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.

Alzheimer\'s disease (AD), the most common neurodegenerative disease worldwide, is caused by loss of neurons and synapses in central nervous system. Several causes for neuronal death in AD have been introduced, the most important of which are extracellular amyloid β (Aβ) accumulation and aggregated tau proteins. Increasing evidence suggest that targeting the process of Aβ production to reduce its deposition can serve as a therapeutic option for AD management. In this regard, therapeutic interventions shown that a disintegrin and metalloproteinase domain-containing protein (ADAM) 10, involved in non-amyloidogenic pathway of amyloid precursor protein processing, is known to be a suitable candidate. Therefore, this review aims to examine the molecular properties of ADAM10, its role in AD, and introduce it as a therapeutic target to reduce the progression of the disease. Video abstract.

Abstract　Immune thrombocytopenia (ITP) is a complex autoimmune disease characterized by less than 100×109/L platelet count in peripheral blood. The pathogenesis of ITP is complex and has not been fully elucidated. Currently, researches on the pathogenesis of ITP mainly focus on the disorders of humoral immunity and cellular immunity. In recent years, some new progress has been made in the study of this pathogenesis, including the platelet clearance pathway that is not dependent on Fc γ R mediation, the metalloproteinase (ADAM) 10 that can regulate T and B cells, and the abnormal expression of micro RNA in genetic factors. Under the joint action of multiple factors, the imbalance of the immune system in the body leads to the occurrence of ITP. This article reviews the research progress on humoral immunity, cellular immunity and other possible new pathogenesis of ITP in recent years.
UNASSIGNED: 原发性免疫性血小板减少症的发病机制研究进展.
UNASSIGNED: 原发性免疫性血小板减少症（Immune thrombocytopenia，ITP）是一种复杂的自身免疫疾病，以外周血中血小板计数＜100×109/L为特点。ITP的发病机制复杂，尚未完全阐明，目前对ITP发病的研究主要针对于体液免疫失调以及细胞免疫失调等方面。近年来，研究该发病机制取得了一些新的进展，包括非依赖Fc γ R 介导的血小板清除途径，可以调节T、B细胞的金属蛋白酶（ADAM）10，遗传因素中的微小RNA的表达异常等。在多种因素的共同作用下，机体免疫系统的失衡，导致ITP的发生。本文就近年来针对ITP研究的体液免疫，细胞免疫以及其他可能的新发病机制研究进展进行综述。.