Somatostatin, tau, and β-amyloid within the anterior olfactory nucleus in Alzheimer disease

Impaired olfaction is an early symptom of Alzheimer disease (AD). This likely to reflect neurodegenerative processes taking place in basal telencephalic structures that mediate olfactory processing, including the anterior olfactory nucleus. Βeta-amyloid (Aβ) accumulation in AD brain may relate to decline in somatostatin levels: somatostatin induces the expression of the Aβ-degrading enzyme neprilysin and somatostatin deficiency in AD may therefore reduce Aβ clearance. We have investigated the expression of somatostatin in the anterior olfactory nucleus of AD and control brain. We report that somatostatin levels were reduced by ∼ 50% in AD brain. Furthermore, triple-immunofluorescence revealed co-localization of somatostatin expression with Aβ (65.43%) with Aβ and tau (19.75%) and with tau (2.47%). These data indicate that somatostatin decreases in AD and its expression may be linked with Aβ deposition.