Ischemic stroke treatment
Given its significant functions, non-muscle myosin 2 (NM2) is becoming an important therapeutic target in various diseases, including stroke, a leading cause of disability and mortality. Currently no effective therapy is available.
Our laboratory developed a biologically safe myosin 2 specific motor protein inhibitor, to repair the damaged brain tissue through the formation of vascular and neuronal networks.
One of our major interests regarding the new inhibitors is their effect on the induction of neurite outgrowth function of human neurons derived from neuronal stem cells (hNSC).
For modelling stroke, transient middle cerebral artery occlusion (MCAO) was used in rats which was followed by the injection of our molecule to the damaged area.
The effects of our newly developed inhibitor were studied using SPECT/CT combined with MRI for up to 21 days after MCAO. To test whether this molecule contributes to recovery and provide an accurate evaluation of neurological function, general and focal deficits were monitored. In treated animals cerebral blood flow evaluation and MRI images revealed increased blood flow and decreased cerebral oedema within the lesion site. A substantial behavioural improvement was also observed.
Monitoring in vivo the cerebral oedema and blood flow during ischemic stroke and after drug treatment by MRI and SPECT in rats.
In treated animals cerebral blood flow evalution and MRI images revealing increased blood flow and decreased cerebral oedema within the lesion site.
Our results suggest that direct myosin 2 inhibition by the newly developed molecule can contribute to the repair of brain damage following ischemic stroke.