Mitochondrial Trafficking and Function in Neuronal Health and Disease

Venue: The Joseph B. Martin Conference Center at Harvard Medical School

Location: Boston, Massachusetts, United States

Event Date/Time: Jun 25, 2012 End Date/Time: Jun 26, 2012
Registration Date: May 08, 2012
Early Registration Date: May 14, 2012
Abstract Submission Date: Apr 30, 2012
Paper Submission Date: Apr 30, 2012
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The regulated trafficking, morphology and function of mitochondria is essential for providing ATP at the correct spatial location to power neural computation. Mitochondria can also sequester and buffer Ca2+, and also play a key role in apoptotic signaling, so their positioning affects local regulation of Ca2+ dynamics and hence neural signaling, and possibly also neuronal death2. In neurons, the concentration of mitochondria in specific regions such as growth cones and synapses is important for correct neuronal function and development. Moreover mutations in proteins regulating mitochondrial trafficking and function compromise neuronal development and the formation, function and plasticity of synapses. Consequently, defective mitochondrial trafficking is increasingly implicated in neurological diseases. This meeting aims to provide the latest insights into understanding the molecular mechanisms that control mitochondrial trafficking, dynamics and function in neurons. How altered mitochondrial trafficking and function contributes to neuronal dysfunction in neurological diseases (e.g. Alzheimer’s, Parkinson’s and Huntington’s diseases) where disrupted mitochondrial trafficking and function have been shown to occur will be a key focus.