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Neurology

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Neurology

Kathleen A. Maguire-Zeiss, Ph.D.

585-273-1503 (office)
585-273-2198 (lab)

Current Titles and Roles

2002- present; Research Assistant Professor (Center for Aging & Developmental Biology)

Degrees, Certifications, and Licenses

  • B.S., Biochemistry, Albright College
  • Ph.D., Pharmacology, Pennsylvania State University College of Medicine
  • Post-doctoral training, University of Pennsylvania, The Wistar Institute of Anatomy & Biology

Prior Work History

1997-2002; Associate, Neurology, Center for Aging & Developmental Biology, University of Rochester of Medicine & Dentistry

1996-1997; Senior Instructor, Neurology, Center for Aging & Developmental Biology, University of Rochester of Medicine & Dentistry

1993-1996; Senior Instructor, Neurology, Geriatric Neurology Unit, University of Rochester of Medicine & Dentistry

1990-1993; Instructor, Neurology, Geriatric Neurology Unit, University of Rochester School of Medicine & Dentistry

Highlights

  • Member Society of Neuroscience
  • Member American Society of Gene Therapy
  • Member Sigma Xi Research Society
  • NIH Individual National Research Service Award, National Cancer Institute, 1987-1990
  • Markey Foundation Pilot Grant, “Regulation of Calbindin D-28k Expression”, 1991-1992
  • Alzheimer's Association Pilot Research Grant, “Calcium binding proteins in Alzheimer’s Disease”, 1991-1992
  • American Health Assistance Foundation Alzheimer's Research Grant, "Calbindin D28k: Distribution & Regulation in AD", 1992-1995
  • Rochester Alzheimer's Disease Center Pilot, "Estrogen Receptor mRNA in AD", 1995-1996

Research

“Development and Application of Single Chain Antibodies for PD Therapy”
Principle Investigator: Howard J. Federoff, M.D., Ph.D.
Co-Investigator: Kathleen Maguire-Zeiss, Ph.D.

Project Number: DAMD17-02-1-0695
Source: DOD Dates of Approved/Proposed Project: 08/01/02-07/31/07

Parkinson’s disease affects over one million Americans and is the second leading neurodegenerative disease. The etiology of Parkinson’s disease is currently unknown but is thought to involve both genetic and environmental triggers. Despite multiple initiating factors, we and others envisage a common pathobiologic model of Parkinson’s disease. Sporadic and genetic forms of Parkinson’s disease display the profound loss of nigrostriatal dopamine neurons and the hallmark pathological feature of intracytoplasmic inclusions called Lewy bodies, comprised of a number of proteins including ?-synuclein. We are investigating the role of dopamine and ?-synuclein in the pathogenesis of Parkinson’s disease. Utilizing both in vitro and in vivo models of Parkinson’s disease we are studying the role of protein aggregation in this neurodegenerative disease. One of the major goals of this project is to establish the utility of single-chain antibody treatment for the attenuation of ?-synuclein aggregation, a posited convergent mechanism of Parkinson's disease pathophysiology.

Academic Activity

  • Lecturer, MBB II: Advanced Basic Sciences, Development & Degeneration: A Life-Long Balance Influencing Brain Function: 2002-Ongoing.
  • Lecturer, Neuroscience Investigative Seminars, Department of Neurosurgery: 2001.
  • Faculty facilitator, Ethics and Professional Integrity (IND 501, CRN 51942): 2001-2003.
  • Thesis Committee Member
  • Thesis Co-Advisor
  • Member Grant Peer Review Panel, American Institute of Biological Sciences, Neurotoxin Exposure & Treatment Research Program-2002
  • Ad Hoc Reviewer, Neurobiology of Aging