Neurobiology of Aging, Available online 3 February 2012
Liyong Wanga, #, Kenju Haraa, d, #, Jessica M. Van Baaren a, Justin C. Price a, Gary W. Beecham a,
Paul J. Gallins a, Patrice L. Whitehead a, Gaofeng Wang a, Chunrong Lu a, Michael A. Slifer a,
Stephan Züchner a, Eden R. Martin a, Deborah Mash b, Jonathan L. Haines c, Margaret A. Pericak-Vance a,
John R. Gilberta, jgilbert at med.miami.edu
a Hussman Institute for Human Genomics, University of Miami Miller School of Medicine (1501) NW 10 Ave, Miami, Florida, USA
b Department of Neurology, Brain Endowment Bank, University of Miami Miller School of Medicine, 3049 Parkinson Building, Miami, Florida, USA
c Center for Human Genetics Research, Vanderbilt University Medical Center, 519 Light Hall, Nashville, Tennessee, USA
d Current address: Department of Neurology, Akita Red Cross Hospital, 222-1 Kamikitate Saruda Nawashiro-sawa Akita City, Japan 010-1495
Genetic studies on late-onset Alzheimer's disease (AD) have repeatedly mapped susceptibility loci onto chromosome 12q13, encompassing the vitamin D receptor (VDR) gene.
Epidemiology studies have indicated vitamin D insufficiency as a risk factor for AD.
Given that VDR is the major mediator for vitamin D's actions, we sought to clarify the role of VDR in late-onset AD.
We conducted an association study in 492 late-onset AD cases and 496 controls with 80 tagging single nucleotide polymorphisms (SNPs).
The strongest association was found at a promoter SNP rs11568820 (P = 9.1×10?6, odds ratio (OR) = 1.69), which resides within the transcription factor Cdx-2 binding site and the SNP has been also known as CDX2.
The risk-allele at rs11568820 is associated with lower VDR promoter activity (p < 10?11).
The overexpression of VDR or vitamin D treatment suppressed amyloid precursor protein (APP) transcription in neuroblastoma cells (p < 0.001).
We provide both statistical evidence and functional data suggesting VDR confers genetic risk for AD.
Our findings are consistent with epidemiology studies suggesting that vitamin D insufficiency increases the risk of developing AD.
- Overview Cognition and vitamin D has lots on Alzheimer's disease - including the following
EVERY SINGLE ONE of the above associations with Alzheimer's Disease is also associated with low vitamin D:
- physical inactivity - not get out in the sun
- depression - a common result of low vitamin D:
- Smoking - well known to consume vitamin D
- mid-life hypertension a result of low vitamin D:
- mid-life obesity - which results from low vitamin D, and Obesity makes vitamin D levels even lower
- Low education - take far fewer nutritional supplements - due to cost, knowledge, belief
Note: low education is also associated with dark skinned people, who get less vitamin D from the sun
- diabetes - a result of low vitamin D:
- Vitamin D Receptor category listing has
265 items along with related searches
The items in both Cognition and Vitamin D Receptor categories:
- Alzheimer’s (1.2X) and Parkenson’s (1.3X) more likely if poor Vitamin D Receptor – meta-analysis March 2019
- Treating herpes reduced incidence of senile dementia by 10 X (HSV1 reduces VDR by 8X) – 2018
- Body may changes gene activation if more Vitamin D is needed by tissue (Schiz. in this case) – Oct 2018
- Alzheimer’s associated with Vitamin D and Vitamin D receptor – video and pdf – Aug 2018
- Cerebral small vessel disease 2.5 X more likely if poor Vitamin D Receptor – Sept 2018
- Alzheimer’s Disease is associated with genes which restrict vitamin D – Aug 2015
- Parkinson's and Alzheimer's: associations with vitamin D receptor genes and race – meta-analysis July 2014
- Alzheimer’s patients 3X more likely to have a malfunctioning vitamin D receptor gene – 2012
- Alzheimer’s patients are genetically 70 percent more likely to be vitamin D in-efficient – Feb 2012
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