Somatostatin and Alzheimerʹs disease

One of the most consistent neurochemical deficits in Alzheimerʹs 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 Alzheimerʹs 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 Alzheimerʹs disease. These findings may be of importance for possible therapeutic approaches using somatostatin-receptor-influencing compounds.