NIH R01 · 2024
Mitochondria and metabolism in neurodegeneration
SUMMARY Currently, ~5.8 million Americans suffer from Alzheimer's disease (AD)1 and there remain no approved therapeutics to lessen the associated neuronal dysfunction and cell death. Various AD clinical trials targeting the “amyloid cascade” have proven unsuccessful, suggesting a dire need to rethink AD disease progression. Alterations in cellular calcium (iCa2+) and mitochondrial function are reported as critical molecular contributors to AD pathogenesis. Our lab has previously shown that genetic modulation of either mCa2+ uptake or efflux is a powerful way to limit mitochondrial dysfunction and cell death in the context of cell stress featuring elevated iCa2+. As causal evidence of…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.