Mitochondrial Trafficking and Function in Neuronal Health and Disease

Start date
June 25, 2012
End date
June 26, 2012
Venue
The Joseph B. Martin Conference Center at Harvard Medical School
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

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Latest news

Save the date:

Conference chairs Josef Kittler (University College London, UK) and Zu-Hang Sheng (NIH, US) have announced an exciting line up of speakers, as well as an ideal location and venue. Register early to receive early bird discounts and secure your place. Do not forget there will be opportunities to present your work. Speaking slots are available as well a networking poster session. 

 

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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.