The core findings of the neuropathology of the disease have led to the discovery of certain changes in the extracellular amyloidal plaques, neuronal death, synaptic deterioration, and intracellular NFTs (Thies and Bleiler, 2011: 208). Upon the examination of tissues, it is easy to see the granulovacuolar degeneration in the patient’s hippocampus and the amyloidal deposition within the blood vessels. Research also revealed that the increased interference of synaptic activity by the amyloidal plaque initiates a series of downstream effects that lead to further increase in intraneuronal dysfunction, and this leads to the death of cells (Hardy, 2009: 1129).One of the most common pathological models of AD is the amyloid hypothesis, and has come to be accepted by various researchers. The model posits that the overproduction of amyloid beta peptides and its consequent accumulation in the plaques lead to the formation of neuritic plaques that signal an early and central event in the pathophysiology of AD (Meraz-Ríos et al., 2010: 1356). On the other hand, the downstream phenomenon is regarded as the cytoskeleton changes arising from the intracellular aggregation to microtubule associated protein known as tau. This then forms the neurofibrillary tangles. The amyloid hypothesis is the most prevalent theory based on the available successes in its utilization in the treatment of AD.Some researchers sub-classify the amyloid plaques based on their composition (Kalaria et al., 2008: 815; Meraz-Ríos et al., 2010: 1357; Hardy, 2009: 1131). All these amyloid plaques contain β-amyloid protein (Aβ). This amino acid peptide forms after a. The Pathophysiological Treatments of Alzheimer's Disease.
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