ReviewPrion2012
Is tau ready for admission to the prion club?
Review in Prion, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- Prion and "Prion-Like" Detection: From Conventional Methods to Microfluidics or Lab-on-Chip Platforms to Monitor Seeding and Spreading of Misfolded Proteins.Sub-cellular biochemistry · 2025Review
- Review
- Role of Microglial Cells in Alzheimer's Disease Tau Propagation.Frontiers in aging neuroscience · 2019Article
- Review
- Involvement of Cellular Prion Protein in α-Synuclein Transport in Neurons.Molecular neurobiology · 2018Article
- Chronic Traumatic Encephalopathy: Is Latency in Symptom Onset Explained by Tau Propagation?Cold Spring Harbor perspectives in medicine · 2018Review
- Spinal cord injury and Alzheimer's disease risk: a population-based, retrospective cohort study.Spinal cord · 2018Article
- Amyloidogenesis of Tau protein.Protein science : a publication of the Protein Society · 2017Review
- Reduced Abundance and Subverted Functions of Proteins in Prion-Like Diseases: Gained Functions Fascinate but Lost Functions Affect Aetiology.International journal of molecular sciences · 2017Review
- β-Amyloid and the Pathomechanisms of Alzheimer's Disease: A Comprehensive View.Molecules (Basel, Switzerland) · 2017Review
- Monoaminergic neuropathology in Alzheimer's disease.Progress in neurobiology · 2017Review
- Tau Protein Hyperphosphorylation and Aggregation in Alzheimer's Disease and Other Tauopathies, and Possible Neuroprotective Strategies.Biomolecules · 2016Review
- Chaperones in Neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Review
- The neuropathology of chronic traumatic encephalopathy.Brain pathology (Zurich, Switzerland) · 2015Review
- Tau depletion prevents progressive blood-brain barrier damage in a mouse model of tauopathy.Acta neuropathologica communications · 2015Article
- Yeast prions and human prion-like proteins: sequence features and prediction methods.Cellular and molecular life sciences : CMLS · 2014Review
- Proteins recruited to exosomes by tau overexpression implicate novel cellular mechanisms linking tau secretion with Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2014Article
- Chronic traumatic encephalopathy: a spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel.Alzheimer's research & therapy · 2014Review
- Tangles, Toxicity, and Tau Secretion in AD - New Approaches to a Vexing Problem.Frontiers in neurology · 2013Review
- Rapid accumulation of endogenous tau oligomers in a rat model of traumatic brain injury: possible link between traumatic brain injury and sporadic tauopathies.The Journal of biological chemistry · 2013Article
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
Aggregation-prone proteins associated with neurodegenerative disease, such as α synuclein and β amyloid, now appear to share key prion-like features with mammalian prion protein, such as the ability to recruit normal proteins to aggregates and to translocate between neurons. These features may shed light on the genesis of stereotyped lesion development patterns in conditions such as Alzheimer disease and Lewy Body dementia. We discuss the qualifications of tau protein as a possible "prionoid" mediator of lesion spread based on recent characterizations of the secretion, uptake and transneuronal transfer of human tau isoforms in a variety of tauopathy models, and in human patients. In particular, we consider (1) the possibility that prionoid behavior of misprocessed tau in neurodegenerative disease may involve other aggregation-prone proteins, including PrP itself, and (2) whether "prionlike" tau lesion propagation might include mechanisms other than protein-protein templating.
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.