ReviewAging and disease2016
Pathophysiological Function of ADAMTS Enzymes on Molecular Mechanism of Alzheimer's Disease.
Review in Aging and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.
- Improving reproducibility of differentially expressed genes in single-cell transcriptomic studies of neurodegenerative diseases through meta-analysis.Nature communications · 2025Pooled it
- Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer's disease risk.Nature genetics · 2019Pooled it
- Novel Alzheimer's disease-associated variants and genetic interactions identified from UK biobank whole-exome sequencing data using IBI-DT.Scientific reports · 2026Article
- Unravelling Synaptic and Metabolic Mechanisms of Cognitive Resilience in Asymptomatic Alzheimer's Disease Across Two Alzheimer's Disease Cohorts.Cellular and molecular neurobiology · 2026Article
- Epigenetic Control of Hyperuricemia and Gout by Gene Writer DNMT1 and RNA Editor ADAR1: Mechanism of Gout and Amyloid Dissolution in Down Syndrome.Biochemical genetics · 2026Article
- GTsurvival: A Hybrid GCN-Neural Decision Tree Model for Restricted Mean Survival Time Prediction with Complex Censored Data.Entropy (Basel, Switzerland) · 2025Article
- NADScience advances · 2025Article
- A Reproducibility Focused Meta-Analysis Method for Single-Cell Transcriptomic Case-Control Studies Uncovers Robust Differentially Expressed Genes.bioRxiv : the preprint server for biology · 2025Article
- Genetic variations in extracellular matrix degradation pathways linking to major depressive disorder: Evidence from a large-scale genetic association study.BioMedicine · 2025Article
- Secretome analysis of oligodendrocytes and precursors reveals their roles as contributors to the extracellular matrix and potential regulators of inflammation.bioRxiv : the preprint server for biology · 2024Article
- Prediction models of persistent taxane-induced peripheral neuropathy among breast cancer survivors using whole-exome sequencing.NPJ precision oncology · 2024Article
- Spatial transcriptomic patterns underlying amyloid-β and tau pathology are associated with cognitive dysfunction in Alzheimer's disease.Cell reports · 2024Article
- Mutations in fibulin-1 and collagen IV suppress the short healthspan of mig-17/ADAMTS mutants in Caenorhabditis elegans.PloS one · 2024Article
- Single nucleus multiomics identifies ZEB1 and MAFB as candidate regulators of Alzheimer's disease-specificCell genomics · 2023Article
- Hypermethylation at CREBBP Is Associated with Cognitive Impairment in a Mexican American Cohort.Journal of Alzheimer's disease : JAD · 2023Article
- Cell type-specific histone acetylation profiling of Alzheimer's disease subjects and integration with genetics.Frontiers in molecular neuroscience · 2022Article
- Serum Glycoproteomics and Identification of Potential Mechanisms Underlying Alzheimer's Disease.Behavioural neurology · 2021Article
- Basal Forebrain Cholinergic Neurons: Linking Down Syndrome and Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- New Insights into ADAMTS Metalloproteases in the Central Nervous System.Biomolecules · 2020Review
- Novel Associations Within the Tumor Microenvironment: Fibulins Meet ADAMTSs.Frontiers in oncology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular matrix (ECM) is an environment that has various enzymes attended in regeneration and restoration processes which is very important to sustain physiological and biological functions of central nervous system (CNS). One of the participating enzyme systems in ECM turnover is matrix metalloproteinases. A disintegrin-like and metalloproteinase with thrombospondin type 1 motifs (ADAMTS) is a unique family of ECM proteases found in mammals. Components of this family may be distinguished from the ADAM (A Disintegrin and Metalloproteinase) family based on the multiple copies of thrombospondin 1-like repeats. The considerable role of the ADAMTS in the CNS continues to develop. Evidences indicate that ADAMTS play an important role in neuroplasticity as well as nervous system pathologies such as Alzheimer's disease (AD). It is hopeful and possible that ADAMTS family members may be utilized to develop therapies for CNS pathologies, ischemic injuries, neurodegenerative and neurological diseases. To understand and provide definitive data on ADAMTS to improve structural and functional recovery in CNS injury and diseases, this review aimed to enlighten the subject extensively to reach certain information on metalloproteinases and related molecules/enzymes. It will be interesting to examine how ADAMTS expression and action would affect the initiation/progression of above-mentioned clinical situations, especially AD.
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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.