A new player in microglial activation driving inflammation and pathology in traumatic brain injury [TBI].

Aim: To determine whether SHIP-1 deficiency in mice leads to hyperactive microglia and exacerbated inflammatory responses in the normal brain as well as following experimental traumatic brain injury (TBI), thereby identifying SHIP-1 as a critical regulator of these brain-resident immune cells, providing scope for SHIP-1 pathway modulation for therapy.

The grant offers $5000 for use to support pilot data towards a larger grant application and to support mid-career researchers.