A research consortium has identified four new genes that may contribute to late-onset Alzheimer’s disease.

Researchers say the findings could mean four different pathways are related to the formation of Alzheimer’s.

Identifying the function of the genes may help researchers detect changes in the brain before any symptoms of memory loss or intellectual decline are apparent.

Genetic profiling may also allow researchers to determine who is at risk of developing the disease and trigger new drug development.

“A significant aspect of our research is that these genes clarify three new pathways,” said Richard Mayeux, MD., MS. Chairman of the Department of Neurology of Columbia University Medical Center.

“APOE-e4 and the other genes identified earlier are related to the accumulation of amyloid in the brain; these new genes are involved in inflammatory processes, lipid metabolism, and the movement of molecules within cells.

“Therefore, we may now have four pathways that are critically related to the disease and that could really make a difference in how we study and potentially prevent and treat it.”

Until recently, only four genes associated with late-onset Alzheimer’s had been confirmed, with the gene for apolipoprotein E-e4 (APOE-e4) having the largest effect on risk.

The Nature Genetics studies add another four: MS4A, CD2AP, CD33, and EPHA1. The studies also contributed to the identification and confirmation of two other genes, BIN1 and ABCA7.

Researchers from 44 universities and research institutions collaborated to study more than 54,000 people with Alzheimer’s disease with the initiative led by Gerard D. Schellenberg, PhD, at Penn.

“This is the culmination of years of work on Alzheimer’s disease by a large number of scientists, yet it is just the beginning in defining how genes influence memory and intellectual function as we age.

“We’re all tremendously excited by our progress so far, but much remains to be done, both in understanding the genetics and in defining how these genes influence the disease process,” Schellenberg said.

The findings appear in the current issue of Nature Genetics.

Source: Columbia University Medical Center