Scientists discover the future that helps your mind to clean itself – and fight Alzheimer’s disease

In Alzheimer’s disease, proteins such as beta amyloid form groups, known as paintings, which cause brain damage.

But in some people, the immune cells called the small glial cells are destroyed by these proteins before causing harm. This leads to a fewer and smaller number – and more moderate symptoms.

Researchers at the University of California, San Francisco, have identified a molecular future that enables small glial cells to get rid of the bita -amyloid paintings.

Without receptors, adgrg1, small glial cells are barely clarified on toxic protein. Using a mouse mouse for Alzheimer’s disease, the researchers noticed how ADGRGG1 loss led to a rapid accumulation of amyloid paintings, nervous degeneration, learning and memory problems.

“We believe this future helps in doing their work in maintaining brain health for many years,” said Xianhua Piao, PhD in Medicine, PhD in Pediatrics at UCSF.

In fact, when the researchers re -analyzed a previous study of genetic expression in the human brain, they found that the individuals who died due to mild Alzheimer’s disease had small glial cells with abundant adgrg1, and moderate cognitive weakness – which means that small glial cells came well and maintained the disease. But for those who died due to severe Alzheimer’s disease, the small glial cells did not have AdGRG1, and the paintings spread.

Adgrg1 is one of the hundreds of G -Protein receptors, which are routinely targeted in the development of the drug. This promises good for a quick translation to discover new treatments.

“Some people are lucky because they have responsible micrographic cells,” said Piao. “But this discovery creates an opportunity to develop medicines to make small glial cells effective against amyloid beta in everyone.”

Authors: Other Ucsf authors are Becca Chu, PhD, Andy Wangsu, PhD, Dianconu, PhD, Tao Lee, PhD, Rachel Schmidt, Stacy L. Grinberg, MD, PHD, Salvatore Spina, MD, PHD, Richard M. Ransohoff, MD, Arnold R. Kriegstein, MD, PHD, William W. Seley, MD, and Tomasz Nowakowski, PHD.

Funding: This work was partially funded by the National Institutes of Health (P01ag019724, P50Ag023501, R01NS094164, R01NS108446, K99ag081694), Unionia Prontotemport Research, The Tau Consortium, The Alzheimer’s Association (23AARG -NTF-1030341), Cure alzheimer box, and BRIGHTFOCUS Foundation Postdocontal (A2021020F).