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Mufson
Elliott
J.
PhD
The Alla V. and Solomon Jesmer Chair in Aging
Professor
Neurological Sciences
1735 W. Harrison
Cohn Research Building
Ste. 310
Chicago,IL 60612

1735 W. Harrison
Cohn Research Building
Ste. 300
Chicago,IL 60612

(312) 563-3583
(312) 563-3571
emufson@rush.edu
Posdoctoral Fellow, Harvard Medical School, 1978

PhD, Downstate Medical Center, SUNY, New York, 1977

MA, Kansas State University, Manhattan, Kan., 1971

BA, Hunter College, New York, 1969

Pathological Conditions Signs and Symptoms
Animal surgery/Modeling, Immunohisto-/immunocytochemistry, In Situ Hybridization, Laser Capture

Research Interests

The focus of the research of Dr. Mufson's laboratory revolves around gaining a greater understanding of the mechanisms underlying the selective vulnerability of neuronal populations which degenerate in people with mild cognitive impairment (MCI), Alzheimer's disease (AD) and Parkinson's disease (PD). In AD he has been performing studies aimed at defining the underlying mechanisms, which play a role in the degeneration of cholinergic basal forebrain neurons. In particular, his laboratory has performed numerous studies aimed at determining the involvement of the neurotrophin NGF and its high affinity trkA receptor as well as the low affinity p75 NTF receptor in the selective vulnerability of cholinergic basal forebrain (CBF) neurons in AD. More recently, Dr. Mufson's laboratory demonstrated that cholinergic deficits are not evident in subjects with early MCI or mild AD, leading to major rethinking of the validity of pathophysiologic markers underlying cognitive decline.

For Parkinson's disease (PD), this laboratory has been evaluating the neurotrophin brain derived neurotrophic factor (BDNF) as a potential factor for the treatment of this disease. Studies are being performed on the tissue samples of the human substantia nigra to evaluate age and disease related changes of the dopamine transporter (DAT) in PD.

Dr. Mufson's laboratory also is investigating the uniquely human galaninergic plasticity response, which occurs within the basal forebrain in AD. The laboratory is examining changes in receptor pharmacology and gene expression for galanin as well as whether its over expression correlates with cognitive decline in AD. Recent findings in galanin-deficient and over-expressing mice have shown a neurotrophic of galanin on cholinergic basal forebrain neurons as reported in PNAS.

The laboratory has also undertaken studies aimed at evaluating the involvement of apolipoprotein E (ApoE) in the pathogenesis of AD. An increased expression of the ApoE allele e4 is a risk factor for the onset of familial and sporadic AD.

Dr. Mufson's laboratory has undertaken molecular biological studies of the genetic profiles of neurons that are selectively impacted in people with MCI. These studies are part of an NIA funded program project entitled "Neurobiology of Mild Cognitive Impairment in the Elderly".

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