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Vitamine D tegen de ziekte van Alzheimer*
Uit een Japanse studie, weliswaar met muizen, blijkt dat vitamine D belangrijk is in het voorkomen van de ziekte van Alzheimer. Uit eerdere studies was al vastgesteld dat lage bloedwaarden vitamine D gerelateerd zijn met de vermindering van geheugen en cognitieve functies bij het ouder worden. In deze studie werd naar het onderliggend mechanisme gezocht. Bij het ouder worden wordt het blijkbaar moeilijker om afbraakproducten als bèta amyloïd uit de hersenen en het hersenvocht te verwijderen. Vitamine D zo blijkt uit de studie zorgt voor een goede afvoer van bèta amyloid door de bloed-hersen-barrière heen zodat het verwijderd wordt.
1α,25-Dihydroxyvitamin D3 enhances cerebral clearance of human amyloid-β peptide(1-40) from mouse brain across the blood-brain barrier
Shingo Ito1,2, Sumio Ohtsuki1,2, Yasuko Nezu1, Yusuke Koitabashi1, Sho Murata1 and Tetsuya Terasaki1,2* 
· * Corresponding author: Tetsuya Terasaki terasaki@mail.pharm.tohoku.ac.jp 
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Fluids and Barriers of the CNS 2011, 8:20 doi:10.1186/2045-8118-8-20
Abstract
Background
Cerebrovascular dysfunction has been considered to cause impairment of cerebral amyloid-β peptide (Aβ) clearance across the blood-brain barrier (BBB). Further, low levels of vitamin D are associated with increased risk of Alzheimer's disease, as well as vascular dysfunction. The purpose of the present study was to investigate the effect of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3), an active form of vitamin D, on cerebral Aβ clearance from mouse brain. 
Methods
The elimination of [125I]hAβ(1-40) from mouse brain was examined by using the Brain Efflux Index method to determine the remaining amount of [125I]hAβ(1-40) radioactivity after injection into the cerebral cortex. [125I]hAβ(1-40) internalization was analyzed using conditionally immortalized mouse brain capillary endothelial cells (TM-BBB4). 
Results
Twenty-four hours after intraperitoneal injection of 1,25(OH)2D3 (1 μg/mouse), [125I]hAβ(1-40) elimination from mouse brain was increased 1.3-fold, and the level of endogenous Aβ(1-40) in mouse brain was reduced. These effects were observed at 24 h after i.p. injection of 1,25(OH)2D3, while no significant effect was observed at 48 or 72 h. Vitamin D receptor (VDR) mRNA was detected in mouse brain capillaries, suggesting that 1,25(OH)2D3 has a VDR-mediated genomic action. Furthermore, forskolin, which activates mitogen-activated protein kinase kinase (MEK), enhanced [125I]hAβ(1-40) elimination from mouse brain. Forskolin also enhanced [125I]hAβ(1-40) internalization in TM-BBB4 cells, and this enhancement was inhibited by a MEK inhibitor, suggesting involvement of non-genomic action. 
Conclusions
The active form of vitamin D, 1,25(OH)2D3, appears to enhance brain-to-blood Aβ(1-40) efflux transport at the BBB through both genomic and non-genomic actions. Compounds activating these pathways may be candidate agents for modulating Aβ(1-40) elimination at the BBB.

Het artikel. (December 2011)