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Microglial cells and inflammatory cytokines in causation of Alzheimers disease
PAGE \* MERGEFORMAT 18
Microglial cells and inflammatory cytokines in causation of Alzheimer’s disease
[Keywords:] microglia cells; inflammatory cytokines; Alzheimer’s disease; causal relationship between
Alzheimer’s disease (Alzheimer’s disease, AD) is a progressive degenerative neurons in the brain diseases, including familial AD and sporadic AD. Major clinical manifestations of progressive memory loss and cognitive impairment. Brain pathology is manifested mainly neurofibrillary tangles (neurafibrillarytangle, NFT) and senile plaques (senile plaque, SP) co-occurrence. Neurons within the NFT is the excessive TAU tubulin phosphorylation and glycosylation forms produced in the cell aggregation, whereas in the extracellular accumulation of SP mainly contains 40 ~ 42 amino acids of β -amyloid protein (amyloid β -protein, Aβ ) component. These pathological changes mainly in the parietal lobe, temporal lobe, frontal joint zones, such as the cerebral cortex, hippocampus and the forebrain. The majority of AD patients with brain Aβ to accumulate in the senile plaques Department, Aβ by β -amyloid precursor protein (amyloid precurso protein, APP) through a series of enzymatic reaction of a soluble product of degradation of APP is released [1]. The process of Aβ release by three kinds of enzymes to control, namely, α , β and γ -secretase [2], β -secretase in the Aβ domain of the first N-terminal methionine and aspartic acid cleavage between the release of a longer soluble APP fragment (solubleAPP-β , SAPP-β ), while the C terminal fragment was still with the (c-terminalfragment, CTF) membrane-bound, followed by γ -secretase cleavage CTF-β produced, ranging from the length of Aβ (39 ~ 43) amino acids, pathological significance of which is that Aβ 40 and Aβ 42 [3], brain Aβ 40 levels much higher than AB42, but Aβ 42 than Aβ 40 aggregation is not only faster, but the latter triggered by agglutination, is the main component of senile plaques. AD patients was fou
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