ReviewInternational journal of molecular sciences2020
Exploring the Potential of Therapeutic Agents Targeted towards Mitigating the Events Associated with Amyloid-β Cascade in Alzheimer's Disease.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
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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
30 citing papers in PubMed, 38 citations in OpenAlex.
- Attenuation of Tau-Mediated β-Amyloid1-42 Aggregation by Native PLGA Nanoparticles and Its Relevance to Alzheimer Disease Pathology.International journal of molecular sciences · 2026Article
- Hydration water dynamics in amyloid-β aggregates using deuterium and oxygen-17 solid-state NMR spectroscopy.The Journal of chemical physics · 2026Article
- Antioxidant, Anti-Cholinesterase, and Neuroprotective Properties ofAntioxidants (Basel, Switzerland) · 2026Article
- Mitochondria as a Therapeutic Target in Neurodegeneration: Strategies for Restoring Cellular Homeostasis.Current neuropharmacology · 2026Review
- Graph and Multi-Level Sequence Fusion Learning for Predicting the Molecular Activity of BACE-1 Inhibitors.International journal of molecular sciences · 2025Article
- Association of statins use and genetic susceptibility with incidence of Alzheimer's disease.The journal of prevention of Alzheimer's disease · 2025Article
- Recent Advances in Therapeutics for the Treatment of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2024Review
- Combination of Tramiprosate, Curcumin, and SP600125 Reduces the Neuropathological Phenotype in Familial Alzheimer Disease PSEN1 I416T Cholinergic-like Neurons.International journal of molecular sciences · 2024Article
- Amyloid beta peptides (Aβ) from Alzheimer's disease neuronal secretome induce endothelial activation in a human cerebral microvessel model.Neurobiology of disease · 2023Article
- Development of Activity Rules and Chemical Fragment Design for In Silico Discovery of AChE and BACE1 Dual Inhibitors against Alzheimer's Disease.Molecules (Basel, Switzerland) · 2023Article
- The Potential Roles of Exosomes Carrying APP and Tau Cleavage Products in Alzheimer's Disease.Journal of clinical medicine · 2023Review
- Metabolic Syndrome as a Risk Factor for Alzheimer's Disease: A Focus on Insulin Resistance.International journal of molecular sciences · 2023Review
- The interaction of peptide inhibitors and Aβ protein: Binding mode analysis, inhibition of the formation of Aβ aggregates, and then exert neuroprotective effects.Frontiers in aging neuroscience · 2023Article
- Effectiveness and safety of monoclonal antibodies against amyloid-betaFrontiers in neurology · 2023Article
- Pharmacotherapy Evolution in Alzheimer's Disease: Current Framework and Relevant Directions.Cells · 2022Review
- Critical appraisal on mitochondrial dysfunction in Alzheimer's disease.Aging medicine (Milton (N.S.W)) · 2022Review
- Reviewing the Traditional/Modern Uses, Phytochemistry, Essential Oils/Extracts and Pharmacology ofAntioxidants (Basel, Switzerland) · 2022Review
- Novel Design of Neuropeptide-Based Drugs with β-Sheet Breaking Potential in Amyloid-Beta Cascade: Molecular and Structural Deciphers.International journal of molecular sciences · 2022Article
- Taurine Stabilizing Effect on Lysozyme.Life (Basel, Switzerland) · 2022Article
- Statins and cognition: Modifying factors and possible underlying mechanisms.Frontiers in aging neuroscience · 2022Review
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the most commonly occurring neurodegenerative disorders, Alzheimer's disease (AD), encompasses the loss of cognitive and memory potential, impaired learning, dementia and behavioral defects, and has been prevalent since the 1900s. The accelerating occurrence of AD is expected to reach 65.7 million by 2030. The disease results in neural atrophy and disrupted inter-neuronal connections. Amongst multiple AD pathogenesis hypotheses, the amyloid beta (Aβ) cascade is the most relevant and accepted form of the hypothesis, which suggests that Aβ monomers are formed as a result of the cleavage of amyloid precursor protein (APP), followed by the conversion of these monomers to toxic oligomers, which in turn develop β-sheets, fibrils and plaques. The review targets the events in the amyloid hypothesis and elaborates suitable therapeutic agents that function by hindering the steps of plaque formation and lowering Aβ levels in the brain. The authors discuss treatment possibilities, including the inhibition of β- and γ-secretase-mediated enzymatic cleavage of APP, the immune response generating active immunotherapy and passive immunotherapeutic approaches targeting monoclonal antibodies towards Aβ aggregates, the removal of amyloid aggregates by the activation of enzymatic pathways or the regulation of Aβ circulation, glucagon-like peptide-1 (GLP-1)-mediated curbed accumulation and the neurotoxic potential of Aβ aggregates, bapineuzumab-mediated vascular permeability alterations, statin-mediated Aβ peptide degradation, the potential role of ibuprofen and the significance of natural drugs and dyes in hindering the amyloid cascade events. Thus, the authors aim to highlight the treatment perspective, targeting the amyloid hypothesis, while simultaneously emphasizing the need to conduct further investigations, in order to provide an opportunity to neurologists to develop novel and reliable treatment therapies for the retardation of AD progression.
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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.