Scientists mapped the step-by-step actions that lead to late-onset Alzheimers disease, research that may offer new paths to developing treatments for the ailment.

People who carried the APOE4 gene, known to increase the risk of acquiring Alzheimers later in life, without having the disease, experienced changes in the expression of genes in their brains that resembled those of Alzheimers patients, according to a study published today in the journal Nature.

The changes in gene expression may point to early markers of the disease, and may help develop drugs for Alzheimers, for which there is no treatment or cure. They also bolster the idea that Alzheimers disease alters the brain long before patients become forgetful, said Dean Hartley, the director of scientific initiatives for the Alzheimers Association, an advocacy organization in Chicago. He wasnt involved in the study.

We do need to understand more about the mechanisms involved in Alzheimers diseases initiation and progression, Hartley said in a telephone interview, noting there havent been any successful clinical trials for drugs that try to alter the diseases path. This paper is important because its trying to look at whats being affected. It may suggest targets or pathways to look for new drugs.

The research also suggests that doctors should look to treat patients before they become forgetful, Hartley said. Studies like this one may help identify places to intervene before symptoms appear, he said.

More than 5 million people in the U.S. have Alzheimers, the most common form of dementia, and the number may increase to as many as 16 million by 2050, according to the Alzheimers Association.

There has been growing interest among scientists in what happens in the brain before a patient is diagnosed with clinical Alzheimers. Todays study is meant to help understand those changes at the molecular and cellular levels, Asa Abeliovich, a study author and neuroscientist at Columbia University in New York, said in a telephone interview.

The APOE4 gene increases the risk of developing late-onset Alzheimers, the most common form of the disease, by 3 times for those who have one copy of the gene, and 10 times in those who have two. That gene was first identified in 1991.

While APOE4 raises the risk of getting Alzheimers, most people with the mutation dont develop dementia, Abeliovich said. That suggests some other factor may be required for Alzheimers to begin. The most important non-genetic risk factor for Alzheimers is age. Understanding how the cellular changes from APOE4 interact with other risk factors may explain why some people develop the disease while others dont.

The researchers found 215 genes worked differently in those who had APOE4. They looked most closely at two, which act on how the body processes amyloid precursor protein, which creates the characteristic Alzheimers protein, beta amyloid.

Excerpt from:
Path of Alzheimer’s Disease Risk Gene Tracked, Scientists Say

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