TTUHSC Paul L. Foster School of Medicine
Neurosciences

Research: Center of Excellence for Neuroscience

Principal Investigators

Ruth Perez, Ph.D.

Associate Professor, Department of Biomedical Sciences and Center of Excellence for Neuroscience


Department of Biomedical Sciences
Center of Excellence for Neuroscience
Texas Tech University Health Sciences Center
5001 El Paso Drive, El Paso TX, Zip Code 79905
Phone: (915) 783-5202

 ruth.g.perez@ttuhsc.edu

Ruth Perez received her B.S. and M.A. degrees from the University of Texas at El Paso and her Ph.D. from the University of Pittsburgh School of Medicine. After postdoctoral training at the Center for Neurologic Diseases at Brigham and Women’s Hospital of Harvard Medical School she joined the faculty of the Allegheny Singer Research Institute, Medical College of Pennsylvania Hahnemann at Allegheny University of the Health Sciences. She returned to the University of Pittsburgh in 1999 and obtained a tenure stream faculty appointment in 2005.  In 2010 she was promoted to Associate Professor of Neurology and had a secondary appointment in the Department of Pharmacology and Chemical Biology. In August of 2011, Dr. Perez returned to El Paso where she is Associate Professor of Biomedical Sciences at the Paul L. Foster School of Medicine. Her laboratory does basic science and translational research on neurodegenerative diseases with a focus on Parkinson’s disease and related disorders. Funding has been provided by the National Institute of Neurological Disorders and Stroke, National Institute on Aging, Michael J Fox Foundation, Ethyl Vincent Charitable Trust, Alzheimer’s Association, Scaife Family Foundation, and the Pittsburgh Foundation.

Research

The Perez lab studies the normal function of the key proteins that “go bad” in brain disorders.  Using biochemistry, cell biology, molecular biology, and mouse models the lab measures the effects of proteins on cell signaling, neuronal function, enzymatic activity and protein phosphorylation. Major projects focus on the contributions of alpha-synuclein and 14-3-3 proteins, two chaperone-like molecules that work in counterpoint to each other to regulate proteins with which they interact. Key projects on Parkinson’s disease (PD), Dementia with Lewy Bodies (DLB), Alzheimer’s disease (AD), and diabetes are in progress. With regard to PD, the Perez lab showed that alpha-synuclein, a protein strongly implicated in PD, is a normal regulator of dopamine synthesis, a brain neurotransmitter that contributes to olfaction, body movements, affect, and cognition.  Alpha-synuclein inhibits the rate limiting dopamine synthesis enzyme, tyrosine hydroxylase.  Dopamine is tightly regulated because it can be is toxic if overproduced and present in the cytosol. Another major regulatory property of alpha-synuclein is its ability to interact with and stimulate the activity of the catalytic subunit of protein phosphatase 2A (PP2A). PP2A dephosphorylates tyrosine hydroxylase and many other brain proteins. Additional data from the lab demonstrate that alpha-synuclein contributes to the release of insulin from pancreatic beta cells by interacting with the inwardly rectifying potassium channel, Kir6.2.  DLB studies reveal that alpha-synuclein aggregation impairs PP2A activity, which then allows hyperphosphorylation of tyrosine hydroxylase as well as tau, a small cytoskeletal protein that forms neurofibrillary tangles in AD brains. Those studies align with Alzheimer-related projects to elucidate the normal function of the amyloid precursor protein (APP) and the role of the Low Density Lipoprotein Receptor-related Protein (LRP) in neuronal development.  Together these projects form a concerted effort to identify novel targets for improving brain function to optimize the quality of life for patients with synucleinopathy. New studies reveal potential new compounds to reverse alpha-synuclein related neuropathology.

Recent Publications