Neuronal trafficking: The Good, the Bad and the Ugly

"The science of living forms is the science of movement and transformation". Static images often tell only a small part of a story, and are often misleading. Frankly they are a bit boring as well. Motility is critical for almost all known functions within a cell, and this is particularly true for neurons.  

We like to watch things move. The vast majority of neuronal proteins are made in tiny cell-bodies and then shipped to distant axons and synapses by axonal transport. Axonal transport occurs throughout the life of a neuron, and is a formidable task - analogous to continuously shipping stuff made in a little office in San Diego all the way up and down the coast of California. Not surprisingly, disturbances of transport occur in neurodegenerative diseases like Alzheimer's and Parkinson's disease, where axonal/synaptic degeneration are key pathologies. Though the precise role of transport deficits in the pathogenesis of most of these diseases remains unclear (the classic chicken v/s egg paradox), familial neurodegenerative diseases with mutations in motor proteins - mechanochemical enzymes that move cargoes - indicate that defective transport can lead to neurodegeneration.


We like to find new things. We have two overall areas of interest, relating to basic and applied neuroscience. 1) We want to understand the overall logic of axonal transport. We are particularly interested in understanding the mechanisms of slow axonal transport that delivers cytosolic proteins to their destinations within axons. Along these lines, we are interested in how cargoes are assembled, how they associate with motors, how the movement is regulated, and related mechanistic aspects. 2) We are interested in how (and if)  trafficking/transport is disrupted in neuro-degenerative diseases. Towards this, we are presently involved in studies related to the pathologic role of alpha-synuclein and amyloid-beta on transport/trafficking. For details, click the "Projects" tab above.

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