Arshad Majid, M.D.
Associate Professor, Neurology

Academic Appointments

• 2006-present: Associate Professor, Michigan State University
• 2002-2006: Assistant Professor, Michigan State University

Postdoctoral Training

• 1998-2001: Resident, University of Pennsylvania, Neurology
• 1996-1998: Fellow, Washington University
• 1994-1996: Intern, University of Glasgow

Education

• M.D., University of Glasgow, 1993
• B.S. Physiology at the University of Wales College of Cardiff, 1988

Arshad Majid graduated with a degree in Medicine from the University of Glasgow, Scotland in 1993. After residency training in Internal Medicine, he was elected Member of the Royal College of Physicians (MRCP) in the United Kingdom. His training also included a Neurology residency at the University of Pennsylvania and Fellowship training at Washington University in St. Louis.

Dr. Majid has published a number of papers in international peer-reviewed journals, and made presentations at national and international meetings. He has been presented with a number of awards in both the United Kingdom and United States for his research. Arshad joined the MSU faculty on July 1, 2002.

His immediate goal is to establish and lead the stroke program at MSU and Sparrow Health System. He will be the head of MSU's Division of Cerebrovascular Disease. His research interests include molecular mechanisms of cell death in neurological disease. 

Research Interests

The research in my lab is focused in two main areas. We are using single cell molecular genetics to identify genes that may play a critical role in the pathogenesis of human diseases like stroke and ALS.

1. Cerebral ischemic pre-conditioning
   
   Using a mouse model of cerebral ischemic preconditioning, we are characterizing changes in expression of genes that may play key roles in neuroprotection after cerebral ischemia in neurons and astrocytes. By comparing differential expression of genes in preconditioned and control animals, we are trying to characterize changes in expression of genes that may play a key role in endogenous neuroprotection. This strategy may open up many new avenues for future therapeutic intervention in stroke.
    
2. Pathogenesis of ALS
   
   The pathogenesis of motor neuron loss in amyotrophic lateral sclerosis (ALS) is still unknown, although a number of hypotheses have been proposed. An intriguing clinical hallmark of ALS is the relative lack of involvement of the nuclei of cranial nerves III, IV and VI, while there is extensive involvement of other brain stem nuclei. This relative resistance to vulnerability of different populations of neurons in ALS is the focus of our research.
   
   We are using human spinal cord and brain stem tissue obtained post-mortem as well as tissue from a mouse model of ALS to analyze gene expression in individual cells before and after clinical and pathological evidence of disease.
   
   

   Ubiquitin immunolabeled motorneurons in human spinal cord.	A single motorneuron has been microdissected.

Selected Publications

• Majid A, He YY, Gidday JM, Kaplan SS, Gonzalez E, Park TS, Fenstermacher JD, Ling W, Choi DW and Hsu CY. (2000). Differences in vulnerability to permanent focal cerebral ischemia in common mutant mouse strains. Stroke 31:2701-2706.
• Majid A, Kantor J and Delanty N. (2001). Antiplatelet agents in the secondary prevention of ischemic stroke. Annals Pharmacother 35:1241-7.
• Majid A, Galetta SL, Sweeney CJ, Robinson C, Mahlingham R, Smith J, Forghani B and Gilden DH. (2002). Epstein-Barr virus myeloradiculitis and encephalomyeloradiculitis. Brain 125:159-65.

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