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Research article summary (published 30 May 2002):

The role of the metabolic lesion in Alzheimer's disease.

Full Abstract

This paper discusses the hypothesis that the cerebrometabolic deficiency in Alzheimer's disease(AD) is the proximate cause of the clinical disability. Several sets of observations support this hypothesis. (1) Impaired brain metabolism essentially always occurs in clinically significant AD, and the degree of clinical disability is proportional to the degree of metabolic impairment. The earliest, mildest changes in brain metabolism occur even before the onset of measurable cognitive impairment or atrophy. This observation disproves the now outdated assumption that the decreased metabolism is simply a consequence of decreased mental function or of atrophy. One of the important mechanisms reducing brain metabolism in AD appears to be damage to key mitochondrial components. Another appears to relate to inappropriate responses to insulin, i.e. to diabetes of the brain. (2) Inducing impairments of brain metabolism causes changes in mentation that mimic the clinical disabilities in AD, in both humans and experimental animals. (3) Preliminary results from several units suggest that treatment directed at the impairment of brain metabolism can improve neuropsychological functions in AD patients. The hypothesis presented here in no way negates the importance of other mechanisms in AD, such as amyloid accumulation, vascular compromise, and free radical action. However, those other abnormalities including amyloidosis can occur in people whose mentation is still clinically unimpaired. In contrast, once significant decrease in the rate of brain metabolism occurs, mentation becomes defective.

 

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Author information

Author/s: Blass, John P (JP); Gibson, Gary E (GE); Hoyer, Siegfried (S);

Affiliation: Weill-Cornell Medical College at Burke Medical Research Institute, 785 Mamaroneck Ave, White Plains, NY 10605, USA. jpblass(-atsign-)mail.med.cornell.edu

Journal and publication information

Publication Type: Journal Article; Review

Journal: Journal of Alzheimer's disease : JAD (J Alzheimers Dis), published in Netherlands. (Language: eng)

Reference: 2002-Jun; vol 4 (issue 3) : pp 225-32

Dates: Created 2002/09/12; Completed 2002/10/29; Revised 2005/11/16;

PMID: 12226541, status: MEDLINE (last retrieval date: 11/6/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Associated Chemicals: Amyloid beta-Protein (0)

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