ReviewTranslational neurodegeneration2025
Dual modulation of amyloid beta and tau aggregation and dissociation in Alzheimer's disease: a comprehensive review of the characteristics and therapeutic strategies.
Review in Translational neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mechanistic insights into mesenchymal stem cell therapy for cognitive impairments in Alzheimer's disease models: a systematic review and meta-analysis.Molecular and cellular biochemistry · 2026Pooled it
- Human amniotic mesenchymal stromal cell-derived extracellular vesicles reprogram microglia and prevent neurodegeneration in experimental models of Alzheimer's disease.Translational neurodegeneration · 2026Article
- Micro/Nanoplastics Drive Amyloid‑β Colloidal and Oxidative Reorganization: A Real-World Contaminant Stressor.ACS omega · 2026Article
- Targeting soluble misfolded oligomers in anti-amyloid research.Nature reviews. Chemistry · 2026Review
- RNA-based therapeutics for Alzheimer's disease and related tauopathies: challenges and opportunities.The journal of prevention of Alzheimer's disease · 2026Review
- Biophysical assessment of the molecular mechanisms of Tau aggregation and its role in Alzheimer's disease.Protein science : a publication of the Protein Society · 2026Review
- PLGA Nanoparticle-based Anti-TLR2 scFv Gene Delivery for the Treatment of Alzheimer's Disease.Experimental neurobiology · 2026Article
- Tau and β-Amyloid Relevant Pathology as a Central Therapeutic Target in Alzheimer's Disease.Biomolecules · 2026Review
- Neuropeptides in the Management of Alzheimer's Disease: From Pathophysiology to Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Estradiol ameliorates AD pathology and cognitive deficits by SORLA-mediated APP endosomal trafficking.Alzheimer's research & therapy · 2026Article
- Tau Protein Aggregation Inhibitors-Therapeutic Strategy for Concurrent Tau and Amyloid Aggregation Inhibition.Biomedicines · 2026Review
- AGGRESCAN and its evolution: A two-decade perspective on protein aggregation prediction.Biophysical reviews · 2026Review
- Integrating network pharmacology and experimental validation strategies to investigate the mechanisms and key flavonoids in medicinal and edible citrus plants against Alzheimer's disease.Frontiers in aging neuroscience · 2026Article
- Peptide-Based Therapeutics for Alzheimer's Disease: Medicinal Chemistry, AI-Guided Computational Design, and Blood-Brain Barrier Delivery.Drug design, development and therapy · 2026Review
- Research Progress on the Pathogenesis, Therapeutic Strategies, and Phthalocyanine Compounds for Alzheimer's Disease.Current Alzheimer research · 2026Review
- Monoclonal antibodies and small molecules: on the cutting edge of Alzheimer's disease therapy.Frontiers in cell and developmental biology · 2026Review
- Mechanistic modeling of amyloid dynamics relating to Alzheimer's disease progression.Frontiers in aging neuroscience · 2026Article
- Prions and protein aggregates as pathogens, self-propagating structures, biomarkers, and therapeutic targets.Microbiology and molecular biology reviews : MMBR · 2025Review
- Catalytic Effect of Amyloid-β on Native Tau Aggregation at Physiologically Relevant Concentrations.International journal of molecular sciences · 2025Article
- Carbonic Anhydrase 3 Overexpression Modulates Signalling Pathways Associated with Cellular Stress Resilience and Proteostasis.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Alzheimer's disease (AD) is not a single-cause disease; rather, it is a complex neurodegenerative disease involving multiple pathological pathways influenced by various risk factors. Aggregation and accumulation of amyloid beta (Aβ) and tau are the most prominent features in the brains of AD patients. Aggregated Aβ and tau exert neurotoxic effects in the central nervous system, contributing to the pathogenesis and progression of AD. They also act synergistically to cause neurodegeneration, resulting in memory loss. In this context, dual inhibition of Aβ and tau aggregation, or dissociation of these two aggregates, is considered promising for AD treatment. Recently, dual inhibitors capable of simultaneously targeting the aggregation and dissociation of both Aβ and tau have been investigated. Specific amino acid domains of Aβ and tau associated with their aggregation/dissociation have been identified. Subsequently, therapeutic agents that prevent aggregation or promote disaggregation by targeting these domains have been identified/developed. In this review, we summarize the major domains and properties involved in Aβ and tau aggregation, as well as the therapeutic effects and mechanisms of agents that simultaneously regulate their aggregation and dissociation. This comprehensive review may contribute to the design and discovery of next-generation dual-targeting drugs for Aβ and tau, potentially leading to the development of more effective therapeutic strategies for 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.