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Brain function and mitochondrial Ca2+ homeostasis-its potential as a CNS therapeutic target

Sridhar S. Kannurpatti, PhD - Assistant Professor, Department of Radiology RUTGERS-New Jersey Medical School

 Mar 23, 2023 @ 4:00 p.m.

Mitochondria are important subcellular organelles which play a role in normal cellular signaling and energy metabolism. While most evidence comes from in vitro or ex-vivo studies, it makes human translation a challenge. Using pharmacological perturbation of mitochondrial Ca2+ uptake capacity (MC/UC) and functional imaging in vivo, the dynamic role of mitochondria in regulating both brain neural activity and neurovascular coupling has been identified. Currently, the feedback and feedforward hypotheses provide the biophysical basis for neurovascular coupling based on various in vivo messengers (eg., CO2, NO, K+, lactate, nNOS and PLA2). However, in vivo mitochondrial modulation and its effects on neural activity and functional imaging markers such as cerebral blood flow (CBF) and fMRI blood oxygen contrast (BOLD) responses, provide evidence for a unified hypothesis of MC/UC activity as a central mechanism of neurovascular coupling. As mitochondrial dysfunction is implicated in many neuropathologies, it is an obvious therapeutic target. Whether the central mechanism of MC/UC, which regulates neurovascular activity, can be harnessed as a therapeutic target will be presented. How translational preclinical imaging can help bridge gaps to easier clinical trial decision making will be discussed.

 Medical Center | Upper Auditorium (3-7619)

Host: University of Rochester School of Medicine and Dentistry, Department of Neuroscience and the Del Monte Institute for Neuroscience