Alzheimer gene may shrink brain starting in childhood


A gene associated with Alzheimer’s disease may shrink brain structures and lower thinking skills as early as in childhood, decades before the illness actually appears, says a research.
The findings showed that children with epsilon(E)4 variant of the apolipoprotein-E gene showed differences in their brain development compared to children with E2 and E3 forms of the gene and were more likely to develop Alzheimer’s disease.
In such children the size of the hippocampus — a brain region that plays a role in memory — was found to be approximately 5 per cent smaller.
Specifically, the children as small as of age three showed up to 50 per cent lower scores on tests of executive function, working memory and attention.
Each person receives one copy of the gene (E2, E3 or E4) from each parent, so there are six possible gene variants: E2E2, E3E3, E4E4, E2E3, E2E4 and E3E4, the researchers explained.
Further, children younger than eight and with the E4E4 genotype typically had lower measures on a brain scan as well as had lower scores on a test on memory and thinking skills.
“Studying these genes in young children may ultimately give us early indications of who may be at risk for dementia in the future and possibly even help us develop ways to prevent the disease from occurring or to delay the start of the disease,” said study author Linda Chang from the University of Hawaii in Honolulu, US.
However, children older than 8 with these two genotypes had similar and normal test scores compared to the other children.
“These findings mirror the smaller volumes and steeper decline of the hippocampus volume in the elderly who have the E4 gene,” Chang added in the work published online in the journal Neurology.
For the study, the team analysed 1,187 children from ages three to 20 years who had genetic tests and brain scans and as well as took tests of thinking and memory skills.
The children had no brain disorders or other problems that would affect their brain development, such as prenatal drug exposure.
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