Davis Lab

Albert (Gus) Davis, MD

Parkinson disease and dementia with Lewy bodies are progressive neurodegenerative disorders characterized by motor impairment, dementia, and psychosis. A shared hallmark of these diseases is the accumulation of insoluble aggregates of the protein alpha-synuclein (aSyn) into structures known as Lewy bodies.

Mechanisms of alpha-synuclein aggregation
Although aSyn is a naturally abundant brain protein involved in synaptic function, certain aggregated forms are toxic and contribute to neuronal dysfunction and injury. The molecular and cellular mechanisms that drive aSyn aggregation remain poorly understood, and no disease-modifying therapies currently exist for these disorders, collectively known as synucleinopathies.

Experimental models and research approach
We use a combination of in vitro, cell culture, and in vivo model systems to investigate the mechanisms underlying pathological aSyn aggregation and neurodegeneration. These models help us explore how specific forms of aSyn contribute to disease progression.

Research goals
Our primary goal is to deepen understanding of the basic pathophysiological processes involved in protein aggregation and neurodegeneration in synucleinopathies. This knowledge will support the development of improved diagnostic tools and pave the way for effective disease-modifying treatments.

Principal investigator

Our team

Recent publications