ReviewNature medicine2014
Cell-to-cell transmission of pathogenic proteins in neurodegenerative diseases.
Review in Nature medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 370 papers, 2 of them syntheses 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
370 citing papers in PubMed, 2 syntheses or guidelines pooled it, 639 citations in OpenAlex.
- Alpha-Synuclein Strain Variability in Body-First and Brain-First Synucleinopathies.Frontiers in aging neuroscience · 2022Pooled it
- Meta-Analysis of the Alzheimer's Disease Human Brain Transcriptome and Functional Dissection in Mouse Models.Cell reports · 2020Pooled it
- Network-Based Spreading of Gray Matter Changes Across Different Stages of Psychosis.JAMA psychiatry · 2023Trial
- Widespread synaptic density loss in schizophrenia follows molecular and network architecture.Molecular psychiatry · 2026Article
- The Amyloid State of Mutant p53 in Cancer.JMA journal · 2026Review
- Local autophagy impairment triggers brain-wide presynaptic remodeling and resilience.The EMBO journal · 2026Article
- Exosomes: Mechanisms, Diagnosis, and Therapeutic Progress in Vascular Cognitive Impairment.Molecular neurobiology · 2026Review
- Application of the Allen Human Brain Atlas in Alzheimer's disease and Parkinson's disease.Translational neurodegeneration · 2026Review
- Frontotemporal dementia associated CHCHD10Cell death & disease · 2026Article
- Dysregulation of the Extracellular Matrix in the Synaptic Pathology of Parkinson's Disease: Molecular Mechanisms and Novel Therapeutic Approaches.Life (Basel, Switzerland) · 2026Review
- Exosomes in Amyloid Propagation-Roles in Neurodegeneration.Molecular neurobiology · 2026Review
- Bacillus Calmette-Guérin (BCG) Vaccination and the Immune-Brain Axis: Implications for Neuroprotection and Neurodegenerative Disease.Vaccines · 2026Review
- Perampanel Blocks Transsynaptic α-Synuclein Propagation and Neurodegeneration in a Mouse Model of Lewy Body Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Amyloid-β, Tau Protein, α-Synuclein, TDP-43, and FUS in Mixed Pathology: And Intrinsic Disorder to Rule Them All.International journal of molecular sciences · 2026Review
- Dynamic thermodynamic-informational entropic relationship (TIER) models of selective vulnerability to neurodegeneration.bioRxiv : the preprint server for biology · 2026Article
- Structure-function coupling in the human brainstem.bioRxiv : the preprint server for biology · 2026Article
- Full-length tau seeded by C-shaped tau fibrils is conformationally variable.The Journal of biological chemistry · 2026Article
- Tubulin transforms Tau and α-synuclein condensates from pathological to physiological.Nature communications · 2026Article
- Phosphorylated tau exhibits antimicrobial activity capable of neutralizing herpes simplex virus 1 infectivity in human neurons.Nature neuroscience · 2026Article
- Where do PDD and DLB SYNdromes fit in neuronal alpha-SYNuclein biological frameworks?Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
310 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 at 1 institution in 1 country.
Funding
Abstract
A common feature of many neurodegenerative diseases is the deposition of β-sheet-rich amyloid aggregates formed by proteins specific to these diseases. These protein aggregates are thought to cause neuronal dysfunction, directly or indirectly. Recent studies have strongly implicated cell-to-cell transmission of misfolded proteins as a common mechanism for the onset and progression of various neurodegenerative disorders. Emerging evidence also suggests the presence of conformationally diverse 'strains' of each type of disease protein, which may be another shared feature of amyloid aggregates, accounting for the tremendous heterogeneity within each type of neurodegenerative disease. Although there are many more questions to be answered, these studies have opened up new avenues for therapeutic interventions in neurodegenerative disorders.
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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.