Lee-Way Jin, M.D., Ph.D.

Director, Brain and Tissue Bank, M.I.N.D. Institute; Associate Professor, Department of Medical Pathology, School of Medicine

UC Davis M.I.N.D. Institute
2825 50th Street
Sacramento, CA 95817
E-mail:  lee-way.jin@ucdmc.ucdavis.edu  

Dr. Jin is a neuropathologist and neuroscientist with expertise in brain banking and the molecular analysis of degenerative brain diseases. Before his move to Davis, he was the PI of the NIA-funded Neuropathology Core of the Alzheimer’s Disease Research Center at the University of Washington, which is renowned for research on a familial form of early onset Alzheimer’s disease and its brain banking practices. Dr. Jin’s laboratory performs neuropathological and behavioral characterization of various transgenic models of brain disorders, including Alzheimer’s disease, Parkinson’s disease, spinobulbar muscular atrophy, and Niemann-Pick type C disease. He is particularly interested in the toxicity induced by misfolded proteins in brain diseases, and his laboratory is testing methods to reduce this toxicity.

Jin LW, Claborn K, Kurimoto M, Geday M, Maezawa I, Sohraby F, Estrada M, Kaminsky W, Kahr B. Linear birefringence and dichroism imaging of amyloid plaques. Proc Natl Acad Sci USA. 100:15294-15298, 2003. We evaluated a novel optical method to study the structural parameters of amyloid plaques in the brain. This method reveals a central disorganized core of plaques and provides clues to the mechanism of Congo red binding to amyloid. This study points out the potential of using optical properties of tissues in the development of new microscopy method and the possibility of detecting in situ structural abnormalities of macromolecules in disease status in a high throughput manner.

Jin L-W, Maezawa I, Vincent I, Bird T. Intracellular accumulation of amyloidogenic fragments of APP in neurons with Niemann-Pick type C defects is associated with early endosomal abnormalities. Am J Pathol. 164:975-9852004. Niemann-Pick type C disease is a progressive neurological disease characterized by cerebellar dysfunction, dystonia, dysarthria, and mental retardation. We found that the intraneuronal accumulation of the amyloidogenic fragments of APP might contribute to neuronal death in the cerebellar cortex and hippocampus, and the accumulation was associated with endosomal abnormalities.

Intraneuronal accumulation of Aß in the pathogenesis of Alzheimer’s disease, UC Davis M.I.N.D. Institute, Sacramento, CA, October 2003

Parkinson’s disease caused by a-synuclein locus triplication, UC Davis Department of Pathology, Sacramento, CA, December 2003.

The role of phospholipid transfer protein in the pathogenesis of Alzheimer’s disease, Emory University Center for Neurodegenerative Diseases, Atlanta, GA, March 2004.

Co-Principal Investigator: Model of SBMA Motor Neuron Degeneration, NINDS, 2001-2006, $225,000 annually. This study will develop mouse models and cell culture models of X-linked spinal and bulbar muscular atrophy in order to understand the molecular basis of motor neuron degeneration secondary to expansion of the polyglutamine tract in the androgen receptor protein.

Co-Principal Investigator: Functions of FE65 and its role in dementias of the Alzheimer’s type, NIA, 2001-2006, $216,000 annually. This study investigates the mechanisms whereby FE65 regulates expression of GSK-3β and several other candidate genes. It also investigates the role of FE65 on Aß production/deposition and the rate of APP internalization.

Ad hoc reviewer for Proteomics, Brain Research, Journal of Neuroscience Research, and Journal of Neuropathology and Experimental Neurology
Ad hoc scientific reviewer for the Alzheimer Association