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Grant: Project Grant

University of Toronto

$1,090,125.00

Exploring the role of ALK and LTK in axon remodelling.

FY 2024-25

Summary
Neurons have long protrusions called dendrites or axons. Formation of these protrusions occurs during development of the nervous system and are essential for proper neuronal function. Neurons of the central nervous system have a very limited capacity to recover from damage caused by injury and cannot re-grow axons. We discovered a pathway that plays a key role in limiting the growth of axons during embryonic development. Moreover, we observed that treating normal neurons or those subjected to damage with a drug that inhibits the pathway can promote the regrowth of neuronal axons. Here, we propose to undertake studies using both in vitro and in vivo mouse models to better understand the molecular mechanisms for these effects during normal development and upon damage. Results from our work will provide insights on new approaches to promote survival and regeneration of damaged neurons in diverse contexts.
Program
Project Grant
Location
Ontario, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
510792
Name
Attisano Liliana
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Cell Biology - Disease
Projecttitle
Exploring the role of ALK and LTK in axon remodelling.
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$1,090,125
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Axon Regeneration; Cns Injuries; Neurons; Signal Transduction
Abstract
Neurons have long protrusions called dendrites or axons. Formation of these protrusions occurs during development of the nervous system and are essential for proper neuronal function. Neurons of the central nervous system have a very limited capacity to recover from damage caused by injury and cannot re-grow axons. We discovered a pathway that plays a key role in limiting the growth of axons during embryonic development. Moreover, we observed that treating normal neurons or those subjected to damage with a drug that inhibits the pathway can promote the regrowth of neuronal axons. Here, we propose to undertake studies using both in vitro and in vivo mouse models to better understand the molecular mechanisms for these effects during normal development and upon damage. Results from our work will provide insights on new approaches to promote survival and regeneration of damaged neurons in diverse contexts.
Competitiondate
202409
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Attisano, Liliana
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,090,125~ $0~