ArticleFrontiers in aging neuroscience2025
Asrij/OCIAD1 contributes to age-associated microglial activation and neuroinflammation in mice.
Article in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aging is characterized by chronic low-grade neuroinflammation, which increases the risk of neurodegenerative disorders. Neuroinflammation, driven by the activation of astrocytes and microglia, underlies age-associated cognitive deficits. Amplified neuroinflammatory responses to immune challenges are attributed to microglial activation in the aged brain. Despite extensive clinical and experimental evidence linking neuroinflammation to aging, the molecular players that control age-associated neuroinflammatory responses in the brain are not fully understood. Genome-wide association studies (GWAS), proteomics, and transcriptomic datasets have revealed that Asrij/OCIAD1 is a novel aging and Alzheimer's disease (AD)-associated factor. Asrij levels are increased in patients with AD and are known to promote amyloid-beta (Aβ) pathology and microglia-mediated neuroinflammation, which are associated with cognitive dysfunction in AD. Increased levels of Asrij are also reported in the brains of aged wild-type (WT) mice; however, whether this may promote neuroinflammation or be a protective response during aging is not known. To test this, we used young and aged WT and
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