Improving early recanalization and preventing neurovascular damage at the acute phase of ischemic stroke are the main objectives of current stroke research. In contrast, much less attention is being paid to the possibility of reversing and repairing post-stroke neurological damage. Previous studies, including ours, have indicated that pro-angiogenic and immunomodulation-based therapies can stimulate post-stroke cerebral remodeling and healing, thus decreasing infarct volume, improving sensorimotor deficit but also preventing cognitive decline. Remarkably, although the healing properties of platelets have long been known and taken advantage of in regenerative medicine, data on the role of platelets in post-stroke cerebral plasticity are scarce. Our previous studies and preliminary results show that in addition to storing large amounts of growth factors, platelets are the main source of various factors involved in post-stroke recovery, including brain-derived neurotrophic factor, angiopoietin-1, TGF-beta, serotonin and dopamine. In fact, our results obtained from a cohort of thrombocytopenic patients show that low platelet counts are associated with a significant decrease in those factors' plasma levels. In addition, our results obtained in experimental stroke models in mice indicate that platelets play a vital role in the days following an ischemic stroke, and that platelet inhibition by aspirin as used in secondary prevention post- Stroke worsens cognitive decline. In this context, our translational research project aims at determining the mechanistic contribution of platelets to cognition and post-stroke cerebral plasticity. This is of utmost importance since antiplatelet therapy is the main treatment given to stroke patients for secondary prevention.