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Hypercortisolism and its possible neural bases.

R M Sapolsky1, P M Plotsky

  • 1Department of Biological Sciences, Stanford University, California 94305-5020.

Biological Psychiatry
|May 1, 1990
PubMed
Summary

Biological psychiatrists study dexamethasone (DEX) resistance and hypercortisolism in neuropsychiatric disorders. Research suggests these endocrine abnormalities may stem from neural dysregulation within the complex adrenocortical axis.

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Area of Science:

  • Neuroendocrinology
  • Psychiatry
  • Endocrinology

Background:

  • Biological psychiatrists are interested in dexamethasone (DEX) resistance and hypercortisolism in neuropsychiatric disorders.
  • Endocrine abnormalities in these disorders are increasingly used as diagnostic and prognostic markers.
  • The complex adrenocortical axis involves CNS control, shifting hormonal sensitivities, and feedback regulation.

Purpose of the Study:

  • To review data on the neural basis of DEX resistance and hypercortisolism.
  • To propose models for how neural defects cause these endocrine abnormalities, drawing from rodent literature.

Main Methods:

  • Review of existing literature on DEX resistance and hypercortisolism.
  • Analysis of data suggesting neural involvement in endocrine defects.
  • Examination of rodent models to understand mechanisms.

Main Results:

  • Hypercortisolism in affective disorders, anorexia nervosa, Alzheimer's disease, and chronic stress is not uniform.
  • Elevated basal cortisol and DEX resistance can occur independently or together.
  • These endocrine abnormalities are suggested to be, at least partly, neural in origin.

Conclusions:

  • The endocrine dysregulation seen in various neuropsychiatric conditions likely has a significant neural component.
  • Understanding these neural mechanisms is crucial for developing better diagnostic and prognostic tools.
  • Further research into rodent models can elucidate the pathways underlying DEX resistance and hypercortisolism.

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