A study by Canada-based researchers suggests that Alzheimer's disease could begin in womb or just after birth if the fetus or newborn does not get enough vitamin A. The study, which was performed on genetically-engineered mice, found that even a mild deficiency of vitamin A increased the production of a protein which aids in killing neurons during Alzheimer's and facilitates the disease.

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The study, conducted at the University of British Columbia, also demonstrates that supplements given to newborns with low levels of vitamin A could be effective in slowing the degenerative brain disease. Dr. Weihong Song, a professor of psychiatry and Canada Research Chair in Alzheimer's Disease, said that the study clearly shows that even a marginal deficiency of vitamin A has a detrimental effect on brain development and a long-lasting effect that can facilitate Alzheimer's disease in later life.

As a part of the research, Song started building on previous studies that have linked low levels of vitamin A with cognitive impairments. After collaborating with Dr. Tingyu Li and others at Children's Hospital of Chongqing Medical University, they examined the effects of vitamin A deficiency in the womb and infancy on Alzheimer's model mice.

The researchers found that even a mild vitamin A deficiency increased the production of amyloid beta, the protein that forms plaques that ultimately kill neurons in Alzheimer's disease. They also found that these mice, with deficiency of vitamin A, performed worse as adults on a standard test of learning and memory. Even the mice deprived of vitamin A in the womb, provided with a normal diet as pups, performed worse than mice who received a normal amount of the nutrient in the womb but were deprived after birth. In other words, the damage was already done in the womb.

The study was published in Acta Neuropathologica. The research was partly funded by the National Natural Science Foundation of China and Canadian Institutes of Health Research.