Jan. 27 (UPI) — Research from the University of British Columbia has found that biochemical reactions in brain tissue that cause Alzheimer’s disease can start in the womb.
The study, which was based on experiments with genetically engineered mice, found that a vitamin A deficiency in a fetus or newborn could start the biochemical reaction. Conversely, vitamin A supplements given to newborns could slow the progression of the disease.
Researchers examined the effects of vitamin A deficiency in the womb and in infancy on Alzheimer’s model mice, where critical stages of development of brain tissue programming occur.
The study found that a vitamin A deficiency in the womb caused mice to perform worse on standard tests of learning and memory. A mild vitamin A deficiency increased the production of amyloid beta, a protein that forms plaques that kill neurons in Alzheimer’s disease. Mice that were deprived of vitamin A in the womb but were then given a normal amount of the vitamin after birth performed poorly compared to mice that received a normal amount of vitamin A in the womb but were deprived after birth.
“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,” Dr. Welhong Song, a professor of psychiatry, Canada Research Chair in Alzheimer’s disease and author of the study, said in a press release.
Researchers also found that mice who were deprived in utero but were given supplements immediately after birth performed better than mice who were not given supplements pointing to a possible reversal of damage.
“In some cases, providing supplements to the newborn Alzheimer’s disease model mice could reduce the amyloid beta level and improve learning and memory deficits,” Song said. “It’s a matter of the earlier, the better.”
The study was published in Acta Neuropathologica.
