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

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. Examination of GPR34 effection on microglia in 5XFAD mice.