August 19, 2024 – A groundbreaking study has revealed that neurons aren’t the only brain cells involved in the production of amyloid beta proteins, which have long been associated with Alzheimer’s disease. Researchers at the Max Planck Institute for Multidisciplinary Sciences in Germany have discovered that oligodendrocytes, the cells that support neurons, also contribute to the formation of amyloid beta clumps, potentially reshaping our understanding of this devastating disease.
New Perspective on Amyloid Beta Production
Amyloid beta proteins occur naturally in the brain but are linked to the development of Alzheimer’s disease when they aggregate into plaques. These plaques are believed to contribute to the neurodegeneration seen in Alzheimer’s patients. Until now, it was thought that neurons were the primary source of amyloid beta, making them the main target for new drug therapies. However, the limited success of these treatments suggests that other factors may be involved.
In a new study led by neurogeneticist Andrew Octavian Sasmita, the research team found that oligodendrocytes, a type of brain cell responsible for supporting neurons and forming the insulating myelin sheath around nerve fibers, also produce amyloid beta. By knocking out the gene responsible for the enzyme BACE1, which is crucial for amyloid beta production, in oligodendrocytes, the researchers observed a significant reduction in brain plaque formation about 30 percent fewer plaques compared to normal conditions.
Implications for Alzheimer’s Treatment
This discovery opens new avenues for Alzheimer’s treatment. “Potentially, selective targeting of BACE1 in oligodendrocytes could spare the detriments of widespread BACE1 inhibition,” the researchers suggest. Previous attempts to inhibit BACE1 broadly in the brain have led to negative side effects, including memory decline and reduced brain volume, due to BACE1’s role in neuron proliferation. However, targeting only oligodendrocytes may avoid these issues while still reducing plaque formation.
Despite these promising findings, some scientists caution against an overemphasis on amyloid beta as the sole cause of Alzheimer’s. There is ongoing debate in the scientific community about whether amyloid beta plaques are a cause or a consequence of the disease. Nonetheless, the involvement of oligodendrocytes in both amyloid beta production and myelin sheath formation another process that appears to be disrupted in Alzheimer’s suggests that these support cells could play a crucial role in the disease’s progression.
As Alzheimer’s continues to affect millions worldwide, with a new dementia diagnosis being made every three seconds, the need for effective treatments is more urgent than ever. This new research, published in Nature Neuroscience, adds a crucial piece to the puzzle, potentially paving the way for more targeted and effective therapies that could alleviate the symptoms or even slow the progression of Alzheimer’s disease.
As the scientific community continues to explore the complex mechanisms behind Alzheimer’s, this study highlights the importance of looking beyond neurons to fully understand and combat this elusive and devastating condition.
