ReviewCellular and molecular neurobiology2016
The Distinct Role of ADAM17 in APP Proteolysis and Microglial Activation Related to Alzheimer's Disease.
Review in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 71 citations in OpenAlex.
- Gene-specific DNA methylation responses to PbEnvironmental epigenetics · 2026Article
- Integrated single-cell genomics, transcriptomics, and pathomics to identify potential biomarkers in muscle-invasive bladder cancer.Translational andrology and urology · 2025Article
- NEU1-Mediated Extracellular Vesicle Glycosylation in Alzheimer's Disease: Mechanistic Insights into Intercellular Communication and Therapeutic Targeting.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Article
- ADAM17 Inhibition Protects Cognition in Intermittent Hypoxia: The Role of TREM2.Nature and science of sleep · 2025Article
- Article
- ADAM17 as a promising therapeutic target: from structural basis to inhibitor discovery in human diseases.Frontiers in pharmacology · 2025Review
- Role of NLRP3 in Parkinson's disease: Specific activation especially in dopaminergic neurons.Heliyon · 2024Review
- Novel Social Stimulation Ameliorates Memory Deficit in Alzheimer's Disease Model through Activating α-Secretase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Effects of Cerebrospinal Fluids from Alzheimer and Non-Alzheimer Patients on Neurons-Astrocytes-Microglia Co-Culture.International journal of molecular sciences · 2024Article
- Multi-cohort cerebrospinal fluid proteomics identifies robust molecular signatures for asymptomatic and symptomatic Alzheimer's disease.Research square · 2024Article
- Role of Metalloproteinases in Diabetes-associated Mild Cognitive Impairment.Current neuropharmacology · 2024Review
- Article
- The Cytokine CX3CL1 and ADAMs/MMPs in Concerted Cross-Talk Influencing Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Naturally-aged microglia exhibit phagocytic dysfunction accompanied by gene expression changes reflective of underlying neurologic disease.Scientific reports · 2022Article
- Integrated network-based multiple computational analyses for identification of co-expressed candidate genes associated with neurological manifestations of COVID-19.Scientific reports · 2022Article
- Analysis of post COVID-19 condition and its overlap with myalgic encephalomyelitis/chronic fatigue syndrome.Journal of advanced research · 2022Review
- Interval-Based Secretomics Unravels Acute-Phase Response in Hepatocyte Model Systems.Molecular & cellular proteomics : MCP · 2022Article
- Immunomodulatory role of metalloproteinase ADAM17 in tumor development.Frontiers in immunology · 2022Review
- Impact of SARS-CoV-2 on Host Factors Involved in Mental Disorders.Frontiers in microbiology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 α-secretase happens inside the Aβ domain. ADAM17 is supposed to be the regulated α-secretase 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 membrane-bound 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 AD-related APP shedding and neuroinflammatory microglial activation will be carefully discussed.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.