Grant: Operating Grant
McGill University
$836,640.00
Investigating the mechanism of Amyloid-beta GxxxG-motif-targeting agents
EF 2013-14
Résumé
Alzheimer disease (AD) is the most prevalent neurodegenerative disorder, estimated to currently affect over 35 million
people worldwide. As the most common form of AD is age-related and life expectancy continues to increase, a dramatic rise
in the incidence of AD is anticipated and the number of people suffering from this debilitating disease is expected to nearly
double every 20 years. This clearly demonstrates that AD is among the most significant social, health and economic burdens
of the 21st century.
The degenerative process is made worse by the toxic actions of a specific protein that accumulates inside the Alzheimer
brain, known as amyloid (Abeta). Since healthy aging is possible, we assume that cognitive decline is not an inevitable
outcome. Given the significance of toxic amyloid aggregates for the pathogenesis of AD, our exciting new approach is that
we propose to test selected drugs active in inhibiting and/or neutralizing the neurotoxic properties. The overarching objective
of this proposal is to find out exactly how such agents target the toxic amyloid and how they interfere with the formation of
these disease-causing aggregates.
In summary the proposed studies are a direct response to (i) the new interest in understanding molecular processes of
amyloidogenesis and (ii) the recent developments in prevention and early detection of amyloid aggregates. The anticipated
results could generate novel therapeutic approaches based on a better mechanistic understanding of amyloid sequence
interactions. This work will lead to the development of novel preventive or curative AD treatments and contribute towards a
better understanding of AD pathogenesis.
Programme
Operating Grant
Bénéficiaire
Emplacement
Quebec, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
291449
Name
Multhaup Gerhard
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Aging
Theme2
Biomedical
Prcname2
Biochemistry & Molecular Biology - A
Projecttitle
Investigating the mechanism of Amyloid-beta GxxxG-motif-targeting agents
Programtype2
Operating Grants
Orgnameinp2
McGill University
Cihramount2
$836,640
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Aggregation; Alzheimer Disease; Amyloid; Cellular And Organotypical Slice Cultures; Drosophila Melanogaster In Vivo; Electrophysiological Recordings; Gxxxg Motif; Size Exclusion Chromatography; Surface Plasmon Resonance; Toxicity
Abstract
Alzheimer disease (AD) is the most prevalent neurodegenerative disorder, estimated to currently affect over 35 million
people worldwide. As the most common form of AD is age-related and life expectancy continues to increase, a dramatic rise
in the incidence of AD is anticipated and the number of people suffering from this debilitating disease is expected to nearly
double every 20 years. This clearly demonstrates that AD is among the most significant social, health and economic burdens
of the 21st century.
The degenerative process is made worse by the toxic actions of a specific protein that accumulates inside the Alzheimer
brain, known as amyloid (Abeta). Since healthy aging is possible, we assume that cognitive decline is not an inevitable
outcome. Given the significance of toxic amyloid aggregates for the pathogenesis of AD, our exciting new approach is that
we propose to test selected drugs active in inhibiting and/or neutralizing the neurotoxic properties. The overarching objective
of this proposal is to find out exactly how such agents target the toxic amyloid and how they interfere with the formation of
these disease-causing aggregates.
In summary the proposed studies are a direct response to (i) the new interest in understanding molecular processes of
amyloidogenesis and (ii) the recent developments in prevention and early detection of amyloid aggregates. The anticipated
results could generate novel therapeutic approaches based on a better mechanistic understanding of amyloid sequence
interactions. This work will lead to the development of novel preventive or curative AD treatments and contribute towards a
better understanding of AD pathogenesis.
Competitiondate
201309
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Multhaup, Gerhard
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $836,640~ $0~