Brain Research Institute

Karen Gylys, Ph.D.

Email Address:
kgylys@sonnet.ucla.edu

Work Address:
Office
Factor Building
Los Angeles, CA 90095
UNITED STATES

Work Phone Number:
310 794-5472
310-206-3840

Department / Division Affiliations

Associate Professor, School of Nursing

Member, Neuroscience Graduate Program, Brain Research Institute

Bio:

Karen Hoppens Gylys is a neuroscientist who joined the faculty of the School of Nursing and the Brain Research Institute in 1998. Dr. Gylys earned a B.S. degree in Nursing and a M.S. degree in Human Development at the University of Texas, Dallas. She received her Ph.D. in Neuroscience, with a major in neuropharmacology, at UCLA in 1993, and did postdoctoral work on molecular mechanisms of opioid tolereance in the NPI. Since joining the faculty of the School of Nursing, she has taught pharmacology and research in the School of Nursing and is actively involved in the BRI. Her laboratory research is focused on understanding the dysfunction and loss of synapses that occurs in Alzheimer's disease, which is thought to underly the earliest cognitive impairments.

Publications:

Gylys Karen H., Fein Jeffrey A., Yang Fusheng, Miller Carol A., Cole Gregory M. Increased Cholesterol in Amyloid beta-positive Nerve terminals from Alzheimers Disease Cortex. Neurobiology of Aging ; in press: .

Gylys, Karen H., Fein, Jeffrey A, Yang, F, and Cole, Gregory M. Enrichment of Pre- and Post-synaptic Markers by Size-Based Gating Analysis of Synaptosome Preparations from Rat and Human Cortex. Cytometry, Part A 2004; 60A: 90-96.

Gylys KH, Fein JA, Tan AM, Cole GM Apolipoprotein E Enhances Uptake of Soluble but not Aggregated Amyloid-beta Protein into Synaptic Terminals. Journal of Neurochemistry 2003; 84(6): 1442-51.

Gylys, Karen H., Fein, Jeffrey A and Cole, Gregory M. Flow cytometry analysis of a crude synaptosomal fraction (P-2) from rat brain. J. Neurosci. Res. 2000; 61: 186-192.

Gylys, KH Fein, JA Yang, F Wiley, DJ Miller, CA Cole, GM Synaptic changes in Alzheimer's disease: increased amyloid-beta and gliosis in surviving terminals is accompanied by decreased PSD-95 fluorescence.. The American journal of pathology. . 2004; 165(5): 1809-17.