ReviewActa neurologica Belgica2024
The probable role of tissue plasminogen activator/neuroserpin axis in Alzheimer's disease: a new perspective.
Review in Acta neurologica Belgica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 18 papers.
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.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- A new era in neuropharmacology: assessing the efficacy and safety of novel anti-amyloid and non-amyloid drug targets for Alzheimer's disease.Journal of neurology · 2026Review
- Senescence as a Central Node in Alzheimer's Disease: Molecular Triggers, Cellular Effectors, and RNA-Based Interventions.Neurochemical research · 2026Review
- The potential role of adenosinergic pathway and methylxanthines in Parkinson's disease: Blowing in the wind or not.Purinergic signalling · 2026Review
- The Double-Edged Sword Effect of the Fibrinolytic System in Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Neuroserpin, Tissue Plasminogen Activator, Brain-Derived Neurotrophic Factor and Interleukin-6 Serum Levels in Patients with Bipolar Disorder.Noro psikiyatri arsivi · 2026Article
- Unveiling the Neuroprotective Effect of Paraoxonase 1 in Neurodegenerative Diseases Focusing on Alzheimer's Disease.Molecular neurobiology · 2025Review
- Are pNF-H, IL-6, BDNF, and NSP Reliable Biomarkers of Cognitive Function in Prostate Cancer Patients?International journal of molecular sciences · 2025Article
- Alzheimer disease: Amyloid peptide controversies and challenges of anti-Aβ immunotherapy.The Journal of pharmacology and experimental therapeutics · 2025Review
- Unlocking Alzheimer's Disease: The Role of BDNF Signaling in Neuropathology and Treatment.Neuromolecular medicine · 2025Review
- The Conceivable Role of Metabolic Syndrome in the Pathogenesis of Alzheimer's Disease: Cellular and Subcellular Alterations in Underpinning a Tale of Two.Neuromolecular medicine · 2025Review
- Alterations in the Processing of Platelet APP (Amyloid Beta Precursor Protein) in Alzheimer Disease: The Possible Nexus.Neuropsychopharmacology reports · 2025Review
- Internet of Medical Things (IoMT) for Alzheimer Patient's Outcome.CNS & neurological disorders drug targets · 2025Review
- Amyloid-β and heart failure in Alzheimer's disease: the new vistas.Frontiers in medicine · 2025Review
- The Aggravating Role of Failing Neuropeptide Networks in the Development of Sporadic Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Therapeutic Potential Effect of Glycogen Synthase Kinase 3 Beta (GSK-3β) Inhibitors in Parkinson Disease: Exploring an Overlooked Avenue.Molecular neurobiology · 2024Review
- Hypoglycemia and Alzheimer Disease Risk: The Possible Role of Dasiglucagon.Cellular and molecular neurobiology · 2024Review
- BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy.Journal of cellular and molecular medicine · 2024Review
- Quantitative Proteomics Reveal Region-Specific Alterations in Neuroserpin-Deficient Mouse Brain and Retina: Insights into Serpini1 Function.Proteomes · 2024Article
Corrections and comments
- Expression of concern
Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common type of dementia associated with amyloid beta (Aβ) deposition. Dysfunction of the neuronal clearance pathway promotes the accumulation of Aβ. The plasminogen-activating system (PAS) is controlled by various enzymes like tissue plasminogen activators (tPA). Neuronal tPA enhances the conversion of plasminogen to plasmin, which cleaves Aβ; this function is controlled by many inhibitors of PAS, including a plasminogen-activating inhibitor (PAI-1) and neuroserpin. Therefore, the objective of the present narrative review was to explore the potential role of tPA/neuroserpin in the pathogenesis of AD. PAI-1 activity is increased in AD, which is involved in accumulating Aβ. Progressive increase of Aβ level during AD neuropathology is correlated with the over-production of PAI-1 with subsequent reduction of plasmin and tPA activities. Reducing plasmin and tPA activities promote Aβ by reducing Aβ clearance. Neuroserpin plays a critical role in the pathogenesis of AD as it regulates the expression and accumulation of Aβ. Higher expression of neuroserpin inhibits the neuroprotective tPA and the generation of plasmin with subsequent reduction in the clearance of Aβ. These observations raise conflicting evidence on whether neuroserpin is neuroprotective or involved in AD progression. Thus, neuroserpin over-expression with subsequent reduction of tPA may propagate AD neuropathology.
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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.