Immunization with Cop-1 promotes neuroprotection and neurogenesis after ischemic stroke.

Cerebrovascular diseases are considered to be amongst the most serious public health issues, since they are the third leading cause of death (WHO, 2014) and the most common cause of disability worldwide. Its monetary significance is evidenced by the economic burden imposed on health care systems, given that the cost of medical care for a patient that has suffered a stroke is around $25,741 US dollars every 5 years (Luengo-Fernandez et al., 2012). A stroke occurs as a result of a disturbance or interruption of cerebral blood flow that significantly reduces the supply of oxygen and glucose to the neural tissue. Consequently, several cell death mechanisms (secondary lesion mechanisms) such as necrosis, excitotoxicity, free radical production and inflammation are triggered (Castillo, 2000). Over the last decades, a variety of therapies with thrombolytic, neuroprotective, and restorative properties have been investigated. However, the results of these studies appear to be limited. That is the case of the tissue plasminogen activator (tPA) – the first line of treatment for decades – which is associated with low rates of recanalization and high rates of morbidity. Also, endovascular intervention, particularly mechanical thrombectomy, has been proposed as a promising therapeutic adjunct to tPA for the treatment of stroke; however, until recently, the efficacy of this therapeutic approach has been controversial (Ding, 2015). Innovative theurapeutic options are currently being developed in order to restore affected neuronal circuits following a cerebral ischemic event. Some of these innovative therapeutic approaches are based on stem cell transplantation and/or induction of neurogenesis.