Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.brainresbull.2009.12.007
DC FieldValue
dc.titleResveratrol is neuroprotective because it is not a direct activator of Sirt1-A hypothesis
dc.contributor.authorTang, B.L.
dc.date.accessioned2011-11-29T05:58:42Z
dc.date.available2011-11-29T05:58:42Z
dc.date.issued2010
dc.identifier.citationTang, B.L. (2010). Resveratrol is neuroprotective because it is not a direct activator of Sirt1-A hypothesis. Brain Research Bulletin 81 (4-5) : 359-361. ScholarBank@NUS Repository. https://doi.org/10.1016/j.brainresbull.2009.12.007
dc.identifier.issn03619230
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/28723
dc.description.abstractThe plant polyphenol resveratrol (3,5,4′-trihydroxystilbene) has been touted to have multiple health benefits. A commonly cited mechanism of resveratrol action is via the activation of the longevity factor Sir2/Sirt1, whose deacetylase activity on several transcription factors has stress resistance and pro-survival effects. Resveratrol has been shown to be beneficial in various in vitro and in vivo models of central nervous system (CNS) neuron death and degeneration, presumably acting through Sirt1. However, accumulating recent evidence suggests that Sirt1 inhibitors are also neuroprotective. These contradictory results leave us with an apparently irreconcilable paradox. Based on other recent findings that resveratrol also activate AMP-activated protein kinase (AMPK), particularly in neurons, we hypothesize that reseveratrol does not exert its neuroprotective effect via direct Sirt1 activation. In fact, resveratrol is neuroprotective precisely because it does not activate Sirt1 during the acute phase of neuronal cell demise. However, its activation of AMPK may be neuroprotective. Furthermore, resveratrol may indirectly increase Sirt1 activity in recovering or spared cells via AMPK's elevation of NAD levels, which then translates into an overall beneficial outcome. The hypothesis could potentially be tested via selective AMPK silencing in various neuronal death and degeneration models, to see if the neuroprotective effect of resveratrol will be blunted. If proven true, the hypothesis has important ramifications in how reseveratrol, as well as novel Sirt1 activators, may be best used in treatment of CNS injuries and disorders. © 2009 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.brainresbull.2009.12.007
dc.sourceScopus
dc.subjectNeuron
dc.subjectNeuroprotection
dc.subjectResveratrol
dc.subjectSirt1
dc.typeOthers
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.1016/j.brainresbull.2009.12.007
dc.description.sourcetitleBrain Research Bulletin
dc.description.volume81
dc.description.issue4-5
dc.description.page359-361
dc.description.codenBRBUD
dc.identifier.isiut000274972800001
Appears in Collections:Staff Publications

Show simple item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

34
checked on Sep 24, 2020

WEB OF SCIENCETM
Citations

31
checked on Sep 24, 2020

Page view(s)

274
checked on Sep 22, 2020

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.