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Beta amyloid suppresses the expression of the vitamin d receptor gene and induces the expression of the vitamin d catabolic enzyme gene in hippocampal neurons.

Authors: Dursun, Erdinç  Gezen-Ak, Duygu  Yilmazer, Selma 
Citation: Dursun E, etal., Dement Geriatr Cogn Disord. 2013;36(1-2):76-86. doi: 10.1159/000350319. Epub 2013 Jun 7.
Pubmed: (View Article at PubMed) PMID:23752060
DOI: Full-text: DOI:10.1159/000350319


BACKGROUND/AIMS: The beta amyloid aggregations present in Alzheimer's disease affect neurons through various toxic alterations. The aim of this study was to determine the expression of the vitamin D receptor (VDR), 25-hydroxyvitamin D3 24-hydroxylase (an accelerator of vitamin D catabolism), and the L-type voltage-sensitive calcium channel A1C (LVSCC-A1C) in hippocampal neurons in response to beta amyloid and vitamin D treatments to test the protective effects of vitamin D and the probable effects of beta amyloid on vitamin D catabolism.
METHODS: The expression of the VDR, 24-hydroxylase (24OHase) and LVSCC-A1C mRNAs were studied using quantitative real-time polymerase chain reaction, and the cytotoxicity levels were determined by an ELISA in primary hippocampal neuron cultures prepared from Sprague-Dawley rat embryos.
RESULTS: Our results demonstrated that beta amyloid suppressed the expression of VDR mRNA and induced the expression of 24OHase and LVSCC-A1C mRNAs.
CONCLUSION: Beta amyloid may disrupt the vitamin D-VDR pathway and cause defective utilization of vitamin D by suppressing the level of the VDR and elevating the level of 24OHase.

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CRRD Object Information
CRRD ID: 13432075
Created: 2017-09-18
Species: All species
Last Modified: 2017-09-18
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.