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Stress, the Aging Brain, & the Mechanisms of Neuron Death

by Sapolsky, Robert M.

Stress, the Aging Brain, & the Mechanisms of Neuron Death cover
  • ISBN: 9780262193207
  • ISBN10: 0262193205

Stress, the Aging Brain, & the Mechanisms of Neuron Death

by Sapolsky, Robert M.

  • Binding: Hardcover
  • Publisher: MIT Press
  • Publish date: 02/01/2009
  • ISBN: 9780262193207
  • ISBN10: 0262193205
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Description: Looking beyond the now widely recognized relationships between stress and physical illness, this accessible and engagingly written book suggests that stress and stress-related hormones can also endanger the brain. Strategies to reduce stress and methods to protect neurons from further damage are proposed, and the relevance for humans of the animal research findings are clearly delineated.

Sapolsky provides an extensive review of the recent, exciting data on glucocorticoids, the adrenal steroid hormones (hydrocortisone or cortisol in humans) that are released during stress. Excessive exposure to these hormones can damage the brain and make neurons more vulnerable to neurological insults. The findings he reports and ideas he synthesizes may have profound implications for understanding brain aging and resistance of the brain to the damaging effects of strokes, seizures, and possibly Alzheimer's disease.

In part I Sapolsky focuses on how the failure of glucocorticoid regulation and subsequent excessive secretion combine to cause a complex cascade of degeneration in the brain during aging. In part 11 he addresses the implications of glucocorticoid neurotoxicity for neurology. Each chapter includes a helpful summary of the major points discussed as well as a capsule review of information from the previous chapters.

Robert M. Sapolsky is Associate Professor of Biology and Neuroscience at Stanford University. He is also Research Associate at the Institute for Primate Research, National Museums of Kenya, Nairobi, and a MacArthur Fellow.
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Product notice Returnable at the third party seller's discretion and may come without consumable supplements like access codes, CD's, or workbooks.
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