Grant: Operating Grant
Centre hospitalier de l'Université de Montréal (CHUM)
$547,835.00
Further studies of the pathophysiology of vitamin B1 deficiency: effects on neural progenitor cell function
EF 2009-10
Résumé
Wernicke's encephalopathy (WE) is one of two components of the Wernicke-Korsakoff syndrome, a neuropsychiatric
disorder resulting from vitamin B1 (thiamine) deficiency (TD), that often develops in alcoholic patients and other individuals
with a grossly impaired nutritional status. WE is associated with irreversible brain damage, particularly in forebrain and
midbrain structures. These patients often have a history of recurrent bouts of TD. While thiamine administration represents a
well-established treatment for acute WE nowadays, such lesions and the resulting neurological impairment are not responsive to thiamine treatment. Thus, we plan to 1) examine the effects of TD on neural precursor cells capable of forming new neurons and thereby replacing the damaged structures, and 2) the ability of these cells to respond to the injury when administered to the intact TD animal.
Programme
Operating Grant
Emplacement
Quebec, Canada
Type de bénéficiaire
Not-for-profit organization or charity
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
202451
Name
Hazell Alan S
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Nutrition, Metabolism and Diabetes
Theme2
Biomedical
Prcname2
Nutrition, Food & Health
Projecttitle
Further studies of the pathophysiology of vitamin B1 deficiency: effects on neural progenitor cell function
Programtype2
Operating Grants
Orgnameinp2
Centre hospitalier de l'Université de Montréal (CHUM)
Cihramount2
$547,835
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Astrocyte; Excitotoxicity; Neural Stem Cells; Neurogenesis; Nmr Spectroscopy; Oxidative Stress; Rna Interference
Abstract
Wernicke's encephalopathy (WE) is one of two components of the Wernicke-Korsakoff syndrome, a neuropsychiatric
disorder resulting from vitamin B1 (thiamine) deficiency (TD), that often develops in alcoholic patients and other individuals
with a grossly impaired nutritional status. WE is associated with irreversible brain damage, particularly in forebrain and
midbrain structures. These patients often have a history of recurrent bouts of TD. While thiamine administration represents a
well-established treatment for acute WE nowadays, such lesions and the resulting neurological impairment are not responsive to thiamine treatment. Thus, we plan to 1) examine the effects of TD on neural precursor cells capable of forming new neurons and thereby replacing the damaged structures, and 2) the ability of these cells to respond to the injury when administered to the intact TD animal.
Competitiondate
201003
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Hazell, Alan S
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $547,835~ $0~