We are interested in understanding the pathological mechanisms of Alzheimer’s disease. About 95% of the Alzheimer’s disease cases are sporadic while 5% of the cases are familial. Most of the current Alzheimer’s research has been focused on the familial models. We are using our unique mouse model of sporadic Alzheimer’s disease to understand the pathogenic mechanisms underlying the majority of Alzheimer’s disease cases.
If you are interested in finding out more about our research program or joining our research team, please feel free to contact us!
Undergraduate students are welcome
For more information, please contact:
Kevin Park, PhD
Department of Psychology
Biochemistry, Cellular and Molecular Biology Graduate Program
Park,K and Barrett,T (2020). Neuroinflammation precedes Abeta and tau pathologies in the neuronal cell cycle re-entry mouse model of Alzheimer’s disease (under review)
Barrett, T., Marchalant, Y., Park, K.
(2019) p35 hemizygous deletion in 5xFAD mice increases Abeta plaque load in males but not in females.
(in press). Read the article here
Park, K.H.J., Franciosi, S., Parrant, K., Lu, G., and Leavitt, B.R. (2017) p35 hemizygosity activates Akt but does not improve motor function in the YAC128 mouse model of Huntington’s disease.
Park KHJ (2015). Mechanisms of muscle denervation in aging: insights from a mouse model of amyotrophic lateral sclerosis.
Aging and Disease 6 (5): 380-389.
Park KHJ, Franciosi S, Leavitt BR (2013). Postnatal muscle modification by myogenic factors modulates neuropathology and survival in an ALS mouse model.
Nat Commun, 4:2906.
Park KHJ, Lu G, Fan J, Raymond LA, Leavitt BR (2012). Decreasing levels of the cdk5 activators, p25 and p35, reduces excitotoxicity in striatal neurons.
Journal of Huntington’s Disease, 1(1):89-96.
Park KHJ, Hallows JL, Chakrabarty P, Davies P, Vincent I (2007). Conditional neuronal simian virus 40 T antigen expression induces Alzheimer-like tau and amyloid pathology in mice.
J Neurosci, 27(11): 2969-2978.