Potential for Neuroprotective Drug Discovery

Much of the opportunity for pharmacological intervention to preserve neurological function after acute central nervous system (CNS) injuries such as stroke, TBI, and SCI is based on the fact that most of the vascular and neurodegeneration that follows these injuries is not due to the primary ischemic, hemorrhagic, or mechanical (i.e., shearing of blood vessels, and nerve cells) insults, but rather to secondary injury events set in motion by the primary injury. For example, most SCIs do not involve actual physical transection of the cord, but rather the spinal cord is damaged as a result of a contusive, compressive, or stretch injury. Some residual white matter, containing portions of the ascending sensory and descending motor tracts, remains intact, which allows for the possibility of neurological recovery. However, during the first minutes and hours following injury a secondary degenerative process, which is proportional to the magnitude of the initial insult, is initiated by the primary mechanical injury. Nevertheless, the initial anatomical continuity of the injured spinal cord in the majority of cases, together with our present knowledge of many of the factors involved in the secondary injury process, has led to the notion that pharmacological treatments that interrupt the secondary cascade, if applied early, could improve spinal cord tissue survival, and thus preserve the necessary anatomic substrates for functional recovery to take place. Similarly, the extent of neurological damage and the potential for a good outcome after stroke or TBI is mainly determined by the extent of the potentially treatable secondary pathophysiology and neurodegeneration. The goal of interfering with this process is referred to as 'neuroprotection'.

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