Davidson Fellows - 2012 Laureate Michael Yan


         

Michael Yan

$50,000 Scholarship Recipient

Age: 18
Pepper Pike, OH
Category: Science
Project Title: “Genetic Mutation of LRRK2 Causes Autosomal Parkinson’s Disease by Disrupting Mitochondrial Dynamics.”

 
 


In the past decades, numerous mutations factors have been linked to Parkinson’s disease (PD) pathogenesis. Despite abundant research implicating various risk factors in PD pathogenesis, the underlying mechanisms involved in PD pathogenesis have remained elusive. Likewise, additional studies have provided greater insights into pathophysiological features of PD. Michael’s work reconciles mutations in LRRK2, which constitute the single most common cause of autosomal dominant PD, with PD pathophysiological features, but it also comprehensively identifies the underlying biomechanism by which LRRK2 mutations cause PD.

Specifically, mitochondria are of imperative importance to the survival of neurons in the brain; neurons are the most energy-intensive organ in the brain. This is because mitochondria play a large role in energy production, maintaining transition metal homeostasis, being a key part of the apoptotic cycle, maintaining regular polarity through their dynamic movements, etc. The results of Michaels’ study indicate that LRRK2 PD-associated mutations increase recruitment of DLP1 to mitochondria through a physical interaction involving kinase activity, thus increasing mitochondrial fission. This event results in mitochondrial dysfunction in terms of excessive mitochondrial fragmentation. Since normal mitochondrial dynamics serve many important purposes in mitochondrial functions, dysfunctional mitochondrial dynamics occurs concomitantly with decreased efficiency of the electron transport chain and energy production as well as increased reactive oxygen species production and neuronal susceptibility to oxidative stress and cell death. This directly explains how mutations in LRRK2 causes PD pathophysiological features like increased oxidative stress, cellular hypometabolism, and severely elevated neuronal loss, thereby also giving great insights into PD pathogenesis on the whole and PD etiology.

Michael graduated from Orange High School, in the fall he will attend the Massachusetts Institute of Technology (MIT). He is aiming to complete a double major in biology and chemistry, and hopes to pursue a Ph.D. in biomedical sciences and/or become a biology professor at MIT.



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