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GPR34 senses demyelination to promote neuroinflammation and cognition impairment in Alzheimer's disease

GSE216209 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2025/02/05 Platform GPL24247
Summary
Sterile neuroinflammation initiated by damage-associated molecular patterns (DAMPs) has been regarded as an important driver in Alzheimer's disease (AD) and can occur prior or independently of the deposition of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles (NFTs). Genetic ablation or pharmacological inhibition of GPR34 reduced microglia activation, Aβ deposition and cognition impairment. Moreover, GPR34 inhibition prevented aging associated neuroinflammation and cognition impairment without the presence of Aβ plaques.
Published in
Demyelination-derived lysophosphatidylserine promotes microglial dysfunction and neuropathology in a mouse model of Alzheimer's disease
Zhou Y, Huang Z, Lin B et al. · Cellular & molecular immunology 2025 · PMID 39741193 · doi:10.1038/s41423-024-01235-w
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Also filed as BioProject PRJNA892590 and SRA study SRP403679. Searching any of these in the dataset finder brings you back here.

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