ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Tau-induced defects in synaptic plasticity, learning, and memory are reversible in transgenic mice after switching off the toxic Tau mutant.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 178 papers.
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Who cites it
178 citing papers in PubMed, 294 citations in OpenAlex.
- Carbon-12 and Gamma-Rays Combined Irradiation Ameliorates Behavioral and Biochemical Alterations in Tau P301S Homozygous Transgenic Mice.Molecular neurobiology · 2026Article
- When Pathologies Collide: The Intersection of Tau and Alpha-Synuclein in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Profiling Protein Aggregate Size Using Single-Molecule Array Technology.Analytical chemistry · 2026Article
- Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease.bioRxiv : the preprint server for biology · 2026Article
- Tau T205 phosphorylation modulates engram cell recruitment and remote memory in mice.Nature communications · 2026Article
- Targeting tau in Alzheimer's Disease: rationale, approach and challenges.Molecular neurodegeneration · 2026Review
- Investigating the role of EFhd2 protein in modulating tau pathology in a tauopathy mouse model.Frontiers in molecular neuroscience · 2026Article
- Computer-aided Drug Design for Alzheimer's Disease: Recent Advancements and Future Perspectives.Current topics in medicinal chemistry · 2026Review
- Seeding Alzheimer's disease-associated tau pathology in MAPT knock-in primary neurons causes early axonopathy and synaptic dysfunction.Scientific reports · 2025Article
- Making tau amyloid models in vitro: a crucial and underestimated challenge.FEBS letters · 2025Review
- Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice.Neurobiology of disease · 2025Article
- Limitations and Applications of Rodent Models in Tauopathy and Synucleinopathy Research.Journal of neurochemistry · 2025Review
- Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice.bioRxiv : the preprint server for biology · 2025Article
- Paradoxical attenuation of early amyloid-induced cognitive impairment and synaptic plasticity in an aged APP/Tau bigenic rat model.Acta neuropathologica communications · 2024Article
- Akt-activated GSK3β inhibitory peptide effectively blocks tau hyperphosphorylation.Archives of pharmacal research · 2024Article
- Transgenic sensors reveal compartment-specific effects of aggregation-prone proteins on subcellular proteostasis during aging.Cell reports methods · 2024Article
- Dendritic spine head diameter predicts episodic memory performance in older adults.Science advances · 2024Article
- Synapses tagged, memories kept: synaptic tagging and capture hypothesis in brain health and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- Nanoligomers targeting NF-κB and NLRP3 reduce neuroinflammation and improve cognitive function with aging and tauopathy.Journal of neuroinflammation · 2024Article
- KIBRA repairs synaptic plasticity and promotes resilience to tauopathy-related memory loss.The Journal of clinical investigation · 2024Article
118 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This report describes the behavioral and electrophysiological analysis of regulatable transgenic mice expressing mutant repeat domains of human Tau (Tau(RD)). Mice were generated to express Tau(RD) in two forms, differing in their propensity for β-structure and thus in their tendency for aggregation ("pro-aggregant" or "anti-aggregant") (Mocanu et al., 2008). Only pro-aggregant mice show pronounced changes typical for Tau pathology in Alzheimer's disease (aggregation, missorting, hyperphosphorylation, synaptic and neuronal loss), indicating that the β-propensity and hence the ability to aggregate is a key factor in the disease. We now tested the mice with regard to neuromotor parameters, behavior, learning and memory, and synaptic plasticity and correlated this with histological and biochemical parameters in different stages of switching Tau(RD) on or off. The mice are normal in neuromotor tests. However, pro-aggregant Tau(RD) mice are strongly impaired in memory and show pronounced loss of long-term potentiation (LTP), suggesting that Tau aggregation specifically perturbs these brain functions. Remarkably, when the expression of human pro-aggregant Tau(RD) is switched on for ∼ 10 months and off for ∼ 4 months, memory and LTP recover, whereas aggregates decrease moderately and change their composition from mixed human plus mouse Tau to mouse Tau only. Neuronal loss persists, but synapses are partially rescued. This argues that continuous presence of amyloidogenic pro-aggregant Tau(RD) constitutes the main toxic insult for memory and LTP, rather than the aggregates as such.
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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.