Memory loss, confusion, speech problems – Alzheimer's disease is the most common cause of dementia, affecting about 35 million people worldwide, and the number is growing. The protein amyloid beta, which occurs naturally in the brain, plays a central role in the disease: It accumulates in patients in insoluble clumps that form plaques between neurons in the brain, damaging them. Researchers at the Max Planck Institute (MPI) for Multidisciplinary Sciences have now shown that, in addition to neurons, special glial cells in the brain also produce amyloid beta.
This finding could open up new avenues for future therapies. There is no cure for Alzheimer's disease. However, there are therapeutic approaches to reduce the amyloid plaques in the brain.
That can slow down the progression of the disease, but it cannot reverse or stop it. "Until now, neurons were thought to be the main producers of amyloid beta and have been the main target for new drugs," explains Klaus-Armin Nave, Director at the MPI for Multidisciplinary Sciences. Results from his Department of Neurogenetics have now shown: In addition to neurons, special glial cells – called oligodendrocytes – play an important role in plaque formation.
"One of the tasks of oligodendrocytes is to form myelin – an insulating layer – and wrap it around the nerve fibers to speed up signal transmission," explains Andrew Octavian Sasmita, one of the first authors of the study now published in Nature Neuroscience and a former PhD .