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The Neuroscientist, Vol. 5, No. 4, 238-253 (1999)
DOI: 10.1177/107385849900500413

Reviews

Review : Gene Expression after Cerebral Ischemia

Sean I. Savitz

Department of Neurology, Neuroscience, Albert Einstein College of Medicine Bronx, New York

Daniel M. Rosenbaum

Department of Neurology, Neuroscience and Ophthalmology Albert Einstein College of Medicine Bronx, New York

Global and focal ischemias induce a variety of gene families, including immediate early genes, cytokines, neurotransmitter receptors, and heat-shock proteins. The Janus-like effects of several of these gene prod ucts promote neuronal survival and degeneration. Therefore, determining the molecular pathways respon sible for the differential regulation of these genes is of paramount importance. The discovery of apoptosis as a mediator of delayed neuronal death has led to the identification of a number of other genes involved in postischemic brain damage. Future neuroprotective therapies for cerebral ischemia may be directed at preventing alterations in gene expression. NEUROSCIENTIST 5:238-253, 1999

Key Words: KEY WORDS Antioxidants • Apoptosis • Cytokines • Glutamate • Heat-shock proteins • Immediate early genes


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