Researchers Discover A New Cause For Alzheimer’s

The findings give doctors a new target for treatment.

DNA image via shutterstock.

DNA image via shutterstock.

Researchers at the MassGeneral Institute for Neurogenerative Disease at Massachusetts General Hospital announced that they have discovered and validated a new genetic cause for the most common form of Alzheimer’s disease.

Late-onset Alzheimer’s, which sets in after the age of 60, is the most common form of the disease, and according to MGH scientists, two recently discovered mutations in the the gene called ADAM10 may be the cause. The mutations in ADAM10 cause increased accumulation of a toxic protein in the brain and decreased production of cells in the part of the brain responsible for learning and memory.

An earlier study by this team of scientists suggested that both of these two ADAM10 mutations caused an increased risk of late-onset Alzheimer’s in seven different families. Bearing this study in mind, researchers set out to understand how ADAM10 and possible mutations in it can affect the brain’s learning and memory functions.

Experiments in mice with Alzheimer’s markers revealed that these two mutations reduced the ADAM10 gene’s function which resulted in accumulation of plaques, certain neurodegenerative signs associated with Alzheimer’s, and reduced production of new neurons to the hippocampus which is the brain’s center for learning and memory.

These new findings give doctors a target to look for and to treat in future late-onset Alzheimer’s patients.

Dr. Rudolph Tanzi, senior author of the study and director of the Genetics and Aging Research Unit at MGH, said in a press release:

 “What we found regarding the many effects of these two rare mutations in ADAM10 strongly suggests that diminished activity of this enzyme can cause [Alzheimer's disease], and these findings support ADAM10 as a promising therapeutic target for both treatment and prevention.”

Future studies, researchers say, will involve finding ways to increase ADAM10 productivity in order to keep new neurons firing to the hippocampus and prevent build-up of the toxic protein—both causes that led to Alzheimer’s related signs during mice experiments.

The researchers’ findings will be published in a paper in the October 16th edition of Neuron.