This protein could stop Alzheimer's disease

Researchers are exploring a promising new avenue for treating Alzheimer's disease by focusing on a specific protein that could enhance the removal of amyloid plaques in the brain.


A team from the Icahn School of Medicine at Mount Sinai has made a major breakthrough in Alzheimer's disease research. Their study, published in Nature Neuroscience on May 27, identifies a promising method to slow or even halt the progression of the disease by targeting reactive astrocytes and the protein plexin-B1.

This innovative research focuses on manipulating the protein plexin-B1 to enhance the brain's ability to clear amyloid plaques, a hallmark of Alzheimer's disease. Reactive astrocytes, brain cells activated in response to injury or disease, play a crucial role in this process by regulating the space around amyloid plaques.

Roland Friedel, PhD, Associate Professor of Neuroscience and Neurosurgery at Mount Sinai, emphasizes that this discovery offers a new pathway for developing treatments by improving cellular interactions with these harmful plaques. This research builds on complex data analyses comparing healthy individuals with those affected by Alzheimer's disease.

Hongyan Zou, PhD, Professor of Neurosurgery and Neuroscience at Mount Sinai, highlights the broader implications of these findings, underscoring the importance of cellular interactions in developing treatments for neurodegenerative diseases. The study also validates multiscale gene network models of Alzheimer's, significantly advancing our understanding of the disease.

Bin Zhang, PhD, Professor of Neurogenetics at Mount Sinai, states that this study lays the groundwork for developing new treatments targeting these predictive gene networks. The researchers stress the need for continued research to translate these discoveries into treatments for patients.