Northwestern University

Oct
23
Mon 4:00 PM

"Mitochondrial Transport and Energy Homeostasis in Synaptic Transmission, Neuronal Degeneration and Regeneration"

When: Monday, October 23, 2017
4:00 PM - 5:00 PM  

Where: Ward Building, 5-230, 303 E. Chicago Avenue, Chicago, IL 60611 map it

Audience: Faculty/Staff - Student - Public - Post Docs/Docs - Graduate Students

Contact: Alexa Nash   312.503.4893

Group: Department of Pharmacology Seminars

Category: Lectures & Meetings

Description:

The Department of Pharmacology is pleased to welcome Dr. Zu-Hang Sheng, Ph.D., Senior Principal Investigator and Chief of the Synaptic Function Section at NINDS.

The following, is an overview of this seminar, as described by Dr. Sheng:

The research in the Sheng laboratory is focused on mechanisms regulating axonal transport in healthy and diseased neurons. Using genetic mouse models, his group is addressing several fundamental questions: (1) how mitochondrial transport is regulated to sense changes in synaptic activity, mitochondrial integrity, axon injury and pathological stress; (2) how neurons coordinate late endocytic transport and autophagy-lysosomal function to maintain cellular homeostasis and synaptic function; (3) how impaired transport contributes to synaptic dysfunction and axonal pathology in several major neurodegenerative diseases. His lab has used a broad range of approaches to tackle these problems, notably the development of neuronal cultures from adult disease mouse models and live imaging of various organelle transport in axons. These studies have led to the identification of motor adaptor and anchoring proteins that regulate axonal transport of mitochondria, endo-lysosomes, and synaptic cargoes. The long-term goal of the laboratory is to decipher mechanisms enhancing autophagy-lysosomal function for efficient clearance of dysfunctional mitochondria that are associated with several major neurodegenerative diseases. Pursuing these investigations will advance our knowledge of fundamental processes that may affect human neurological disorders.

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