Somatostatin and Alzheimer's disease

One of the most consistent neurochemical deficits in Alzheimer's disease is a reduction in cortical somatostatin concentrations. The probability of a predominant regulatory change is heightened by the finding that 90% of somatostatin positive nonpyramidal neurons are also positive for NADPH, an...

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Bibliographic Details
Main Authors: Vécsei László
Klivényi Péter
Format: Article
Published: 1995
Series:ARCHIVES OF GERONTOLOGY AND GERIATRICS 21
doi:10.1016/0167-4943(95)00640-7

mtmt:1032275
Online Access:http://publicatio.bibl.u-szeged.hu/10549
Description
Summary:One of the most consistent neurochemical deficits in Alzheimer's disease is a reduction in cortical somatostatin concentrations. The probability of a predominant regulatory change is heightened by the finding that 90% of somatostatin positive nonpyramidal neurons are also positive for NADPH, and NADPH neurons are 'protected' in Alzheimer's disease and do not appear to be lost. The first evidence that somatostatin influences learning and memory processes in experimental animals was published more than a decade ago. These reports of somatostatin effects on cognitive functions in rats were later confirmed by several other studies. The somatostatin depleting substance cysteamine inhibited the learning and memory performance of rats in active and passive avoidance behavior tests. Post-mortem human studies suggest that although somatostatin concentration is reduced, the somatostatin receptors are less affected in the brain in Alzheimer's disease. These findings may be of importance for possible therapeutic approaches using somatostatin-receptor-influencing compounds.
Physical Description:35-41
ISSN:0167-4943