Synuclein Interest Group (SIG)
Two complementary frameworks guide how we think about α-synuclein (αS). First, αS is a key protein implicated in Parkinson’s disease (PD) and related disorders. However, its normal function is poorly understood. Second, αS regulates neurotransmission and is linked to PD and related disorders. However, its role in disease progression and pathogenesis is poorly understood. These perspectives are not mutually exclusive. Our research integrates both views by first defining the fundamental biology of αS and determining how/to what extent its normal functions become disrupted in disease states. Through this approach, we aim to uncover mechanistic insights that bridge basic synaptic biology with neurodegeneration.
Research Areas
α-Synuclein homeostasis in health and disease
In the SIG, we are interested in how the brain functions and how it goes awry in disease at the cellular and organismal levels. Why did α-Synuclein (αS) become our main research interest? 1) αS is one of the most abundant proteins in the human brain; 2) αS is implicated in the second most common neurodegenerative disease, Parkinson’s disease (PD), as well as a variety of other “synucleinopathies” including dementia with Lewy Bodies (DLB), multiple system atrophy, and certain forms of Alzheimer’s disease; 3) Finally, even after 30 years since its discovery, αS function is either ignored or debated. Therefore, much remains to be learned about this protein in the healthy and diseased brains. Towards this end, our research aims to define the pathophysiological landscape of αS.
