Due to the site upgrade, your MY ACCOUNT logins will need to be updated. Please access Forgot Your Password to make this change. If you do not have an account, click here.

Mouse study shows that Vitamin D may be required to prevent Alzheimer’s disease

Jul 19, 2011

Scientists from Tohoku University in Japan have found a role for vitamin D in clearing the brain of beta amyloid, a toxic compound that accumulates in the plaques that occur in the brains of Alzheimer’s disease patients.  In the researchers words “It was reported that single nucleotide polymorphisms in the vitamin D receptor (VDR) gene increase the risk of impairment of cognitive function and developing Alzheimer’s disease, suggesting a relation between serum vitamin D levels and risk of Alzheimer’s disease”. This means that people who genetically do not handle Vitamin D appropriately in their brain have an increased risk of Alzheimer’s disease however the study itself was in mice.  

Professor Tesuya Terasaki and his colleagues at Tohuko University’s Graduate School of Pharmaceutical Sciences injected mice with 1 alpha,25-dihydroxyvitamin D3; the active form of vitamin D3 in the body. They also in some injected the herbal compound Forskolin, or a control substance.  The animals were then examined to determine the rate of amyloid beta clearance and brain levels after 24 hours.

The rate of elimination of amyloid beta across the blood brain barrier was 1.3 times greater in mice that received vitamin D compared to those that received the control substance.  At 24 hours, endogenous amyloid beta levels were significantly lower in the vitamin D-treated group.

Forskolin was also shown to enhanced amyloid beta removal from the animals’ brains and while its action appears to be nongenomic (not related to genes), vitamin D’s actions were determined to be both genomic and nongenomic. "Vitamin D appears increase transport of amyloid β across the blood brain barrier (BBB) by regulating protein expression, via the vitamin D receptor, and also by regulating cell signaling via the MEK pathway,” Professor Terasaki explained. “These results lead the way towards new therapeutic targets in the search for prevention of Alzheimer's disease." The study is published online ahead of print in the journal Fluids and Barriers of the CNS.