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COURTESY AMANDA SHELL, JABSOM
Dr. Linda Chang in the control room of the UH-Queen’s Medical Center MR Research Center.
A national study of 1,187 children — including 256 kids from Hawaii — who carry variations of the gene linked to Alzheimer’s disease showed altered brain development at a young age, according to a University of Hawaii neurologist who led the study released today.
Children under the age of 10 who carry the epsilon(ε)4 variant of the apolipoprotein-E gene had “slightly delayed brain development and cognitive function,” said study author Dr. Linda Chang of UH’s John A. Burns School of Medicine, who is also a fellow of the American Academy of Neurology. “Therefore, these findings indicate that these genes not only can influence the development of Alzheimer’s disease later in life, but can also affect early brain development.”
However, Chang said “it’s important to emphasize that the older children with these genotypes showed normal brain structure and function.”
The study, conducted between 2010 and 2012, looked at individuals ages 3 to 20 who carry the epsilon(ε)4 variant of the apolipoprotein-E gene in nine communities across the country.
Those children are more likely to develop Alzheimer’s disease than people with the other two variants of the gene, ε2 and ε3, according to the study.
“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,” Chang said.
Researchers from UH, UCLA, USC, UC-San Diego, Johns Hopkins, Harvard, Yale, Cornell and the University of Massachusetts studied children in their communities. But the plurality of children who were studied came from Hawaii, Chang said.
“Hawaii was the site that collected 20 percent of the data,” she said, adding that the genetic work was performed at the Scripps Research Institute in San Diego.
In the future, Chang said, “The findings of this study might provide early indications of who might benefit from preventive measures when they become available.”
The study appears in today’s online issue of the Minneapolis-based Neurology, the medical journal of the American Academy of Neurology, the world’s largest neurology organization.
Wow! This is a big deal study both for diagnostics and for policy. ”Effects related to common genetic risk loci distributed throughout the genome are detectable among individuals without dementia. The influence of this genetic risk may begin in early life and make an individual more susceptible to cognitive impairment in late life.”