Page - (000284) - in Biomedical Chemistry: Current Trends and Developments

erodes the ability for neurons to communicate and results in a wide variety of symptoms in patients suffering from MS, ranging from physical disability to psychiatric and cognitive deficits. The progression of MS has been observed to occur either in isolated “attacks” and a slower degenerative progression. In each case, permanent damage is done as the disease advances, however, it appears that some functions can be relearned likely through network plasticity. Presently, the molecular cause of MS is not fully elucidated but much evidence points to a failure of the immune system in which the myelin- producing cells are attacked. Glutamate-mediated excitotoxicity has also been implicated as a root cause. As discussed previously, the oligodendrocytes, the cells that provide the myelin sheath for neurons in the CNS, are also susceptible to excitotoxicity. In a recent study in an animal model of MS, glutamate receptor blockers were found to increase the survival of oligodendrocytes and prevent some of the molecular mechanism from over-stimulation (Suhs, 2014). 3.2.6.3 Alzheimer’s Disease (AD) Characterized by progressive death and degeneration of neurons, Alzheimer’s disease leads to increasing memory loss and eventual dementia. A small percentage of cases (Ballard, 2011) have been found to be caused by a congenital defect and these cases are classified as Familial Alzheimer’s Disease (FAD). The majority of Alzheimer’s disease cases are classified as sporadic Alzheimer’s and there is presently no known direct cause. Two classic indications of the disease that can be observed in brain tissue of both FAD and sporadic Alzheimer’s sufferers are the presence of neurofibrillary tangles of hyperphosphorylated tau inside of neurons and plaques consisting primarily of extracellular aggregations of beta-amyloid (Aβ) peptide fragments. Aβ clusters have been found to influence glutamate transmission in several ways, some of which could lead to excessively high concentrations of calcium and thus excitotoxicity. It was shown that the presence of Aβ impairs the ability of glutamate transporters to help remove glutamate from the extracellular area around the synapse, potentially resulting in excitotoxic effects (Li, 2009). Aβ clusters also