ReviewPrion
Alzheimer disease: a tale of two prions.
Review in Prion. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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
37 citing papers in PubMed, 112 citations in OpenAlex.
- NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation.Neuroimmunomodulation · 2026Review
- P-tau217 as a Reliable Blood-Based Marker of Alzheimer's Disease.Biomedicines · 2024Review
- Structural and functional damage to neuronal nuclei caused by extracellular tau oligomers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Alzheimer's Disease as Type 3 Diabetes: Common Pathophysiological Mechanisms between Alzheimer's Disease and Type 2 Diabetes.International journal of molecular sciences · 2022Review
- Microglia activation linking amyloid-β drive tau spatial propagation in Alzheimer's disease.Frontiers in neuroscience · 2022Article
- Article
- Potential Mechanisms Underlying Resistance to Dementia in Non-Demented Individuals with Alzheimer's Disease Neuropathology.Journal of Alzheimer's disease : JAD · 2022Review
- Cofilin Signaling in the CNS Physiology and Neurodegeneration.International journal of molecular sciences · 2021Review
- All Roads Lead to Rome: Different Molecular Players Converge to Common Toxic Pathways in Neurodegeneration.Cells · 2021Review
- Longitudinal predictive modeling of tau progression along the structural connectome.NeuroImage · 2021Article
- Protein and Imaging Biomarkers in the Eye for Early Detection of Alzheimer's Disease.Journal of Alzheimer's disease reports · 2021Review
- Are Heat Shock Proteins an Important Link between Type 2 Diabetes and Alzheimer Disease?International journal of molecular sciences · 2020Review
- A physics-informed geometric learning model for pathological tau spread in Alzheimer's disease.Medical image computing and computer-assisted intervention : MICCAI ... International Conference on Medical Image Computing and Computer-Assisted Intervention · 2020Article
- A Glimmer of Hope: Maintain Mitochondrial Homeostasis to Mitigate Alzheimer's Disease.Aging and disease · 2020Review
- Bridging the Gap Between Fluid Biomarkers for Alzheimer's Disease, Model Systems, and Patients.Frontiers in aging neuroscience · 2020Review
- FeMolecular neurobiology · 2019Article
- Recent Developments in Metal-Based Drugs and Chelating Agents for Neurodegenerative Diseases Treatments.International journal of molecular sciences · 2019Review
- Drug Development for Alzheimer's Disease: Microglia Induced Neuroinflammation as a Target?International journal of molecular sciences · 2019Review
- Amyloid Beta and MicroRNAs in Alzheimer's Disease.Frontiers in neuroscience · 2019Review
- A longitudinal model for tau aggregation in Alzheimer's disease based on structural connectivity.Information processing in medical imaging : proceedings of the ... conference · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer disease (AD) has traditionally been thought to involve the misfolding and aggregation of two different factors that contribute in parallel to pathogenesis: amyloid-β (Aβ) peptides, which represent proteolytic fragments of the transmembrane amyloid precursor protein, and tau, which normally functions as a neuronally enriched, microtubule-associated protein that predominantly accumulates in axons. Recent evidence has challenged this model, however, by revealing numerous functional interactions between Aβ and tau in the context of pathogenic mechanisms for AD. Moreover, the propagation of toxic, misfolded Aβ and tau bears a striking resemblance to the propagation of toxic, misfolded forms of the canonical prion protein, PrP, and misfolded Aβ has been shown to induce tau misfolding in vitro through direct, intermolecular interaction. In this review we discuss evidence for the prion-like properties of both Aβ and tau individually, as well as the intriguing possibility that misfolded Aβ acts as a template for tau misfolding in vivo.
Indexed as
Identifiers
What OpenQuestion holds
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.