Retinoic acid normalizes nuclear receptor mediated hypo-expression of proteins involved in beta-amyloid deposits in the cerebral cortex of vitamin A deprived rats.
Neurobiology of Disease. 2006-07-01; 23(1): 1-10
DOI: 10.1016/j.nbd.2006.01.008
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1. Neurobiol Dis. 2006 Jul;23(1):1-10. Epub 2006 Mar 10.
Retinoic acid normalizes nuclear receptor mediated hypo-expression of proteins
involved in beta-amyloid deposits in the cerebral cortex of vitamin A deprived
rats.
Husson M(1), Enderlin V, Delacourte A, Ghenimi N, Alfos S, Pallet V, Higueret P.
Author information:
(1)Unité de Nutrition et Signalisation Cellulaire (E.A. MENRT; USC INRA) ISTAB,
Université Bordeaux 1, Avenue des Facultés, 33405 Talence cedex, France.
Recent data have revealed that disruption of vitamin A signaling observed in
Alzheimer’s disease (AD) leads to a deposition of beta-amyloid (Abeta). The aim
of this study was to precise the role of vitamin A and its nuclear receptors
(RAR) in the processes leading to the Abeta deposits. Thus, the effect of vitamin
A depletion and subsequent administration of retinoic acid (RA, the active
metabolite of vitamin A) on the expression of RARbeta, and of proteins involved
in amyloidogenic pathway, e.g., amyloid precursor protein (APP), beta-secretase
enzyme (BACE), and APP carboxy-terminal fragment (APP-CTF) was examined in the
whole brain, hippocampus, striatum, and cerebral cortex of rats. Rats fed a
vitamin A-deprived diet for 13 weeks exhibited decreased amount of RARbeta,
APP695, BACE, and of APP-CTF in the whole brain and in the cerebral cortex.
Administration of RA is able to restore all expression. The results suggest that
fine regulation of vitamin A mediated gene expression seems fundamental for the
regulation of APP processing.
DOI: 10.1016/j.nbd.2006.01.008
PMID: 16531051 [Indexed for MEDLINE]