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

Abstract:

: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.

journal_name

Exp Neurol

journal_title

Experimental neurology

authors

Saiz-Sanchez D,Ubeda-Bañon I,de la Rosa-Prieto C,Argandoña-Palacios L,Garcia-Muñozguren S,Insausti R,Martinez-Marcos A

doi

10.1016/j.expneurol.2009.06.010

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

347-50

issue

2

eissn

0014-4886

issn

1090-2430

pii

S0014-4886(09)00237-4

journal_volume

223

pub_type

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