Affiliates

Administrative Staff  |  Research Staff  |  Post-Doctoral Fellows and Research Associates  |  Doctoral Candidates

Administrative Staff

Esam E. El-Fakahany, Ph.D.
Associate Director of the Center; Professor of Psychiatry, Neuroscience and Pharmacology,

elfak001@umn.edu
612-624-8432

As a researcher I have been interested in studying new therapies for the treatment of Alzheimer's disease. My responsibilities in the CMRC include coordination and growth of its basic and translational research and clinical care.

Pauline Sharpe
Secretary
BA, Child psychology, University of Minnesota

sharp005@umn.edu
612-625-0963

I provide administrative support to the members of the Center.

Research Staff

Colleen Forster
Scientist
BS, Business Administration, Cardinal Strich University
Qualified and Certified in Immunohistochemistry, American Society for Clinical Pathology

cforster@umn.edu
612-626-1930

I do the histological work in the mouse models. This includes grossing in the tissue, processing, embedding and staining.  I also assist with protocol design when new projects are developed. It is a great advantage to work with the team before projects begin, as it allows me to give them the best results possible.  I have a vested interest in Alzheimer's disease, as several people I know are afflicted with it; I am proud to be part of this important venture.

Marianne Grant
Scientist
B.A. Biology from MaCalester, St. Paul, MN.

Grant032@umn.edu
612-625-5654

Focuses on performing quantitative measurements of proteins that contribute to memory loss in Alzheimer’s disease

Lisa Kemper
Principal Laboratory Technician
BA, Biology, Whittier College

kempe050@umn.edu
612-625-5654

I co-manage the mouse husbandry unit, do behavioral testing on transgenic mice, and data analysis.

Linda Kotilinek
Scientist
BS, Biology, Medical Technology, Moorhead State University
Medical Technologist, American Society for Clinical Pathology

kotil001@umn.edu
612-626-0608

I co-manage the mouse behavioral testing, husbandry and biochemistry units.

Jen Paulson
Scientist
BS, Molecular Biology, Winona State University
MBS, Molecular Biology and Neuroscience, University of Minnesota

pauls075@umn.edu
612-625-5654

My responsibilities include creating and modifying DNA constructs for the creation of transgenic mouse models of Alzheimer’s disease. Once we have developed a model, I am also involved in monitoring the biochemical, pathological, and behavioral changes in the mice as they age to identify how well they mirror Alzheimer’s disease.

Anastasia Rupp-Moody
Junior Scientist
B.A. Biology from MaCalester, St. Paul, MN.

ruppm005@umn.edu
612-625-5654

Megan Schmidt
Principal Laboratory Technician
BS, Neuroscience, University of Minnesota

schm1181@umn.edu
612-625-5654

I help maintain the mouse colonies and do behavioral testing and data analysis.

Ulka Shrikhande
Scientist
M.S. Molecular Biology; Purdue University.

shrik002@umn.edu
612-625-5654

Main responsibility is to clone genes and create new mouse models of Alzheimer’s disease

Mathew Sherman
Assistant Scientist
BA, Biology, Gustavus Adolphus College

sherm044@umn.edu
612-625-5654

I work in all aspects of the lab, including colony maintenance, genotyping, and behavioral testing. More specifically, I am involved in protein biochemistry and look at Aβ species in both mouse and human brains, and how they relate to neurocognitive decline.

top

Post-Doctoral Fellows and Research Associates

Laura Hemmy, PhD
Post-doctoral Fellow
PhD, Neuropsychology, University of Minnesota

hemmy001@umn.edu
612-624-0144
 
I am interested in the neuropsychology of cognitive reserve in Alzheimer’s disease.

Brian Hoover
Post-doctoral Fellow
PhD, Neurobiology, University of California, Irvine
BA, Biology, Bucknell University, Lewisburg, Pennsylvania

hoove086@umn.edu
612-624-9198

I am studying the effects of tau on neuron function in in vitro models of Alzheimer’s disease in collaboration with Dr. Dezhi Liao in the Department of Neuroscience at the University of Minnesota.

Sylvain Lesné
Research Associate
PhD, Molecular and Cell Biology/Neuroscience, Université de Caen, France
BSc, Neuroscience and Immunology, Université de Caen, France

lesne002@umn.edu
612-626-2105

My studies aim at deciphering the culprit of memory decline in Alzheimer’s disease and the underlying cellular and molecular mechanisms leading to neuronal dysfunction.

Peng Liu
Post-doctoral Fellow
PhD, Biochemistry and Molecular Biology, University of Florida, Gainesville, Florida
BSc, Biotechnology, Peking University, College of Life Sciences, Beijing, China

liuxx726@umn.edu
612-624-9983

My current project focuses on optimizing purification of Aβ*56 from forebrain extracts of two different transgenic mouse lines, Tg2576 and J20, using a standard approach of immunoaffinity plus size exclusion chromatography.  Optimization is being performed with a goal to obtain high microgram to milligram yields for characterizing Aβ*56 in relation to biochemical stability, biophysical properties and molecular structure using techniques such as 2-D gels, mass spectrometry and X-ray crystallography.  

Miranda Reed
Post-doctoral Fellow
PhD, Behavioral Pharmacology, Auburn University, Auburn, Alabama
BA, Psychology, Auburn University, Auburn, Alabama

reedx264@umn.edu
612-624-9983

My research focuses on animal models of Alzheimer's disease and the effects of potentially therapeutic drugs on memory and learning in these animals.

top

Doctoral Candidates

Maureen Handoko
BA, Biochemistry, College of Saint Benedict , Saint John’s University

mhandoko@umn.edu
612-624-9983

I am developing capture reagents for Aβ*56, using phage display or aptamer technology, in order to measure Aβ*56 in spinal fluid, blood, or urine from humans with a high degree of sensitivity and specificity.  I will use these measurements to ascertain the ability of Aβ*56 to predict Alzheimer’s disease in pre-symptomatic individuals.

Zeb Kurth-Nelson
BS, Computer Science, Iowa State University

kurt0073@umn.edu
612-624-5946

I am investigating whether Aβ*56 is an antagonist of NMDA receptors. Other studies have established that amyloid-β oligomers can inhibit long-term potentiation (LTP), which could explain the memory loss that occurs early in the disease course. If we identify the responsible oligomer and its mechanism of action, then new therapies can selectively target this oligomer.

top