cihr_grants: 170522
This data as json
| external_id | title | project_lead_name | co_researchers | institution | province | country | competition_year | award_amount | program | program_type | theme | research_subject | keywords | abstract | duration | source_url |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 170522 | HMG-CoA reductase in Alzheimer's Disease: Identification of a novel protective variant and unique polymorphisms that modulate Alzheimer pathophysiology. | Poirier Judes | Poirier, Judes | CIUSSS de l'Ouest-de-l'Ile-de-Montréal-Douglas Hospital | Québec | Canada | 200809 | 671999.0 | Operating Grant | Operating Grants | Biomedical | Aging | Alzheimer'S Disease; Cell Biology; Cholesterol; Genetics; Lipid; Molecular Biology | This renewal proposal seeks to further characterize the molecular mechanisms involved in the loss of specific brain cells in common Alzheimer's disease (AD). Over the recent years, our laboratory has documented a complex mechanism that controls the synthesis, recycling and transport of the cholesterol in response to neuronal cell death and local reinnervation in the adult brain. More recently, our team has identified novel genetic anomalies (called mutations) in proteins involved in the production cholesterol in the brain that selectively destroy specific groups of brain cells in AD. This research revealed that a protein known as 3-hydroxy-3-Methylglutaryl-Coenzyme A reductase (HMG CoA reductase) which normally controls the production of cholesterol in the brain is abnormally behaving in the brain of Alzheimer subjects and accelerates the onset of the disease in some cases. Recently, we found a novel and very specific genetic variation in the same HMG CoA reductase gene that confers natural protection against common Alzheimer's disease in humans born with this peculiar genetic trait. More importantly, it provide us with important insights as to how we could to slow down disease progression with specific medications and may be, delay the onset of the disease in people who are genetically "at risk" of developing the disease. Accordingly, the research program submitted here for funding proposes to extend our recent findings in order to examine the fine structure of this gene, its expression level and function in the brain, to eventually determine the exact mechanisms by which of these genetic anomalies (DNA variants) in the HMG-CoA reductase gene play a role in triggering and/or protecting humans against the common form of Alzheimer's disease. | 5 yrs 0 mth | https://webapps.cihr-irsc.gc.ca/decisions/p/project_details.html?applId=170522&lang=en |