A review on the relationship between vitamin D and low-density lipoprotein receptor-related protein (LRP-1) has revealed that the two may work together to possibly clear amyloid-beta (Aβ), whose deposition is considered linked to the progression of neurological dysfunction.
LRP-1 is a large receptor present on the body’s cells and is widely expressed, or present in several tissues. It’s a member of the LDL receptor family, which plays various different roles related to enzyme activation, the entry of bacterial toxins and viruses into cells and the metabolism of proteins that transport and combine with fats in the blood.
But LRP-1 has also been identified as a Aβ scavenger receptor that can remove Aβ from the brain through the blood-brain barrier. However, its expression is decreased in patients with neurological dysfunction.
This review points to recent evidence that after supplementation with the active form of vitamin D, 1,25 (OH)2D3, LRP1 expression increases significantly both in-vivo and in-vitro. This is because so many vitamin D receptors are expressed in the brain.
Several studies also suggest that vitamin D receptor (VDR, the receptor to which vitamin D binds to in the body) deficiency, or inhibition, could be a risk factor for neurodegenerative disease. This review establishes a strong connection between vitamin D, LRP-1, and their potential Aβ clearance abilities.
By neurological dysfunction, they mean Alzheimer’s disease. To review my previous blogs on this subject just type in “Alzheimer’s” in the search box in the upper left hand corner of my blog site. The formation of clusters of amyloid-beta plaque is a classic finding in Alzheimer’s disease. Previous studies have linked the uncoupling of copper by toxins and infection to the formation of these clusters. This study suggests that vitamin D plays a vital role in removing these triggers from the brain.
The active form of vitamin D is not what is typically measured in laboratory testing. That is because the levels in the blood fluctuate by the minute. What we typically measure is the inactive form 25 (OH)D3. However, there is good correlation with the inactive form in the blood and the active form in the tissues.
Some of us make the precursor to the inactive form when sunlight strikes the skin and converts cholesterol into D3. It is then transported to the liver to be converted to 25 (OH)D3. In turn, the inactive form is converted to the active form by the kidneys or by individual cells. Making vitamin D from sunlight is dependent on the vitamin D receptor (VDR receptor). Approximately 25% of the population has a defect in the VDR gene from one parent, limiting their ability to convert vitamin D from cholesterol. Eight percent of the population has the defect from both parents and cannot make the conversion.
More evidence of the need to supplement vitamin D. I recommend supplementation of vitamin D3 at 4,000 IU daily with laboratory testing at least annually. The laboratory norms are 30-100 ng/mL but the optimal range is 42-80 ng/mL.
Source: April 18, 2019 Biotics Research