Glutamate Signaling and Mitochondrial Dysfunction in Models of Parkinson's Disease
Final rept. 1 Dec 2012-30 Nov 2013, Option year 2
NORTHWESTERN UNIV CHICAGO IL
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The central hypothesis of the proposal is that in the early stages of PD, an elevation in synaptically released glutamate leads to persistent activation of NMDARs that synergizes with Cav1 calcium channels to significantly increase mitochondrial oxidant stress and neurodegeneration.
- Anatomy and Physiology
- Medicine and Medical Research