Interferon signalling plays a key role in immune surveillance of the central nervous system, not only in parenchyma but also at the border niches including blood-brain-barrier. However, chronic interferon levels in brain ageing impair brain function and cognition, thereby contributing to the priming of Alzheimer’s disease (AD). We previously identified the interferon-responsive gene, OAS1, as a genetic risk factor for AD with decreased expression, and found that OAS1 limits the pro-inflammatory responses of microglia during interferon activation. However, the mechanisms by which dsRNA sensors like OAS1 and antiviral immune responses modulate the AD development or progression through microglia are unclear.