Mathew T. Mizwicki completed his PhD at the University of California, Riverside and postdoctoral studies at UCR and UCLA. At the time of this webinar he was an Assistant Researcher at the David Geffen School of Medicine, in the Department of Surgery: Liver and Pancreas Transplantation. He has published more than 25 papers. He has since moved to Baxter International.

In this GrassrootsHealth webinar Mizwicki describes the proteins in the brain that are changed by Alzheimer's disease, one of these being the increase in Amyloid beta (1-42) plaques or A β1-42.

Work in Mizwicki's lab led to the finding that vitamin D in the circulatory system has an anti-inflammatory, or healing, affect in the brain. Vitamin D helps support the function of macrophages, which in turn help to prevent or slow down the progression of Alzheimer's disease.
 

Slide from webinar - healthy brain

In a healthy brain A β is produced and deposited in the brain through normal aging or trauma. A neuron "sees" the A β and recruits a macrophage from the periphery to bind to the A β plaque. The macrophage then returns to the circulatory system, with the A β on board, where it flows away from the brain and is eventually eliminated.

In a brain with Alzheimer's, when the A β is deposited a macrophage is recruited and binds to A β, but it may or may not return to the circulatory system. Sometimes the macrophage simply deposits the A β in other parts of the brain or within the blood-brain barrier. As Alzheimer's progresses, there is a build-up of A β  deposits in the brain.

Vitamin D, in the activated form of 1,25D3, plays a role in preventing or slowing the progression of Alzheimer's by regulating the function and survival of the immune cells, the macrophages, and being a neuro-protective hormone.
Mizwicki cannot recommend a definitive level of vitamin D that is optimal, but when working with patients he recommends a goal of 60 ng/ml (of 25OHD) and calls for more large RCTs to truly test the optimal serum level to prevent Alzheimer's.

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Does Vitamin D reduce the risk of dementia?
William B. Grant, PhD
Sunlight, Nutrition, and Health Research Center
2009
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This paper is written by an epidemiologist.  Dr. Grant studies the patterns, causes, and effects of health and disease in populations. This paper explores the hypothesis that "vitamin D can reduce the risk of developing dementia" with data from both observational and laboratory studies.

Grant presents data to validate that vitamin D can reduce the risk of many health conditions that are considered risk factors for dementia - cardiovascular diseases, diabetes, mellitus, depression, dental caries, osteoporosis, and periodontal disease. He also explains some of the studies on the brain, A β, and how vitamin D functions in the brain.

While his hypothesis is not proven in this paper, the supporting evidence is compelling and Grant recommends keeping a healthy vitamin D level, above 40 ng/ml. He states, "There is observational epidemiological evidence that vitamin D reduces the risk of several types of diseases that are risk factors for or can precede dementia. This evidence is supported by identification of mechanisms that vitamin D protects neurocognitive function.... However, until RCTs are performed, the hypothesis cannot be considered a fact."

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Serum Vitamin D Deficiency as a Predictor of Incident Non-Alzheimer Dementias: A 7-Year Longitudinal Study
Cedric Annweiler et al.
January 2012
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This study concluded that baseline vitamin D deficiency, in this case a serum 25-hydroxyvitamin D level < 10 ng/ml, predicted the onset of non-Alzheimer dementias within 7 years.  The study used forty high-functioning older women from Toulouse France who were then divided into two groups based on their vitamin D levels. They followed up after seven years. Non-Alzheimer dementia was found in 6 women with more cases observed from the vitamin D deficient group. They found the association between low vitamin D at baseline and the onset of non-Alzheimer dementia as a factor of 19 to 1.

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John Cannell, MD

Vitamin D Council

September 24, 2015

In this blog, Cannell reviews the evidence of the association between baseline 25(OH)D serum levels and the risk of dementia. Included is a summary and discussion about a recently published paper by Miller et al., which clearly demonstrated a considerable effect of vitamin D deficiency on brain function, with significant differences in the course of cognitive performance in association with 25(OH)D and the greatest rates of cognitive decline associated with 25(OH)D < 20 ng/ml.

Cognitive aspects of frailty: Mechanisms behind the link between frailty and cognitive impairment
Meltem G�lhan Halil et al.
March 2015
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Vitamin D deficiency may have some effects on underlying mechanisms of both frailty and cognitive decline. This review examines the relationship between frailty and cognitive decline and explores the role of vascular changes, hormones, vitamin D, inflammation, insulin resistance, and nutrition in the development of physical frailty and cognitive problems, as potential underlying mechanisms behind this link.