In this provocative mouse study, researchers demonstrated that marginal vitamin A deficiency in utero may have large implications on cognitive function later in life, particularly in the development of Alzheimer's disease. It revealed that vitamin A deficiency increases the potential for amyloid beta to form in the brain, a hallmark of Alzheimer’s disease. Amyloid beta is a type of protein that forms tangles in the brain of Alzheimer’s patients, eventually leading to plaque formation and ultimately manifesting as major cognitive dysfunction and severe memory loss.
Specifically, amyloid precursor protein (generally benign when it stays intact) becomes amyloid beta when it is acted upon by a special enzyme that cleaves it. Vitamin A deficiency increases the activity of this enzyme, thus increasing the production of amyloid beta in the brain. When therapeutic doses of vitamin A was administered to mice, memory was restored, suggesting that “vitamin A supplementation might be a potential approach for Alzheimer’s disease prevention and treatment.”
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