Authors: Meng Qian Xiaoqiang Shen Huanhuan Wang
Publish Date: 2015/06/29
Volume: 36, Issue: 4, Pages: 471-482
Abstract
Alzheimer’s disease AD is a progressive neurodegenerative disease with the symptom of cognitive impairment The deposition of amyloid β Aβ peptide is believed to be the primary cause to neuronal dystrophy and eventually dementia Aβ is the proteolytic product from its precursor amyloid precursor protein APP by β and γ secretase An optional cleavage by αsecretase happens inside the Aβ domain ADAM17 is supposed to be the regulated αsecretase of APP Enhanced activity of ADAM17 leads to the increasing secretion of neuroprotective soluble APP α fragment and reduction of Aβ generation which may be benefit to the disease ADAM17 is then considered the potential therapeutic target for AD Microglia activation and neuroinflammation is another important event in AD pathogenesis Interestingly ADAM17 also participates in the cleavage of many other membranebound proteins especially some inflammatory factors related to microglia activation The facilitating role of ADAM17 in inflammation and further neuronal damage has also been illustrated In results the activation of ADAM17 as the solution to AD may be a tricky task The comprehensive consideration and evaluation has to be carried out carefully before the final treatment In the present review the distinct role of ADAM17 in ADrelated APP shedding and neuroinflammatory microglial activation will be carefully discussed
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