Regulation of cell distancing in peri-plaque glial nets by Plexin-B1 affects glial activation and amyloid compaction in Alzheimer's disease.
Yong HuangMinghui WangHaofei NiJinglong ZhangAiqun LiBin HuChrystian Junqueira AlvesShalaka WahaneMitzy Rios de AndaLap HoYuhuan LiSangjo KangRyan NeffAna KosticJoseph D BuxbaumJohn F CraryKristen J BrennandBin ZhangHongyan ZouRoland H FriedelPublished in: Nature neuroscience (2024)
Communication between glial cells has a profound impact on the pathophysiology of Alzheimer's disease (AD). We reveal here that reactive astrocytes control cell distancing in peri-plaque glial nets, which restricts microglial access to amyloid deposits. This process is governed by guidance receptor Plexin-B1 (PLXNB1), a network hub gene in individuals with late-onset AD that is upregulated in plaque-associated astrocytes. Plexin-B1 deletion in a mouse AD model led to reduced number of reactive astrocytes and microglia in peri-plaque glial nets, but higher coverage of plaques by glial processes, along with transcriptional changes signifying reduced neuroinflammation. Additionally, a reduced footprint of glial nets was associated with overall lower plaque burden, a shift toward dense-core-type plaques and reduced neuritic dystrophy. Altogether, our study demonstrates that Plexin-B1 regulates peri-plaque glial net activation in AD. Relaxing glial spacing by targeting guidance receptors may present an alternative strategy to increase plaque compaction and reduce neuroinflammation in AD.
Keyphrases
- neuropathic pain
- coronary artery disease
- late onset
- spinal cord
- single cell
- spinal cord injury
- early onset
- inflammatory response
- lipopolysaccharide induced
- traumatic brain injury
- cell therapy
- gene expression
- lps induced
- stem cells
- genome wide
- induced apoptosis
- dna methylation
- cognitive decline
- mesenchymal stem cells
- cell death
- bone marrow
- endoplasmic reticulum stress
- cerebral ischemia
- copy number