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The Cellular Basis of Delirium and Its Relevance to Age-Related Disorders Including Alzheimer's Disease

Published online by Cambridge University Press:  07 January 2005

Gary E. Gibson ,
John P. Blass ,
Hsueh-Meei Huang  and
Gary B. Freeman
Gary E. Gibson
Affiliation:
Cornell University Medical College, Burke Medical Research Institute, White Plains, New York, U.S.A.
John P. Blass
Affiliation:
Cornell University Medical College, Burke Medical Research Institute, White Plains, New York, U.S.A.
Hsueh-Meei Huang
Affiliation:
Cornell University Medical College, Burke Medical Research Institute, White Plains, New York, U.S.A.
Gary B. Freeman
Affiliation:
Cornell University Medical College, Burke Medical Research Institute, White Plains, New York, U.S.A.
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Abstract

A wide variety of conditions lead to delirium (i.e., metabolic encephalopathies) in human beings and animals. Despite the varied etiology the clinical consequences are relatively stereotyped which suggests that the diverse insults that cause delirium may act by common metabolic and cellular “final pathways.” Related molecular and cellular mechanisms may be involved in aging and Alzheimer's disease, conditions that predispose to the development of delirium. Animal models of delirium better reflect age-related disorders such as Alzheimer's disease than those that impair a single neurotransmitter system such as the cholinergic system; the metabolic encephalopathies produce global cognitive disturbance, which is more typical of these disorders. Thus, research related to delirium has far-reaching implications for normal and abnormal brain function.

Type
Etiological Models and their Phenomenological Variants: Deficit Models
Information
International Psychogeriatrics , Volume 3 , Issue 2 , December 1991 , pp. 373 - 395
Copyright
© 1991 Springer Publishing Company

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