Alzheimer’s disease affects 32 million people globally, with research ongoing to find ways to slow or stop its progression. A team of researchers from the Icahn School of Medicine at Mount Sinai in New York found that changing certain cellular interactions can help clear out beta-amyloid plaques in the brain, a sign of Alzheimer’s disease. This discovery could lead to new treatment options for the condition. Plexin-B1, a protein identified as crucial in late-onset Alzheimer’s disease, was the focus of the study. The team of researchers found that activating plexin-B1 in reactive astrocytes, cells in the central nervous system that respond to disease or injury, prevents proper plaque clearance. By targeting plexin-B1, researchers hope to develop new therapies for Alzheimer’s disease.
The study, led by Roland H. Friedel, PhD, Hongyan Zou, MD, PhD, and Bin Zhang, PhD, showcases a team approach from three different labs, exploring the function of plexin-B1 in Alzheimer’s disease for the first time. By investigating how plexin-B1 interacts with reactive astrocytes, the researchers found that activating plexin-B1 impaired the ability of these cells to clear plaques, while removing plexin-B1 led to better amyloid clearance. The three researchers are working on identifying potential drugs or antibodies to modulate plexin-B1 function in reactive astrocytes, aiming to contribute significantly to Alzheimer’s disease research efforts.
Karen D. Sullivan, PhD, a neuropsychologist not involved in the study, sees promise in the findings, suggesting that targeting glia cells to reduce neuroinflammation and compact amyloid plaques could potentially slow down the progression of Alzheimer’s disease. However, she stresses that the research is still in the preliminary, preclinical stage and needs further validation in human studies. Similarly, Clifford Segil, DO, a neurologist not associated with the study, expresses skepticism about targeting plaque build-up as an effective strategy for treating Alzheimer’s disease. He highlights the lack of evidence showing that removing amyloid plaque improves cognitive function in patients with the disease.
Segil questions the emphasis on targeting beta-amyloid plaques in Alzheimer’s research, given reports of modest improvements in cognition with current anti-amyloid medications. He suggests that alternative approaches, such as investigating the role of plexin-B1 in brain neuron support cells or microglia, may offer new insights into treating memory loss in Alzheimer’s patients. Segil calls for more research on brain microglia and the brain lymphatic system to uncover novel ways to address cognitive decline in Alzheimer’s disease. Despite differing opinions on the best approaches to treating Alzheimer’s, researchers remain dedicated to finding innovative solutions to combat this challenging neurodegenerative disease.
