Targeting SEMA4D/PLXN signaling through reactive glia as a common pathology for the treatment of neurodegenerative disorders

Abstract

Background: Semaphorin 4D (SEMA4D, CD100) and its receptors Plexin B1, B2 have been identified in multiple transcriptomic/genomic studies as a key signaling pathway associated with reactive gliosis and disease risk in Alzheimer’s Disease (AD), Huntington’s Disease (HD), Multiple Sclerosis, and vascular dementia.

The paper