT1 also protects against amyloid-β toxicity in cell culture and neurodegeneration in the p25/CDK5 mouse model, which recapitulates aspects of Alzheimer's disease pathology and tauopath”
Multiple roles of HDAC inhibition in neurodegenerative conditions (2009, background): “Paradoxically, in rare cases, the activity rather than the inhibition of certain HDAC isoforms has neuroprotective effects, and these include HDAC1 in the AD model, and SIRT1 in AD and ALS models [104].”
SIRTUIN 1 AND SIRTUIN 3: PHYSIOLOGICAL MODULATORS OF METABOLISM (2012, background): “Recent studies have suggested that SIRT1 is responsible for protection from neuronal, and specifically axonal, degeneration (16, 90, 169, 336), suggesting that the activation of SIRT1 might be important in the treatment of Alzheimer’s disease or other neurodegenerative diseases such as Huntington’s ”
Therapeutic application of histone deacetylase inhibitors for central nervous system disorders (2008, background): “Activation of SIRT1, either pharmacologically or genetically, and conditional calorie restriction can both exert neuroprotective effects in various disease model”
Neuroprotective role of SIRT1 in mammalian models of Huntington’s disease through activation of multiple SIRT1 targets (2011, neutral): “We thank L. Tsai at Massachusetts Institute of Technology for providing Sirt1 and H363Y retrovirus constructs, S. Imai at Washington University for providing Sir2 complementary DNAs (cDNAs), M. Macdonald at Harvard Medical School for providing STHdh Q7/Q7 and STHdh Q111/Q111 cells, S. Li n p g”
Acetylation of tau inhibits its degradation and contributes to tauopathy. (2010, positive): “Overexpressing SIRT1 protects against neuronal loss in the inducible p25 transgenic mouse, a model of AD and tauopathy (Kim et al., 2007).”
DNA damage and its links to neurodegeneration (2014, positive): “However, a separate study noted that overexpression of the NAD+-dependent deacetylase, SIRT1, can also prevent neuronal loss in CK-p25 mice (Kim et al., 2007).”
Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders (2010, positive): “It has also been reported that the SIRT1 activator resveratrol can protect neurons against degeneration in experimental models of Alzheimer’s disease and amyotrophic lateral sclerosis (229).”
SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, background): “Part of the difficulty has arisen from the fact that doses of resveratrol given to animals are wildly variable and concentrations used on cells vary greatly as well (Kim et al., 2007; Park et al., 2012).”
Animal models of Alzheimer's disease and frontotemporal dementia (2008, background): “When mice overexpressing p25, an activator of the tau kinase cdk5, were injected with the anti-oxidant resveratrol, hippocampal neurodegeneration was reduced, learning deficiencies were prevented and a decrease in the acetylation of the known SIRT1 substrates PGC-1α and p53 was observe”
Autophagy and apoptosis dysfunction in neurodegenerative disorders. (2014, neutral): “Macroautophagy Chaperon-mediated autophagy Potential therapeutic modulators Alzheimer's disease Macroautophagy is transcriptionally up-regulated (Lipinski et al., 2010) Autophagosome maturation is impaired (Yu et al., 2005) Macroautophagy is inhibited by mutated presinilin-1 in a familial form of AD”