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Myron D. Ginsberg, MD

Arch Neurol. 1996;53(10):1065-1067.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

THE POINT of contention implicit in the title of this article would, at first glance, appear to have little basis in reality. To challenge the validity of rodent studies of brain ischemia would seem on a par, for example, with questioning whether primate kidney cell cultures are a valid model for cultivating the human poliomyelitis virus.¹ A vast body of scientific literature spanning more than 3 decades attests to the utility of the rodent brain in modeling ischemic-anoxic injury.² Certain truths deserve emphasis here. As discomfiting as this may appear to certain members of our highly evolved species, it is nonetheless firmly established that there is a very high degree of genetic homology between humans and rodents.³ Thus, the use of rodents to study genes, messages, enzymes, second messengers, receptors, and neurotransmitters would be expected to lead to insights more relevant than not to the human brain. . . . [Full Text PDF of this Article]

Author Affiliations
From the Cerebral Vascular Disease Research Center, Department of Neurology, University of Miami School of Medicine, Miami, Fla.

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