Homeostatic Plasticity in Mouse Model of Jordan's Syndrome

NIH RePORTER · NIH · R21 · $201,875 · view on reporter.nih.gov ↗

Abstract

ABSTRACT The identification of gene mutations that cause autism and syndromes associated with severe intellectual disability has greatly advanced both research and new therapeutic development. Yet, the mechanisms that link gene loss of function to impaired brain function remain poorly understood in almost every instance. There is a pressing need to elucidate how individual gene mutations lead to deficits in brain function, with the potential to identify common grounds for therapeutic intervention that will benefit the largest patient population. Recently, homeostatic plasticity was demonstrated to have a potent ability to counteract neurological disease onset and progression. This is referred to as Homeostatic Neuroprotection. Based on preliminary data, we propose that the mechanisms of homeostatic neuroprotection also apply to the onset and progression of impaired hippocampal function, based on work examining a new mouse model of severe intellectual disability. This work has the potential to open a new approach toward therapeutic development in psychiatric disease.

Key facts

NIH application ID
10451713
Project number
5R21HD106516-02
Recipient
UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
Principal Investigator
GRAEME W DAVIS
Activity code
R21
Funding institute
NIH
Fiscal year
2022
Award amount
$201,875
Award type
5
Project period
2021-07-15 → 2023-12-31