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Vitamin A deficiency linked with Alzheimer’s disease

By Tim Sandle     Feb 5, 2017 in Health
Brain tissue could be "programmed" for life during early development in the womb and during infancy. One key factor is Vitamin A, and deficiency could be linked to developing Alzheimer's disease later in life.
This finding is the basis of a new study conducted in mice and it follows on from earlier research about levels of vitamin A and an association with cognitive deficits. According to scientists from the University of British Columbia, when genetically-engineered mice have a slight vitamin A deficiency this leads to an increased production of amyloid beta in the brain. Conversely, giving vitamin A supplements given to newborn mice slows down development of the degenerative disease.
Amyloid beta is the probable cause of Alzheimer’s disease, when plaque forms in the brain over time. Amyloid plaques, as Digital Journal has reported, are a form of adhesive build-up that can accumulate outside nerve cells. When it is associated with Alzheimer’s disease the protein divides improperly (by folding). This creates a form called beta amyloid. This folded protein is toxic to neurons in the brain (and consequently neural death occurs.)
Commenting on the new research to Bioscience Techniques, principal scientist Dr. Weihong Song explains: “Our study clearly shows that marginal deficiency of vitamin A, even as early as in pregnancy, has a detrimental effect on brain development and has long-lasting effect that may facilitate Alzheimer’s disease in later life.”
The researcher explains that developmental damage can occur in the womb, as modelled on mice that were deprived of vitamin A in utero. Importantly, when these mice were fed a normal diet after birth this did not sufficiently address the problem. In later life these mice performed far worse in tests compared with rodents who received a sufficient amount of the vitamin when in the womb.
One positive sign, however, was when the mice deprived of vitamin A in the womb were given additional supplements containing vitamin A (above what is found in a normal diet) during the first few weeks following birth, they showed a slower rate of cognitive decline and performed better in the tests.
The extent to which the findings relate to people becomes the next phase of research. Key here will be to see if higher doses of vitamin A in early life make a difference. The problem us there is no easy way to run an accelerated study and gaining data will take the course of human life to demonstrate the vitamin A effect. It is known, however, from medical records that there is a link between vitamin A deficiency and dementia later in life in humans.
The findings are published in the journal Acta Neuropathologica, in the paper “Marginal vitamin A deficiency facilitates Alzheimer’s pathogenesis.”
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