A recent study published in the journal Nature Neuroscience revealed that Plexin-B1, encoded by PLXNB1 , regulates the activation of peri-plaque glial nets in Alzheimer’s disease (AD). AD is a significant medical challenge, as no effective treatment is available. While amyloid plaques are a hallmark of AD pathology, factors driving amyloid-beta (Aβ) deposition, clearance, and plaque compaction are poorly understood.
Recent studies have shed light on microglial engulfing and processing of Aβ. Study: Regulation of cell distancing in peri-plaque glial nets by Plexin-B1 affects glial activation and amyloid compaction in Alzheimer’s disease . Image Credit: Juan Gaertner / Shutterstock Microglial phagocytic activity promotes plaque compaction, limiting the healthy neuron exposure to plaque.
Furthermore, microglial coverage of plaques serves as a barrier limiting neurite exposure to neurotoxic protofibrillar Aβ hotspots. Amyloid plaques are also surrounded by reactive astrocytes. As such, the microglia and reactive astrocytes closely interact with Aβ and one another, forming peri-plaque glial nets.
Plexin-B1 is an axon guidance receptor; plexins and their cognate ligands mediate cell-cell communication during development, cancer, and adult physiology. Previously, the authors identified plexin-B1 as a hub gene in a sub-network underlying late-onset AD. In addition, other studies have independently implicated plexin-B1 in AD pathophysiology; however, functional in vivo data ar.
