背景:研究表明,A整合素和金属蛋白酶10(ADAM10)是淀粉样前体蛋白(APP)的非淀粉样蛋白裂解中的主要α-分泌酶,避免淀粉样β肽(Aβ)的产生,阿尔茨海默病(AD)的病理标志之一。
目的:研究脑脊液(CSF)和血浆/血清中的ADAM10作为AD的潜在生物标志物。
方法:在MEDLINE/PubMed,WebofScience,Embase,和Scopus数据库使用术语和布尔运算符:\"阿尔茨海默氏症\"和\"ADAM10\"和\"生物标志物\"。还采用了引文搜索。纳入标准是AD患者血液或CSF中ADAM10的原始研究。使用用于观察队列和横断面研究的质量评估工具评估偏倚的风险。分析方法在PROSPERO数据库(#CRD42021274239)中注册。
结果:在筛选的97条记录中,17人被包括在内。有强有力的证据表明,与认知健康参与者相比,AD患者的血小板中ADAM10水平较低。另一方面,在血浆中发现更高水平的ADAM10。关于CSF,与健康老年人相比,AD患者的ADAM10水平较低和较高,结果有争议。差异可能是由于不同的原因,包括不同的样本收集和处理以及不同的抗体,强调标准化实验和选择合适的抗体进行ADAM10检测的重要性。
结论:有证据表明,ADAM10水平在血小板中发生改变,等离子体,血清,和患有AD的个体的CSF。这种改变在疾病的所有阶段都很明显,因此,该蛋白质可以代表该疾病的互补生物标志物。然而,必须进行更多的研究来确定ADAM10水平的临界值,以区分AD参与者和认知未受损的老年人.
BACKGROUND: Studies have shown that A Disintegrin and Metalloproteinase 10 (ADAM10) is the main α-secretase in the non-amyloidogenic cleavage of the amyloid precursor protein (APP), avoiding the production of amyloid-β peptide (Aβ), one of the pathological hallmarks of Alzheimer\'s disease (AD).
OBJECTIVE: To investigate ADAM10 from cerebrospinal fluid (CSF) and plasma/serum as a potential biomarker for AD.
METHODS: A systematic
review was carried out in the MEDLINE/PubMed, Web of Science, Embase, and Scopus databases using the terms and Boolean operators: \"Alzheimer\" AND \"ADAM10\" AND \"biomarker\". Citation searching was also adopted. The inclusion criteria were original studies of ADAM10 in blood or CSF in patients with AD. The risk of bias was assessed using the Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies. The analysis methods were registered in the PROSPERO database (#CRD42021274239).
RESULTS: Of the 97 records screened, 17 were included. There is strong evidence for lower levels of ADAM10 in platelets of persons with AD compared to cognitively healthy participants. On the other hand, higher levels of ADAM10 were found in plasma. Regarding CSF, controversial results were found with lower and higher levels of ADAM10 in persons with AD compared to healthy older adults. The differences may be due to diverse reasons, including different sample collection and processing and different antibodies, highlighting the importance of standardizing the experiments and choosing the appropriate antibodies for ADAM10 detection.
CONCLUSIONS: Evidence shows that ADAM10 levels are altered in platelets, plasma, serum, and CSF of individuals with AD. The alteration was evident in all stages of the disease, and therefore, the protein may represent a complementary biomarker for the disease. However, more studies must be performed to establish cut-off values for ADAM10 levels to discriminate AD participants from cognitively unimpaired older adults.