Utveckling av ny strokebehandling

Stroke affects about 12 million people worldwide annually. Of the approximately 6 million survivors, about 50% suffer from long-lasting or permanent disability.

No efficient therapy is currently available, except for the removal of the occluding blood clot during the first hours after ischemic stroke.

Plasticity responses in spared brain regions are a major contributor to functional recovery, while secondary neurodegeneration in remote brain regions impedes the long-term outcome after stroke.We hypothesize that the receptor for complement peptide C3a (C3aR) is a modifier of neural cell responses to stroke.

We showed that C3aR signaling stimulates brain plasticity after ischemic stroke. Most importantly, we showed that intranasal treatment with C3a accelerates functional recovery.

As the treatment was effective even when started 7 days after stroke, the broad therapeutic window means that the majority of stroke survivors could benefit from such a therapy.In this project, we aim to (1) gain a mechanistic insight into stroke-induced neurodegeneration and brain-wide connectivity changes, (2) determine the potential of C3a to inhibit neurodegeneration and (3) to normalize post-stroke hyperconnectivity, (4) determine the efficacy of C3a in improving the outcome after hemorrhagic stroke, and (5) move towards clinical translation of this promising treatment strategy to reduce neurological impairment and improve outcome after stroke, and potentially other types of brain injury.