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Grant: Operating Grant

University of Toronto

$459,204.00

Reversing developmental consequences of NMDA receptor dysfunction in a mouse model of schizophrenia.

FY 2011-12

Summary
The causes of schizophrenia remain unclear, but there is strong evidence to suggest a genetic component to the disease. Even though the susceptibility genes that cause schizophrenia are inherited from birth, the symptoms of the disease are not fully apparent until after adolescence and into early adulthood. We and others hypothesize that improper neural communication and connection during childhood brain development occurs in schizophrenia. Using a genetic mouse model of schizophrenia, we propose to study the emergence of schizophrenia related behaviours through development, and determine whether antipsychotic treatment at early developmental timepoints could improve therapeutic outcomes. Furthermore, we propose to study the ability of the brain to improve function by restoring proper neuronal communication at different developmental stages. In performing these studies, we may gain insight into early diagnostic criteria for schizophrenia, and may determine whether early therapeutic intervention is beneficial for brain function in schizophrenic patients.
Program
Operating Grant
Location
Ontario, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
238167
Name
Ramsey Amy J
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Neurosciences, Mental Health and Addiction
Theme2
Biomedical
Prcname2
Behavioural Sciences - A: Neurobiological Basis of Behavioural Processes
Projecttitle
Reversing developmental consequences of NMDA receptor dysfunction in a mouse model of schizophrenia.
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$459,204
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Antipsychotics; Memory; Nmda Receptor; Postnatal Development; Schizophrenia; Social Behaviour; Striatum; Synapse; Transgenic Mouse
Abstract
The causes of schizophrenia remain unclear, but there is strong evidence to suggest a genetic component to the disease. Even though the susceptibility genes that cause schizophrenia are inherited from birth, the symptoms of the disease are not fully apparent until after adolescence and into early adulthood. We and others hypothesize that improper neural communication and connection during childhood brain development occurs in schizophrenia. Using a genetic mouse model of schizophrenia, we propose to study the emergence of schizophrenia related behaviours through development, and determine whether antipsychotic treatment at early developmental timepoints could improve therapeutic outcomes. Furthermore, we propose to study the ability of the brain to improve function by restoring proper neuronal communication at different developmental stages. In performing these studies, we may gain insight into early diagnostic criteria for schizophrenia, and may determine whether early therapeutic intervention is beneficial for brain function in schizophrenic patients.
Competitiondate
201109
Approvedterm2
3 yrs 0 mth
Pinamesdelim
Ramsey, Amy J
Approvedterm
3 ans 0 mois
Cihrcontribution2
~ $459,204~ $0~