Icahn Mount Sinai researchers find PLXNB1, a hub gene predicted to drive a gene subnetwork causally linked to human AD, is upregulated in reactive astrocytes surrounding amyloid plaques.
Credit: Bin Zhang, PhD, Icahn Mount Sinai
Credit: Bin Zhang, PhD, Icahn Mount Sinai
Researchers at the Icahn School of Medicine at Mount Sinai have made a significant breakthrough in Alzheimer’s disease research by identifying a novel way to potentially slow down or even halt disease progression. The study, which focuses on the role of reactive astrocytes and the plexin-B1 protein in Alzheimer's pathophysiology, provides crucial insights into brain cell communication and opens the door to innovative treatment strategies. It was published in Nature Neuroscience (DOI 10.1038/s41593-024-01664-w) on May 27.