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Cognitive Impairment Of Alzheimer 's Disease

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Q3: Mild cognitive impairment (MCI) is a decline in cognitive function that does not meet the standards of dementia but is worse than what is expected for the patient’s age and educational background (Petersen et al., 1999). While a patient with MCI is at increased (10-20%) risk of developing Alzheimer’s disease (AD) compared to the normal population, it is not necessary to classify patients as having MCI until they develop any further preclinical AD symptoms (Petersen et al., 1999). The diagnostic criteria for MCI includes: (1) impaired in memory that is greater than expected for age and general cognition is not effected (2) capable of performing daily activities and (3) not demented (Albert et al., 2011; Petersen et al., 1999). …show more content…

When AD is suspected, patients will undergo MRI, PET Scans, and lumbar punctures to look for brain atrophy, beta-amyloid plaques, or increased phosphorylated tau in cerebral spinal fluid (Hyman et al., 2012). The two main biomarkers of AD are beta-amyloid (Aβ) and tau and are highly debated in regards to their function in AD pathophysiology. The production of beta-amyloid plaques may be due to improper functioning of the proteasome preventing the breakdown of Aβ. Support for this theory comes from research indicating that the 20S proteasome is responsible for Aβ degradation and that alterations to the kinetics of the proteasome increased Aβ levels (Zhao & Yang, 2010). These accumulated levels of Aβ plaques leads to lower levels of soluble Aβ, which is needed for memory formation. This may occur through activation of nicotinic acetylcholine (ACh) receptors and AChE levels are drastically reduced in AD patients. (Garcia-Osta & Alberini, 2009). The microtubule stabilizing protein tau may become hyper-phosphorylated in AD due to the presence of high levels of Aβ. Hoshi et al (1996) showed that Aβ exposure to rat hippocampal neurons in vitro produced increased levels of the tau kinase GSK-3 (glycogen synthase kinase 3) which in turn hyper-phosphorylated tau leading to cellular death. (Hoshi et al., 1996) The neurotoxicity of tau may not be produced solely because of GSK-3, but may be due to

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