Alzheimer's Amyloid Hypothesis
Alzheimer's disease (AD) is an irreversible progressive neurological disorder affecting memory and cognitive abilities (Qiu et al., 2009). As Estimated, patients diagnosed with AD may not survive the disorder within three to nine years since their diagnosis. AD is the leading cause of dementia in elderly patients, with increased incidence of prevalence with age. Every year, 1275 cases per 100,000 persons aged more than 65 are diagnosed, with a doubling in the incidence every five years in patients older than 65 (Reitz et al., 2011). AD is a multifactorial disease with a unique pathogenic protein aggregations, including accumulation of hyper–phosphorylated tau and the accumulation and misfolding of Amyloid–β (Aβ) (Querfurth and LaFerla, 2010). ... Show more content on Helpwriting.net ...The spontaneous self–aggregation of Aβ into multiple coexisting physical forms, including oligomers (two to six peptides), leads to their coalescence into intermediate assemblies. In addition to this, β–amyloid can also grow into fibrils, which arrange themselves into β–pleated sheets to form the insoluble fibers of advanced amyloid plaques. Soluble oligomers and intermediate amyloids are the most neurotoxic forms of Aβ. In brain–slice preparations, synapses are toxified by dimers and trimers of Aβ. However, the severity of the cognitive defect in Alzheimer's disease is in correlation with the levels of oligomers in the brain, not the total burden of Aβ. Neuronal activation rapidly increases Aβ secretion at the synapse, a process tied to the normal release of vesicles containing
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