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Exp Neurol. 2010 Jun;223(2):347-50. doi: 10.1016/j.expneurol.2009.06.010. Epub 2009 Jun 25.

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

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Laboratorio de Neuroanatomía Humana, Departamento de Ciencias Médicas, Facultad de Medicina, Centro Regional de Investigaciones Biomédicas, Universidad de Castilla-La Mancha, 02006 Albacete, Spain.


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. Betaeta-amyloid (Abeta) accumulation in AD brain may relate to decline in somatostatin levels: somatostatin induces the expression of the Abeta-degrading enzyme neprilysin and somatostatin deficiency in AD may therefore reduce Abeta 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 approximately 50% in AD brain. Furthermore, triple-immunofluorescence revealed co-localization of somatostatin expression with Abeta (65.43%) with Abeta and tau (19.75%) and with tau (2.47%). These data indicate that somatostatin decreases in AD and its expression may be linked with Abeta deposition.

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