Somatostatin and Alzheimer's disease.

摘要: Alzheimer's disease (AD) is characterized by the cerebral deposition of senile plaques that are mainly composed a set peptides referred to as amyloid beta-peptides (Abeta). Among numerous neuropeptides produced in intrinsic cortical and hippocampal neurons, somatostatin (SRIF) has been found be most consistently reduced brain cerebrospinal fluid AD patients. SRIF receptors (SSTR), which mediate neuromodulatory signals SRIF, also markedly depleted brain, there being subtype-selective alterations areas. In rat temporal cortex, we have shown intracerebroventricular infusion Abeta25-35 results decrease SRIF-like immunoreactivity receptor subtype 2 (SSTR2) mRNA protein levels, correlation with SSTR functionality. Insulin-like growth factor-I prevents reduction these parameters induced Abeta25-35. Abeta recently demonstrated degraded primarily neutral endopeptidase, neprilysin, brain. regulates levels via modulation neprilysin activity. Because expression declines upon aging various mammals, including rodents, apes humans, aging-dependent hypothesized trigger accumulation suppressing action. Here present an overview recent advances on role its relationship peptides.