Research Field

Deposition of amyloid-like fibrillar protein aggregates is a common pathological feature of many human neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease. Understanding the molecular mechanisms underlying protein misfolding and aggregation might hold the key to unraveling common pathogenic mechanisms for these devastating neurologic disorders. Since the start of my independent research career in 2000, the goal of my research program is to understand the mechanism of abnormal protein aggregations and its roles in neurodegeneration as well as in neuroinflammation. To achieve this goal, my group has been particularly interested in the normal and pathophysiological behavior of -synuclein, a neuronal protein implicated in several human neurodegenerative diseases, including Parkinson’s disease, dementia with Lewy bodies, multiple system atrophy, and Alzheimer’s disease.

Approaches my lab has employed include the followings.
Basic molecular cell biology techniques (viral vectors, fluorescence imaging, subcellular fractionations, etc.)
Protein biochemistry techniques (liquid chromatography, protein fibrillation kinetic analyses, secondary structure analyses, electron microscopy, atomic force microscopy, etc.)
Animal modeling (transgenic mice, stereotaxic brain injection, immunohistochemistry, behavioral analyses, C. elegans model generation and analyses, etc.).

The major interests of my group include the topics, such as the mechanism of disease progression, determinants for disease specificity (eg, Alzheimer vs. Parkinson), and mechanism-based development of pre-symptomatic diagnosis and therapy. Specific questions to address are the followings.
-What is the underlying mechanism for the ‘progression’ of neurodegenerative diseases?
-How do protein aggregation and neuroinflammation feed forward each other during disease progression?
-What is the relationship among protein aggregation, cellular senescence, and neuroinflammation?
-Why does some people get tauopathies, while others get synucleinopathies or TDP43pathies?
-Can we stop the progression of neurodegenerative diseases by interfering with protein aggregate spreading and neuroinflammation?

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Keyword

Neurodegenerative diseases, Parkinson’s disease, dementia, protein aggregation, neuroinflammation