Oral Resveratrol Reduces Neuronal Damage in a Model of Multiple Sclerosis

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Title Journal of Neuro-Ophthalmology, December 2010, Volume 30, Issue 4
Date 2010-12
Language eng
Format application/pdf
Type Text
Publication Type Journal Article
Collection Neuro-ophthalmology Virtual Education Library: NOVEL http://NOVEL.utah.edu
Publisher Lippincott, Williams & Wilkins
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah, 10 N 1900 E SLC, UT 84112-5890
Rights Management © North American Neuro-Ophthalmology Society
ARK ark:/87278/s69g8sxs
Setname ehsl_novel_jno
ID 227120
Reference URL https://collections.lib.utah.edu/ark:/87278/s69g8sxs

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Title Oral Resveratrol Reduces Neuronal Damage in a Model of Multiple Sclerosis
Creator Shindler, Kenneth S; Ventura, Elvira; Dutt, Mahasweta; Elliott, Peter; Fitzgerald, Denise C; Rostami, Abdolmohamad
Affiliation FM Kirby Center for Molecular Ophthalmology, Department of Ophthalmology, University of Pennsylvania
Abstract Neuronal loss in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), correlates with permanent neurological dysfunction. Current MS therapies have limited the ability to prevent neuronal damage. We examined whether oral therapy with SRT501, a pharmaceutical grade formulation of resveratrol, reduces neuronal loss during relapsing-remitting EAE. Resveratrol activates SIRT1, an NAD+-dependent deacetylase that promotes mitochondrial function. Oral SRT501 prevented neuronal loss during optic neuritis, an inflammatory optic nerve lesion in MS and EAE. SRT501 also suppressed neurological dysfunction during EAE remission, and spinal cords from SRT501-treated mice had significantly higher axonal density than vehicle-treated mice. Similar neuroprotection was mediated by SRT1720, another SIRT1-activating compound; and sirtinol, an SIRT1 inhibitor, attenuated SRT501 neuroprotective effects. SIRT1 activators did not prevent inflammation. These studies demonstrate that SRT501 attenuates neuronal damage and neurological dysfunction in EAE by a mechanism involving SIRT1 activation. SIRT1 activators are a potential oral therapy in MS.
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Format application/pdf
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah, 10 N 1900 E SLC, UT 84112-5890
Setname ehsl_novel_jno
ID 227110
Reference URL https://collections.lib.utah.edu/ark:/87278/s69g8sxs/227110