Health
Glial cells identified as key players in Alzheimer's disease
Memory loss, confusion, speech problems – Alzheimer's disease is the most common cause of dementia, affecting around 35 million people worldwide, and the numbers are growing. Amyloid beta, a protein that occurs naturally in the brain, plays a central role in the disease. Amyloid beta accumulates in patients' bodies as insoluble clumps and damages neurons in the brain by forming plaques between them. Researchers at the Max Planck Institute for Multidisciplinary Sciences (MPI) have now revealed that in addition to neurons, specialized glial cells in the brain also produce amyloid beta. This discovery could pave new avenues for future treatments.
There is no cure for Alzheimer's disease. However, there are treatments that reduce amyloid plaques in the brain. These treatments can slow the progression of the disease but cannot reverse or stop it. “Until now, neurons have been thought to be the main source of amyloid beta production and have therefore been the main target for new drugs,” explains Klaus-Armin Nabe, Director of Interdisciplinary Sciences at MPI. His findings from the Neurogenetics Department show that in addition to neurons, specialized glial cells called oligodendrocytes also play an important role in plaque formation.
“One of the roles of oligodendrocytes is to form myelin, an insulating layer that wraps around nerve fibers to speed up signal transmission,” explains Andrew Octavian Susmita, one of the first authors of the now-published study. Nature Neuroscience “In a previous study, the Göttingen researchers had already found that myelin defects in oligodendrocytes exacerbate Alzheimer's disease. Do glial cells play an even bigger role than previously thought?”
“We found that although neurons are the main producers of amyloid-β, oligodendrocytes also produce significant amounts of the protein that is incorporated into plaques.”
Andrew Octavian Susmita, one of the study's first authors
A research group led by Marc-Aurel Bouchet of University College London (UK) recently came to a similar conclusion.
Preventing plaque formation
Cells in the nervous system produce amyloid beta by cleaving larger precursor molecules with the help of an enzyme called BACE1. For their experiments, the researchers specifically knocked out BACE1 in neurons and oligodendrocytes in mice. They then used 3D light-sheet microscopy to study plaque formation throughout the brain, providing a complete picture of amyloid plaques in all brain regions.
“In oligodendrocytes lacking BACE1, plaques were reduced by about 30 percent. Knocking out the BACE1 gene in neurons reduced plaque formation by more than 95 percent,” says Constanze Depp, first author of the study and a former doctoral student in Prof. Nave's department. The scientists also found that “plaque deposits only form if there is a certain amount of neuronal amyloid beta. Oligodendrocytes contribute to these plaques.”
This threshold could be useful in treating Alzheimer's: “If we can successfully inhibit BACE1 before this threshold is reached, plaques may form later,” Nave emphasizes. This could help slow the progression of Alzheimer's disease in its early stages.
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Journal References:
Sasmita, A.O. Others. (2024) Oligodendrocytes produce amyloid-β and contribute to plaque formation together with neurons in Alzheimer’s disease model mice. Nature Neuroscience. doi.org/10.1038/s41593-024-01730-3.
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