Introduction: The number of preclinical studies employing long term behavioral testing is increasing. However, long-term behavioral evaluations in genetic animal models is often confounded by their acute injury severity. In addition, these studies have been primarily focused on motor outcomes despite stroke patients also suffer from a wide range of cognitive and psychiatric disturbances. The purpose of study is to investigate recovery via comprehensive behavior assessments in WT and CD36KO mice. Methods: Male and female mice were subjected to right transient MCA occlusion for different durations: 30 for WT and 40 min for CD36KO (N= 13/group) to normalize their injury size. A battery of tests for i) motor (rotarod, open field), ii) anxiety (plus maze, Light dark box), and iii) depression (sucrose preference, forced swim test) were performed before, and 2 weeks and 7 weeks after stroke. Cognitive function is assessed at 9 weeks using a water maze protocol consisting of a training phase, probe trial, and a visible platform relearning task. Results: At baseline KO animals showed reduced rotarod performance and hypoactivity. Infarct sizes were comparable between genotypes. Stroke induced hyperactivity, motor and hedonic deficit and reduced depression like behavior at 2 and 7w in WT mice. CD36 deficiency ameliorated hyperactivity, anhedonia and normalized the depressive behavior. In the water maze training and probe trial, all groups showed similar performance. However among stroke groups CD36 KO mice performed significantly better compared to WT mice at the visible platform task. (Figure) Conclusion: The study demonstrate that CD36 deficiency attenuates stroke-induced hyperactivity, hedonic deficit, reduced depression and relearning deficit. Strategy switching deficit observed in WT stroke animals resemble the cognitive dysexecutive syndrome observed in some stroke patients. Our findings indicate that CD36 contribute to stroke-induced cognitive deficits.