The finding is leading the researchers to develop an eye test for early signs of Alzheimer’s in both disorders.

“People with Down syndrome develop symptoms of Alzheimer’s-type dementia often by the age of 30,” said study co-author Dr. Lee E. Goldstein, associate professor at Boston University School of Medicine, in a statement. “This is because they have an extra copy of a key Alzheimer’s gene that leads to increased amyloid-beta accumulation in the brain. We discovered that this same protein starts to accumulate very early in the lens of the eye, even in children.”

“The results are striking,” added Dr. David G. Hunter, ophthalmologist-in-chief at Children’s Hospital Boston and vice chairman of the department of ophthalmology at Harvard Medical School. “We have known that these cataracts are prevalent in people with Down syndrome and are sometimes seen at birth, but we never knew how they were related to the disorder. Now we know. These distinctive cataracts appear only in people with advanced Alzheimer’s disease and much earlier in Down syndrome.”

Goldstein said the team is developing an eye scanner to measure amyloid-beta, the protein in question, in the lens. “This approach may provide a way for early detection and monitoring of related pathology in the brain. Effective treatments for the brain disease in Down syndrome and Alzheimer’s disease are on the horizon, and early detection is the key for successful intervention.”

Previous research had suggested that clumps of amyloid protein, which damage neurons and are characteristic of Alzheimer’s disease, begin appearing many years before Alzheimer’s symptoms appear. But the link between the deposits and memory impairment had not been clearly demonstrated in humans.

In the new study, which appears in the July 30 issue of Neuron, U.S. researchers used medical imaging to examine the brains of older people who did not have significant memory impairment.

“Two recent advances in neuroimaging now allow us to explore the early, asymptomatic phase of [Alzheimer's disease], the ability to measure amyloid distribution in living humans and the identification of sensitive markers of brain dysfunction” in the disease, Dr. Reisa Sperling, of the Center for Alzheimer’s Research and Treatment at Brigham and Women’s Hospital in Boston and lead author of the study, said in a news release from the journal’s publisher.

The researchers found that a number of study participants had amyloid deposits and abnormal activity in areas of the brain believed to be involved in memory function.

The results could help in efforts to find ways to predict and treat cognitive decline in people at risk for Alzheimer’s, the study authors noted.

“Longitudinal studies are certainly needed, but our findings are consistent with the premise that cognitively intact older individuals with amyloid pathology may already be in the early stages of [Alzheimer's disease],” Sperling said. “The combination of molecular and functional imaging techniques may prove useful in monitoring disease progression prior to significant clinical symptoms, as well as the response to amyloid-modifying therapeutic agents in subjects at risk for developing [Alzheimer's disease].”