Our results indicated that pretreatment of FGF2 played a neuroprotective role in the early stage of rat mild TBI through alleviating brain edema, reducing neurological deficits, preventing tissue loss, and increasing the number of surviving neurons in injured cortex and the ipsilateral hippocampus.;Here, we demonstrate that lack of FGF-2 results in an increased volume of the striatal target area in mice.;These findings point to differences in the response of aged versus young adult rats to  FGF-2 in cerebral ischemia, and suggest that such differences need to be considered in the development of neuroprotective agents for stroke.