Albert (Gus) Davis, MD, PhD
Assistant Professor of Neurology
Understanding the molecular and cellular mechanisms of protein aggregation and neurodegeneration in Parkinson disease and dementia with Lewy bodies Read More
|Lab Phone:||(314) 273-7763|
|Lab Location:||Biotech 109|
|Keywords:||Mechanisms of protein aggregation and neurodegeneration in Parkinson disease and related synucleinopathies|
Understanding the molecular and cellular mechanisms of protein aggregation and neurodegeneration in Parkinson disease and dementia with Lewy bodies
Parkinson disease and dementia with Lewy bodies are neurodegenerative illnesses that result in progressive motor impairment, dementia, and psychosis. These disorders share the common feature of accumulation of insoluble aggregates of the protein alpha-synuclein (aSyn) into inclusions termed Lewy bodies. The molecular and cellular mechanisms that regulate aggregation of aSyn are not well understood, and there are currently no disease-modifying therapies for this class of disorders, termed synucleinopathies. Although aSyn is an abundant brain protein that plays a normal role in neuronal synaptic function, specific aggregated forms of aSyn are toxic and have been used to induce neuron dysfunction and injury in experimental models of synucleinopathy. We use a combination of in vitro, cell culture, and in vivo model systems to investigate the molecular and cellular mechanisms responsible for pathological aggregation of aSyn and neurodegeneration. The primary goal of our research is to increase our understanding of the basic pathophysiological mechanisms underlying protein aggregation and neurodegeneration in synucleinopathies in order to pave the way for improved diagnostic tests and disease-modifying treatments for these illnesses.