Somatostatin and Alzheimer's disease

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)35-41
Number of pages7
JournalArchives of Gerontology and Geriatrics
Volume21
Issue number1
DOIs
Publication statusPublished - 1995

Fingerprint

Somatostatin
dementia
Alzheimer Disease
avoidance behavior
Somatostatin Receptors
NADP
learning
brain
deficit
animal
Learning
Avoidance Learning
Cysteamine
Neurons
Cognition
performance
evidence
Brain

Keywords

  • Alzheimer's disease
  • Receptors
  • Somatostatin

ASJC Scopus subject areas

  • Ageing
  • Geriatrics and Gerontology
  • Gerontology
  • Health(social science)
  • Medicine(all)

Cite this

Somatostatin and Alzheimer's disease. / Vécsei, L.; Klivényi, P.

In: Archives of Gerontology and Geriatrics, Vol. 21, No. 1, 1995, p. 35-41.

Research output: Contribution to journalArticle

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