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My lab focuses on studying the pathophysiological properties of genetic mutations associated with Parkinson's disease (PD) and ALS using a combination of in vivo mouse modeling and in vitro neurobiological approaches. While most of PD and ALS cases are sporadic, a small fraction is inherited. The specific genetic defects underlying the familial forms of diseases may provide valuable molecular handles for elucidating the pathogenic mechanisms of the diseases. Following this principle, we have generated a series of novel mouse genetic models for PD and ALS to investigate the pathophysiological phenotypes of various PD and ALS-related genetic mutations and test potential therapeutics. Currently, we focus our research on the functions and pathogenic mechanisms of alpha-synuclein and LRRK2 in PD, VAPB in ALS, and dynactin p150glued in Perry syndrome, a subtype of PD with severe mental depression. We are actively exploring the underlying molecular and cellular mechanisms of these genetic mutations in vivo and in primary neuronal cultures using a variety of histology, electrophysiology, cell biology and biochemistry approaches. Meanwhile, we also take advantage of newly developed RNA sequencing techniques to systematically identify molecular networks critical for the degeneration of nigrostriatal dopaminergic (DA) neurons.
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Aging Communicationsno. 1 (2023): 1-1
Research Square (Research Square) (2023)
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Research square (2023)
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Ageing and neurodegenerative diseasesno. 2 (2022): 6-6
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semanticscholar(2022)
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