Wednesday, May 6, 2020
Cognitive Impairment Of Alzheimer s Disease - 1313 Words
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 patientââ¬â¢s age and educational background (Petersen et al., 1999). While a patient with MCI is at increased (10-20%) risk of developing Alzheimerââ¬â¢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).â⬠¦show more contentâ⬠¦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 (Aà ²) 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 Aà ². Support for this theory comes from research indicating that the 20S proteasome is responsible for Aà ² degradation and that alterations to the kinetics of the proteasome increased Aà ² levels (Zhao Yang, 2010). These accumulated levels of Aà ² plaques leads to lower levels of soluble Aà ², 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 Aà ². Hoshi et al (1996) showed that Aà ² 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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