British Columbia

UBC study links pre-birth vitamin A deficiency to increased Alzheimer's risk

The study found that mice deprived of vitamin A before birth were more likely to develop symptoms of the neurodegenerative disease — even if the vitamin deficiency was relatively minor.

Mice deprived of vitamin A in the womb more likely to develop dementia symptoms later in life, study finds

A new study has found that mice deprived of vitamin A before birth are more likely to develop symptoms of Alzheimer's disease. (Robert F. Bukaty/The Associated Press)

A new study led by a UBC researcher has found a link between in-utero vitamin A deficiency and an increased risk for developing Alzheimer's disease.

The study found that mice deprived of vitamin A before birth were more likely to develop symptoms of the neurodegenerative disease — even if the vitamin deficiency was relatively minor.

But the study also found that giving mice vitamin A supplements immediately after birth tended to counteract those effects.

Weihong Song, a professor of psychiatry at UBC and the Canada Research Chair for Alzheimer's Disease, said the study began when colleagues surveyed about 650 elderly people in Chongqing, China.

They found that 75 per cent of their subjects with mild or significant vitamin A deficiencies had symptoms of cognitive impairment, but of those with normal vitamin A levels, only 47 per cent suffered cognitive impairment.

"[We thought] maybe we should do something to see if this vitamin A deficiency will affect dementia, because cognitive decline is a major symptom of Alzheimer's disease," Song said.

Experiment used transgenic mice

So, Song and his colleagues developed an experiment to test the effects of pre-birth vitamin A deficiency in mice genetically modified to be predisposed to develop Alzheimer's disease.

"We found that the vitamin A deficiency in the pregnancy actually affected the brain development," Song said.

They found that mice deprived of vitamin A as fetuses developed more severe cognitive impairment and had increased rates of amyloid beta plaque formation — the plaque that kills neurons in Alzheimer's patients.

This was true even in mice deprived before birth compared to mice that were born healthy, but deprived of vitamin A after birth — meaning damage happens very early during brain development.

If the vitamin-deprived mice were given vitamin A supplements as newborns, their symptoms were almost completely reversed, Song said.

But waiting almost one or two months to give the supplements had a much smaller effect.

"The earlier the better," Song said.

Study focused on marginal deficiencies

Song said a major vitamin A deficiency will have more immediate negative effects, such as impaired retinal development and blindness, so they focused their efforts on marginal deficiencies, which are more common, particularly in developing and lower income countries.

Song said about 200 million preschool children worldwide suffer from marginal vitamin A deficiency. He said marginal deficiencies are hard to detect because they don't tend to cause significant clinical symptoms.

Song cautioned that the study was only done with mice, but would like to see follow-up studies done in humans. Specifically, he would like to see a longitudinal study tracking the cognitive functions of people in developing countries with vitamin A deficiencies.

He is also interested in seeing if vitamin A supplements are useful in reversing the early symptoms of dementia in humans.

The study was published in the journal Acta Neuropathologica.

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