Grant: Project Grant
Centre hospitalier de l'Université de Montréal (CHUM)
$1,193,400.00
Dual regulation of the ALS/FTD relevant target G3BP1
EF 2024-25
Résumé
The development of an effective treatment for most ALS (amyotrophic lateral sclerosis) and FTD (frontotemporal dementia) patients has been difficult, partly because we don't fully understand the molecular causes of these diseases. One promising area of research focuses on stress granules-structures that help protect neurons, the brain's critical cells, from damage caused by harmful conditions or environmental stress. Neurons cannot regenerate, so they rely on stress granules to survive these challenges.
A protein called G3BP1 is essential for forming stress granules, and our research has shown that it is regulated by another important protein called TDP-43. In ALS and FTD patients, TDP-43 is often misplaced within neurons, leading to problems with stress granule formation. By understanding how G3BP1 and TDP-43 interact, we aim to uncover new therapeutic approaches to protect neurons and slow the progression of ALS and FTD.
Programme
Project Grant
Emplacement
Quebec, Canada
Type de bénéficiaire
Not-for-profit organization or charity
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
522681
Name
Vande Velde Christine Diane C
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Cell Biology - Disease 2
Projecttitle
Dual regulation of the ALS/FTD relevant target G3BP1
Programtype2
Operating Grants
Orgnameinp2
Centre hospitalier de l'Université de Montréal (CHUM)
Cihramount2
$1,193,400
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Amyotrophic Lateral Sclerosis; Cell Biology; Frontotemporal Dementia; Mechanisms Of Disease; Neurodegeneration; Neurons; Rna Binding Proteins; Stress Granules; Tdp-43; Transgenic Mice
Abstract
The development of an effective treatment for most ALS (amyotrophic lateral sclerosis) and FTD (frontotemporal dementia) patients has been difficult, partly because we don't fully understand the molecular causes of these diseases. One promising area of research focuses on stress granules-structures that help protect neurons, the brain's critical cells, from damage caused by harmful conditions or environmental stress. Neurons cannot regenerate, so they rely on stress granules to survive these challenges.
A protein called G3BP1 is essential for forming stress granules, and our research has shown that it is regulated by another important protein called TDP-43. In ALS and FTD patients, TDP-43 is often misplaced within neurons, leading to problems with stress granule formation. By understanding how G3BP1 and TDP-43 interact, we aim to uncover new therapeutic approaches to protect neurons and slow the progression of ALS and FTD.
Competitiondate
202503
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Vande Velde, Christine Diane C
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,193,400~ $0~