Summary: A lack of vitamin A during pregnancy or shortly after birth may facilitate Alzheimer’s disease later in life, a new study reports.
Source: University of British Columbia.
Vitamin A deficiency could ‘program’ brain tissue.
Biochemical reactions that cause Alzheimer’s disease could begin in the womb or just after birth if the fetus or newborn does not get enough vitamin A, according to new research from the University of British Columbia.
These new findings, based on studies of genetically-engineered mice, also demonstrate that supplements given to newborns with low levels of vitamin A could be effective in slowing the degenerative brain disease.
“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,” said Dr. Weihong Song, a professor of psychiatry and Canada Research Chair in Alzheimer’s Disease.
For this research, Song built on previous studies that have linked low levels of vitamin A with cognitive impairments. In collaboration with Dr. Tingyu Li and others at Children’s Hospital of Chongqing Medical University, they examined the effects of vitamin A deprivation in the womb and infancy on Alzheimer’s model mice. These early developmental stages are crucial periods during which brain tissue is “programmed” for the rest of a person’s life.
The researchers found that even a mild vitamin A deficiency increased the production of amyloid beta, the protein that forms plaques that smother and ultimately kill neurons in Alzheimer’s disease. He also found that these mice, when deprived of vitamin A, performed worse as adults on a standard test of learning and memory.
Even when the mice deprived of vitamin A in the womb were given a normal diet as pups, they 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 had already been done in the womb.
Still, Song and his collaborators also showed that some reversal is possible: Mice who were deprived in utero but then given supplements immediately after birth performed better on the tests than mice who weren’t given such supplements.
“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,” said Song. “It’s a matter of the earlier, the better.”
The study, published today in Acta Neuropathologica, also included new evidence in humans of the vitamin A-dementia connection in later years. Examining 330 elderly people in Chongqing, Song and his collaborators found that 75 per cent of those with either mild or significant vitamin A deficiency had cognitive impairment, compared to 47 per cent of those with normal vitamin A levels.
However, Dr. Song cautions against overreacting to this news. Vitamin A deficiency, though common in many low-income regions of the world, is rare in North America, and excess intake of the nutrient could be harmful. Pregnant women in particular should not take excessive vitamin A supplements. A balanced diet is the best way to ensure adequate levels of the nutrient.
About this Alzheimer’s disease research article
Funding: A portion of the research was funded by the National Natural Science Foundation of China and Canadian Institutes of Health Research.
Source: Brian Kladko – University of British Columbia Image Source: NeuroscienceNews.com image is in the public domain. Original Research:Abstract for “Marginal vitamin A deficiency facilitates Alzheimer’s pathogenesis” by Jiaying Zeng, Li Chen, Zhe Wang, Qian Chen, Zhen Fan, Hongpeng Jiang, Yili Wu, Lan Ren, Jie Chen, Tingyu Lin, and Weihong Song in Acta Neuropathologica. Published online January 27 2017 doi:10.1007/s00401-017-1669-y
Cite This NeuroscienceNews.com Article
[cbtabs][cbtab title=”MLA”]University of British Columbia”Alzheimer’s Roots May Extend Back As Far As the Womb.” NeuroscienceNews. NeuroscienceNews, 27 January 2017. <https://neurosciencenews.com/vitamin-a-alzheimers-6014/>.[/cbtab][cbtab title=”APA”]University of British Columbia(2017, January 27). Alzheimer’s Roots May Extend Back As Far As the Womb. NeuroscienceNew. Retrieved January 27, 2017 from https://neurosciencenews.com/vitamin-a-alzheimers-6014/[/cbtab][cbtab title=”Chicago”]University of British Columbia”Alzheimer’s Roots May Extend Back As Far As the Womb.” https://neurosciencenews.com/vitamin-a-alzheimers-6014/ (accessed January 27, 2017).[/cbtab][/cbtabs]
Marginal vitamin A deficiency facilitates Alzheimer’s pathogenesis
Deposition of amyloid β protein (Aβ) to form neuritic plaques in the brain is the unique pathological hallmark of Alzheimer’s disease (AD). Aβ is derived from amyloid β precursor protein (APP) by β- and γ-secretase cleavages and turned over by glia in the central nervous system (CNS). Vitamin A deficiency (VAD) has been shown to affect cognitive functions. Marginal vitamin A deficiency (MVAD) is a serious and widespread public health problem among pregnant women and children in developing countries. However, the role of MVAD in the pathogenesis of AD remains elusive. Our study showed that MVAD is approximately twofold more prevalent than VAD in the elderly, and increased cognitive decline is positively correlated with lower VA levels. We found that MVAD, mostly prenatal MVAD, promotes beta-site APP cleaving enzyme 1 (BACE1)-mediated Aβ production and neuritic plaque formation, and significantly exacerbates memory deficits in AD model mice. Supplementing a therapeutic dose of VA rescued the MVAD-induced memory deficits. Taken together, our study demonstrates that MVAD facilitates AD pathogenesis and VA supplementation improves cognitive deficits. These results suggest that VA supplementation might be a potential approach for AD prevention and treatment.
“Marginal vitamin A deficiency facilitates Alzheimer’s pathogenesis” by Jiaying Zeng, Li Chen, Zhe Wang, Qian Chen, Zhen Fan, Hongpeng Jiang, Yili Wu, Lan Ren, Jie Chen, Tingyu Lin, and Weihong Song in Acta Neuropathologica. Published online January 27 2017 doi:10.1007/s00401-017-1669-y