Abstract:
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.
journal_name
Dement Geriatr Cogn Disordjournal_title
Dementia and geriatric cognitive disordersauthors
Dursun E,Gezen-Ak D,Yilmazer Sdoi
10.1159/000350319subject
Has Abstractpub_date
2013-01-01 00:00:00pages
76-86issue
1-2eissn
1420-8008issn
1421-9824pii
000350319journal_volume
36pub_type
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journal_title:Dementia and geriatric cognitive disorders
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journal_title:Dementia and geriatric cognitive disorders
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更新日期:2005-01-01 00:00:00
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journal_title:Dementia and geriatric cognitive disorders
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