Researchers claim that infants who are carriers of the "Alzheimer’s gene" have observable differences in how their brains develop.
A study of 162 healthy infants between two and 25 months of age found that those who had the APOE-E4 gene variant, which is linked to Alzheimer's risk, had different grey and white matter growth compared to those without the gene.
Those are two types of tissue found in the central nervous system involved in neurological processes.
Using an MRI technique developed at Brown University’s Advanced Baby
Imaging Lab, the researchers found that the kids with the genetic variant had increased growth
in the frontal lobe of the brain and less growth in several middle and rear
areas. The low-growth areas were the same ones that have been shown
to be affected in elderly patients with Alzheimer’s, the researchers pointed out.
The changes in grey matter, the tissue involved in sensory perception and muscle control, were related to the density of nerve cells (neurons) and how they connected with cells in the brain. Differences in white matter affected the myelin insulation that helps brain cells form the highways that allow them to correctly transmit information.
“Maybe these changes are developmental,” study author Dr. Eric Reiman, executive director of the Banner Alzheimer’s Institute in Arizona, said to CBSNews.com. “Maybe they provide a foothold in areas of vulnerability where you would see progressive pathology in later ages. More studies need to be done to determine the extent of the progressive changes years later.”} Alzheimer’s disease is the most common form of dementia, making up 50 to 80 percent of dementia cases, according to the Alzheimer’s Association. It is the sixth-leading cause of death in the U.S., and more than 5 million Americans are currently living with the disease.
Most people will develop Alzheimer's when they are 65 and older, but up to 5 percent of the population suffers from an early-onset form of the disease. Alzheimer's gets worse over time and has no cure, but there are some treatments.
Reiman said that about 25 percent of the population have at least one of the APOE-E4 genetic variants, which contribute to their risk of developing Alzheimer’s. Two to three percent of the population will get two copies of the gene, one from each parent.
People who have an APOE genetic variant are four to five more likely to get the disease in older age than those who do not. Those that have two copies are at a higher risk. However, it is important to note that the majority of people with the faulty gene will not go on to get Alzheimer’s.
Reiman pointed out that these infants showed no signs of
developmental delays, and the infants who had the gene were not all destined to get
Alzheimer’s. He worried that some parents might feel they have to get a brain scan or genetics test for their child to determine his or her Alzheimer's risk. The neuroscientist cautioned against those actions, since they would not determine if a child was definitively going to get the disease or be able to help with earlier treatment.
"These tests are not indicated or helpful for either of those purposes," he said.
“This work is about understanding how this gene influences brain development,” senior author Sean Deoni, who oversees Brown University’s Advanced Baby Imaging Lab, added in a press release. “These results do not establish a direct link to the changes seen in Alzheimer’s patients, but with more research they may tell us something about how the gene contributes to Alzheimer’s risk later in life.”
In an accompanying editorial, Drs. John H. Growdon and Bradley T. Hyman, from the Neurology Service at Massachusetts General Hospital in Boston, said that the study proves that the APOE-E4 genotype is a risk factor for Alzheimer’s disease and may make the individual more susceptible to the disease at an earlier age.
“The results also raise intriguing questions about just 'when' AD-related brain alterations might be considered to start,” they wrote.
The study was published in JAMA Neurology on Nov. 25.