ArticleScience translational medicine2019
Aβ and tau prion-like activities decline with longevity in the Alzheimer's disease human brain.
Article in Science translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses 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
78 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Shaping the future of preclinical development of successful disease-modifying drugs against Alzheimer's disease: a systematic review of tau propagation models.Acta neuropathologica communications · 2024Pooled it
- The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion.Frontiers in neuroscience · 2021Pooled it
- Precision Medicine Approach to Alzheimer's Disease: Successful Pilot Project.Journal of Alzheimer's disease : JAD · 2022Trial
- tRNA-derived fragments elevated in Alzheimer's disease promote Tau aggregation.bioRxiv : the preprint server for biology · 2026Article
- Soluble high-molecular-weight amyloid-β species derived from amyloid-β-laden brains induce cerebral β-amyloidosis.Brain communications · 2026Article
- Amyloid-β Seeds in Alzheimer's Disease: Research Challenges and Implications.Journal of neurochemistry · 2025Review
- Direct disassembly of α-syn preformed fibrils into α-syn monomers by an all-D-peptide.NPJ Parkinson's disease · 2025Article
- Microbial Metabolomes in Alzheimer's Disease: From Pathogenesis to Therapeutic Potential.Current issues in molecular biology · 2025Review
- Small-diffusible aggregates, plaques, tangles, and dynamic equilibria: Untangling Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Structural exposure of different microtubule binding domains determines the propagation and toxicity of pathogenic tau conformers in Alzheimer's disease.PLoS pathogens · 2025Article
- Weissella confusa Attenuates Cognitive Deficits in Alzheimer's Disease by Reducing Oxidative Stress Via the SIRT1/PGC-1α Signaling Pathway.Neurochemical research · 2025Article
- Could Blood Transfusion Increase the Risk of Alzheimer's Disease? A Narrative Review.Healthcare (Basel, Switzerland) · 2025Review
- The Unfolding Story of Protein Misfolding Causing Alzheimer Disease in Recipients of Human Pituitary Growth Hormone.Journal of the Endocrine Society · 2025Article
- The role of microglia in the prion-like transmission of protein aggregates in neurodegeneration.Brain communications · 2025Review
- Severe neurodegeneration in brains of transgenic rats producing human tau prions.Acta neuropathologica · 2024Article
- Effect of host and strain factors on α-synuclein prion pathogenesis.Trends in neurosciences · 2024Review
- Structural Variations of Prions and Prion-like Proteins Associated with Neurodegeneration.Current issues in molecular biology · 2024Review
- Cryo-EM structures reveal tau filaments from Down syndrome adopt Alzheimer's disease fold.Acta neuropathologica communications · 2024Article
- Pathogenic soluble tau peptide disrupts endothelial calcium signaling and vasodilation in the brain microvasculature.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
The hallmarks of Alzheimer's disease (AD) are the accumulation of Aβ plaques and neurofibrillary tangles composed of hyperphosphorylated tau. We developed sensitive cellular assays using human embryonic kidney-293T cells to quantify intracellular self-propagating conformers of Aβ in brain samples from patients with AD or other neurodegenerative diseases. Postmortem brain tissue from patients with AD had measurable amounts of pathological Aβ conformers. Individuals over 80 years of age had the lowest amounts of prion-like Aβ and phosphorylated tau. Unexpectedly, the longevity-dependent decrease in self-propagating tau conformers occurred in spite of increasing amounts of total insoluble tau. When corrected for the abundance of insoluble tau, the ability of postmortem AD brain homogenates to induce misfolded tau in the cellular assays showed an exponential decrease with longevity, with a half-life of about one decade over the age range of 37 to 99 years. Thus, our findings demonstrate an inverse correlation between longevity in patients with AD and the abundance of pathological tau conformers. Our cellular assays can be applied to patient selection for clinical studies and the development of new drugs and diagnostics for AD.
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