ReviewFrontiers in aging neuroscience2020
Mechanisms of Pathogenic Tau and Aβ Protein Spreading in Alzheimer's Disease.
Review in Frontiers in aging neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.
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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
109 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exploring the gut-brain axis in alzheimer's disease treatment via probiotics: evidence from animal studies-a systematic review and meta-analysis.BMC neurology · 2024Pooled it
- Prospect in Alzheimer's disease integrative therapy targeting both amyloid-beta and tau.Neural regeneration research · 2026Article
- Photobiomodulation with 808 nm Laser Light Repairs Mitochondrial Integrity and Normalizes ROS, ATP, and Membrane Depolarization in Aβ-Exposed Primary Neurons in Alzheimer's Disease Model.International journal of molecular sciences · 2026Article
- Anatomy of a Setback: A Taxonomy of Clinical Trial Failures in Alzheimer's Disease and Strategic Lessons for the Future.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- The Use of Dynamic Neck Lymphaticovenous Anastomosis in the Adjunctive Treatment of Alzheimer's Disease: A Retrospective Case Series.Archives of plastic surgery · 2026Article
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Molecular Dynamics Study of the Binding of Cationic, Anionic, and Neutral Luminescent Conjugated Ligands to the Alzheimer Folds of Aβ(1-42) and Tau Fibrils.Chembiochem : a European journal of chemical biology · 2026Article
- Simufilam in Alzheimer's Disease: Assessment of Efficacy of a Controversial Drug in Human Neuronal Cell Culture.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Interpretable machine learning model based on multimodal MRI radiomics for Alzheimer's disease diagnosis.Frontiers in aging neuroscience · 2026Article
- Machine learning for Alzheimer's disease progression under extreme class imbalance.Frontiers in neuroscience · 2026Article
- Unraveling the molecular mechanisms in severe Alzheimer's disease based on transcriptomic data using next generation knowledge discovery methods.Pakistan journal of medical sciences · 2026Article
- Longitudinal three-photon imaging for tracking amyloid plaques and vascular degeneration in a mouse model of Alzheimer's disease.Journal of biomedical optics · 2026Article
- Nanoscopic Mapping of the Extracellular Space in Amyloid Plaque-rich Cortex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Extracellular vesicle-based therapies for neurodegenerative diseases.NeuroImmune pharmacology and therapeutics · 2025Review
- Exosome-Mediated Delivery of Amyloid Beta Modulators: A Potential Therapeutic Strategy for Alzheimer's Disease.Molecular neurobiology · 2025Review
- Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets.CNS neuroscience & therapeutics · 2025Review
- Unraveling the structure-activity relationships of organometallic ferrocene-pyrazole and ferrocene-pyrimidine curcumin analogues in amyloid-β aggregation and glioblastoma treatment.Scientific reports · 2025Article
- The Role of Extracellular Vesicles in Neuropsychiatric Disorders.Advanced pharmaceutical bulletin · 2025Review
- High-caloric intake rescues early symptomatic AD-induced hippocampal neurovascular coupling deficits.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Gaultheria leucocarpa inhibits Aβ fibrillization and enhances mitophagy-mediated degradation of pathogenic proteins.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
49 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is pathologically defined by extracellular accumulation of amyloid-β (Aβ) peptides generated by the cleavage of amyloid precursor protein (APP), strings of hyperphosphorylated Tau proteins accumulating inside neurons known as neurofibrillary tangles (NFTs) and neuronal loss. The association between the two hallmarks and cognitive decline has been known since the beginning of the 20th century when the first description of the disease was carried out by Alois Alzheimer. Today, more than 40 million people worldwide are affected by AD that represents the most common cause of dementia and there is still no effective treatment available to cure the disease. In general, the aggregation of Aβ is considered an essential trigger in AD pathogenesis that gives rise to NFTs, neuronal dysfunction and dementia. During the process leading to AD, tau and Aβ first misfold and form aggregates in one brain region, from where they spread to interconnected areas of the brain thereby inducing its gradual morphological and functional deterioration. In this mini-review article, we present an overview of the current literature on the spreading mechanisms of Aβ and tau pathology in AD since a more profound understanding is necessary to design therapeutic approaches aimed at preventing or halting disease progression.
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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.