Abstract
Understanding molecular mechanisms of neuronal viability & neurite outgrowth At present, the treatment of CNS trauma and disease remains largely one of medicine’s unachieved goals. For example, current treatments of spinal injuries and stroke are often purely palliative and fail to provide the means to facilitate functional recovery or offer the patient a return to normal life [1,2]. Current treatment of Parkinson’s disease still only aims at replacing the dopamine missing in higher brain centers, rather than preventing the death of the midbrain dopaminergic neurons [3], and novel treatments for Alzheimer’s disease and amyotrophic lateral sclerosis (ALS) lead only to marginal, if any, improvements [4–6]. Even though genetic linkage studies and basic neuroscience research have identified numerous genes and mechanisms involved in CNS trauma and the progression of Alzheimer’s disease, ALS and Parkinson’s disease [7–13], none of the currently used or tested medications promote efficient survival of neurons and their connections; they simply serve to alleviate the symptoms caused by the lack of function in certain groups of brain cells.
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