ArticleActa neuropathologica2014
Soluble pathological tau in the entorhinal cortex leads to presynaptic deficits in an early Alzheimer's disease model.
Article in Acta neuropathologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 111 citations in OpenAlex.
- Dysregulation of autophagosome-mitochondria contacts contributes to autophagy dysfunction and neurodegeneration in tauopathy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- FKBP51 inhibition by SAFit2 modulates tau pathology and cognitive deficits in PS19 mice.Alzheimer's research & therapy · 2026Article
- Article
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
- Pathophysiological roles of neural stem cells in neuropsychiatric diseases: from plasticity to pharmacological targeting.Acta pharmacologica Sinica · 2026Review
- Plasma growth-associated protein 43 correlates with synaptic loss in Alzheimer's disease.Cell reports. Medicine · 2025Article
- Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease.The Journal of physiology · 2025Review
- Microglia networks within the tapestry of alzheimer's disease through spatial transcriptomics.Molecular neurodegeneration · 2025Review
- Synaptic loss pattern is constrained by brain connectome and modulated by phosphorylated tau in Alzheimer's disease.Nature communications · 2025Article
- Sea Squirt-Derived Peptide WLP Mitigates OKA-Induced Alzheimer's Disease-like Phenotypes in Human Cerebral Organoid.Antioxidants (Basel, Switzerland) · 2025Article
- Mitochondrial bioenergetics stimulates autophagy for pathological MAPT/Tau clearance in tauopathy neurons.Autophagy · 2025Article
- Autophagy in alzheimer disease pathogenesis and its therapeutic values.Autophagy reports · 2025Review
- Marmosets as model systems for the study of Alzheimer's disease and related dementias: Substantiation of physiological tau 3R and 4R isoform expression and phosphorylation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A mouse model of early sporadic tau pathology induces neurogenic plasticity in the hippocampus.PloS one · 2025Article
- Akt-activated GSK3β inhibitory peptide effectively blocks tau hyperphosphorylation.Archives of pharmacal research · 2024Article
- Exploring the Role of Mesenchymal Stem Cell-Derived Exosomes in Diabetic and Chemotherapy-Induced Peripheral Neuropathy.Molecular neurobiology · 2024Review
- PM2.5 triggers tau aggregation in a mouse model of tauopathy.JCI insight · 2024Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- Pathological Impact of Tau Proteolytical Process on Neuronal and Mitochondrial Function: a Crucial Role in Alzheimer's Disease.Molecular neurobiology · 2023Review
- Tau and neuroinflammation in Alzheimer's disease: interplay mechanisms and clinical translation.Journal of neuroinflammation · 2023Review
9 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
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Neurofibrillary tangles (NFTs), a hallmark of Alzheimer's disease, are intracellular silver and thioflavin S-staining aggregates that emerge from earlier accumulation of phospho-tau in the soma. Whether soluble misfolded but nonfibrillar tau disrupts neuronal function is unclear. Here we investigate if soluble pathological tau, specifically directed to the entorhinal cortex (EC), can cause behavioral or synaptic deficits. We studied rTgTauEC transgenic mice, in which P301L mutant human tau overexpressed primarily in the EC leads to the development of tau pathology, but only rare NFT at 16 months of age. We show that the early tau lesions are associated with nearly normal performance in contextual fear conditioning, a hippocampal-related behavior task, but more robust changes in neuronal system activation as marked by Arc induction and clear electrophysiological defects in perforant pathway synaptic plasticity. Electrophysiological changes were likely due to a presynaptic deficit and changes in probability of neurotransmitter release. The data presented here support the hypothesis that misfolded and hyperphosphorylated tau can impair neuronal function within the entorhinal-hippocampal network, even prior to frank NFT formation and overt neurodegeneration.
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.