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J Nutr Biochem. 2019 May;67:123-137. doi: 10.1016/j.jnutbio.2019.01.015. Epub 2019 Feb 11.

Profiling of Alzheimer's disease related genes in mild to moderate vitamin D hypovitaminosis.

Author information

1
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany; Neurodegeneration and Neurobiology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany; Deutsches Institut für DemenzPrävention (DIDP), Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: marcus.grimm@uks.eu.
2
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: Anna.Lauer@uks.eu.
3
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: Sven.Groesgen@uks.eu.
4
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: andrea.thiel@uks.eu.
5
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany; Department of Internal Medicine II-Gastroenterology, Saarland University Hospital, Saarland University, Kirrberger Str. 100, 66421 Homburg/Saar, Germany. Electronic address: Johannes.Lehmann@uks.eu.
6
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: jakob.winkler@uks.eu.
7
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: Daniel.janitschke@uks.eu.
8
Department of Internal Medicine V-Pulmonology, Allergology, Respiratory Intensive Care Medicine, Saarland University Hospital, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: christian.herr@uks.eu.
9
Department of Internal Medicine V-Pulmonology, Allergology, Respiratory Intensive Care Medicine, Saarland University Hospital, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: christoph.beisswenger@uks.eu.
10
Department of Internal Medicine V-Pulmonology, Allergology, Respiratory Intensive Care Medicine, Saarland University Hospital, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: robert.bals@uks.eu.
11
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: heike.grimm@uks.eu.
12
Experimental Neurology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany; Neurodegeneration and Neurobiology, Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany; Deutsches Institut für DemenzPrävention (DIDP), Saarland University, Kirrberger Str. 1, 66421 Homburg/Saar, Germany. Electronic address: tobias.hartmann@uniklinikum-saarland.de.

Abstract

A vast majority of the elderly population shows a mild to moderate vitamin D deficiency. Besides the well-known function of vitamin D, vitamin D receptor is also expressed in brain and is discussed to regulate several genes. However very little is known whether genes are regulated, associated with Alzheimer's disease (AD). Here we investigate 117 genes, known to be affected in AD, in mouse brain samples with a mild vitamin D hypovitaminosis comparable to the vitamin D status of the elderly population (20%-30% deficiency). The 117 genes include two positive controls, Nep and Park7, already known to be affected by both AD and vitamin D hypovitaminosis. The 25 most promising candidates were verified in a second independent mouse cohort, resulting in eleven genes further evaluated against three additional housekeeping genes. Three of the remaining eight significantly altered genes are involved in APP homeostasis (Snca, Nep, Psmb5), and each one gene in oxidative stress (Park7), inflammation (Casp4), lipid metabolism (Abca1), signal transduction (Gnb5) and neurogenesis (Plat). Our results tighten the link of vitamin D and AD and underline that vitamin D influences several genes also in brain, highlighting that a strong link not only to AD but also to other neurodegenerative diseases might exist.

KEYWORDS:

Alzheimer’s disease; Gene expression; Neurodegeneration; Vitamin D hypovitaminosis; Vitamin D receptor

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