Scientists for the first time explained the role of a protein in the slow destruction of brain cells in Alzheimer’s disease, pinpointing a potential new target for treatments.
The protein, called Dkk1, appears in the brains of Alzheimer’s patients at higher levels than in healthy brains. Dkk1 is produced by beta amyloid plaque, a defining feature of the illness, and spurs the breakdown of nerve-fiber connections in the area of the brain linked to learning and memory, scientists at University College London found.
People with Alzheimer’s show signs of cognitive decline well before beta amyloid manifests into a detectable build-up of plaque. The researchers were able to identify Dkk1 and block it in mice, raising the possibility of stopping the destruction of brain tissue before irreversible dementia sets in. There is no cure for Alzheimer’s, and approved therapies only mitigate symptoms.
“The key thing here is to develop therapies to tackle this molecule before people exhibit a substantial loss of memory,” Patricia Salinas, leader of the study at the University College London’s Department of Cell & Developmental Biology, said in an interview. “That’s the great hope.”
Alzheimer’s is a degenerative neurological condition with no approved treatment to slow brain-cell death. As many as 5 million Americans have the disease, according to the U.S. Centers for Disease Control and Prevention in Atlanta.
Using brain slices from mice, scientists monitored how many nerve cells survived in the presence of the antibody that blocks Dkk1 compared with how many survived without the antibody. Brain cells exposed to the antibody remained healthy, with no signs of disintegration, they wrote in the Journal of Neuroscience. Antibodies are molecules produced by the immune system as part of the body’s defenses.
The research was funded by Alzheimer’s Research UK, a British dementia research charity, and the Biotechnology and Biological Sciences Research Council.