WASHINGTON, April 3 (Xinhua) -- In the largest study of its kind, researchers from a consortium led by the University of Pennsylvania School of Medicine, the University of Miami, and the Boston University School of Medicine, identified four new genes linked to Alzheimer's disease. The findings appeared Sunday in the current issue of Nature Genetics.
Each gene individually adds to the risk of having this common form of dementia later in life. These new genes offer a portal into what causes Alzheimer's disease and is a major advance in the field.
The study, conducted by the Alzheimer's Disease Genetics Consortium, reports genetic analysis of more than 11,000 people with Alzheimer's disease and a nearly equal number of elderly people who have no symptoms of dementia. Three other consortia contributed confirming data from additional people, bringing the total number of people analyzed to over 54,000. The consortium also contributed to the identification of a fifth gene reported by other groups of investigators from the United States, the United Kingdom, France, and other European countries.
The study is the result of a large collaborative effort with investigators from 44 universities and research institutions in the United States, led by Gerard Schellenberg at University of Pennsylvania.
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 are 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.
Until recently, only four genes associated with late-onset Alzheimer's have 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 -- and contribute to identifying and confirming two other genes, BIN1 and ABCA7, thereby doubling the number of genes known to contribute Alzheimer's disease.