ArticleJournal of Alzheimer's disease & Parkinsonism2018
Targeting Prion-like Cis Phosphorylated Tau Pathology in Neurodegenerative Diseases.
Article in Journal of Alzheimer's disease & Parkinsonism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 18 citations in OpenAlex.
- Review
- Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy.Cell reports · 2026Article
- From Traumatic Brain Injury to Alzheimer's Disease: Multilevel Biomechanical, Neurovascular, and Molecular Mechanisms with Emerging Therapeutic Directions.International journal of molecular sciences · 2026Review
- Cross-Talk Between Tau O-GlcNAcylation and the Formation of the Early Driver of Neurodegeneration (Cis P-Thr231-Pro Tau) in Primary Cortical Neurons.Molecular neurobiology · 2025Article
- The glymphatic and meningeal lymphatic systems may converge, connecting traumatic brain injury progression with chronic traumatic encephalopathy onset.Molecular and cellular neurosciences · 2025Review
- A Novel Phosphorylated Tau Conformer Implicated in the Tauopathy Pathogenesis of Human Neurons.Biomolecules · 2025Article
- Traumatic brain injury and the pathways to cerebral tau accumulation.Frontiers in neurology · 2023Review
- The regulatory role of Pin1 in neuronal death.Neural regeneration research · 2023Review
- Death-associated protein kinase 1 mediates Aβ42 aggregation-induced neuronal apoptosis and tau dysregulation in Alzheimer's disease.International journal of biological sciences · 2022Article
- Living Proof of Activity of Extracellular Vesicles in the Central Nervous System.International journal of molecular sciences · 2021Review
- Advances and considerations in AD tau-targeted immunotherapy.Neurobiology of disease · 2020Review
- Post-translational Modifications of the Peptidyl-Prolyl Isomerase Pin1.Frontiers in cell and developmental biology · 2020Review
- Peptidyl-ProlylFrontiers in cell and developmental biology · 2020Review
- Death-Associated Protein Kinase 1 Phosphorylation in Neuronal Cell Death and Neurodegenerative Disease.International journal of molecular sciences · 2019Review
- Traumatic Brain Injury-related voiding dysfunction in mice is caused by damage to rostral pathways, altering inputs to the reflex pathways.Scientific reports · 2019Article
- Death-Associated Protein Kinase 1 as a Promising Drug Target in Cancer and Alzheimer's Disease.Recent patents on anti-cancer drug discovery · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Tau is a microtubule-associated protein heavily implicated in neurodegenerative diseases collectively known as tauopathies, including Alzheimer's disease and chronic traumatic encephalopathy. Phosphorylation of tau at Thr231 allows for the isomerization of phosphorylated tau (p-tau) into distinct cis and trans conformations. Cis, but not trans, p-tau is detectable not only in Alzheimer's disease and chronic traumatic encephalopathy, but also right after traumatic brain injury depending on injury severity and frequency both in humans and animal models. Cis p-tau is not only neurotoxic but also spreads from a neuron to another in a prion-like fashion, functioning as a primary driver of neurodegeneration, which can be effectively neutralized by cis p-tau antibody. This represents an exciting new opportunity for understanding disease development and developing early biomarkers and effective therapies of tauopathies.
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.