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Mitochondrial Trafficking and Function in Neuronal Health and Disease
Jun 25, 2012 - Jun 26, 2012
Event Type: Conference
Location: Boston, US
Registration Deadline: Jun 01, 2012
Abstract Submission Deadline: None
Description of event:
Mitochondrial Trafficking and Function in Neuronal Health and Disease
Description
Meeting Chairs: Josef Kittler and Zu-Hang Sheng
Meeting Poster
The regulated trafficking, morphology and function of
mitochondria is essential for providing
ATP at the correct spatial location to power neural computation.
Mitochondria also sequester and
buffer Ca2+, and play a key role in apoptotic
signaling, so their positioning and function also affects regulation of
Ca2+ dynamics and neuronal death. 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 dynamics compromise neuronal development and the formation, function and plasticity of synapses.
Consequently, defective mitochondrial trafficking and function is increasingly implicated in neurological diseases. This meeting will
focus on the latest insights into our understanding of the mechanisms that control mitochondrial trafficking, form and function in neurons. The latest approaches for
imaging cellular bioenergetics and mitochondrial positioning will also be a
focus. How altered mitochondrial dynamics contribute to neuronal dysfunction in neurological diseases including Alzheimer’s, Parkinson’s and Huntington’s diseases will also be a key
focus.
Venue
The Joseph B. Martin Conference Center at Harvard Medical School
Conference Address:
77 Avenue Louis Pasteur
Boston, Massachusetts 02115
USA
Location
Boston, US
Topics
- Regulatory mechanisms of mitochondrial trafficking, fission and fusion
- Mitochondrial regulation of synaptic function and plasticity
-
Imaging mitochondrial function and cellular bioenergetics
in vitro and
in vivo
- Mitochondrial function and neurodegeneration
- Mitochondrial
quality control, mitophagy and the PINK1-Parkin
pathway