Researchers may have found 11 new genetic links to Alzheimer's disease.
The finding could increase the number of therapeutic targets in terms of genetics, a University of Pennsylvania School of Medicine news release reported. The research also gives researchers a "broader view" of the genetic factors that are linked to Alzheimer's.
The immune system was found to have a "genetic overlap" with neurodegenerative diseases such as Parkinson's.
"Human genetic studies are being used with increased frequency to validate new drug targets in many diseases. Here we greatly increased the list of possible drug target candidates for Alzheimer's disease, finding as many new significant genes in this one study as have been found in the last 15 years combined," co-senior author Gerard Schellenberg, PhD, director of the Alzheimer's Disease Genetics Consortium (ADGC) and professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania, said.
"This international effort has given us new clues into the steps leading to and accelerating Alzheimer's disease. We can add these new genetic clues to what we already know and try to piece together the mechanism of this complex disease," he said.
The team looked at 74,076 patients and controls from 15 countries and performed a two-stage meta-analysis. The team found a number of genes that were known biological pathways of Alzheimer's disease.
One of the more significant findings was HLA-DRB5 - DRB1 which is a complex part of the genome that has been linked to inflammation and immune system responses. It has also been linked to Parkinson's and multiple sclerosis, which suggested similar conditions that involve abnormal proteins accumulating in the brain could have a mechanism in common. If this were true, it would mean these conditions have a "common drug target.
"We know that healthy cells are very good at clearing out debris, thanks in part to the immune response system, but in these neurodegenerative diseases where the brain has an inflammatory response to bad proteins and starts forming plaques and tangle clumps, perhaps the immune response can get out of hand and do damage," Schellenberg said.
"Through this powerful international group as well as our own US collaborations, we'll expand the data set even further to look for rare variants and continue our analysis to find more opportunities to better understand the disease and find viable therapeutic targets. Large-scale sequencing will certainly play a part in the next phase of our genetics studies," he said.
