ArticleThe American journal of pathology2007
Early axonopathy preceding neurofibrillary tangles in mutant tau transgenic mice.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 133 citations in OpenAlex.
- Amplification of seeding-competent tau aggregates by PMCA in human and experimental tauopathies.Acta neuropathologica communications · 2026Article
- N-terminally acetylated Met11-Tau: a new pathological truncated Tau species with functional relevance in Alzheimer's disease.Translational neurodegeneration · 2026Article
- Article
- Impairment of neuronal activity occurs at the early stages of the aggregation cascade of Aβ1-42 and mutant Tau.Disease models & mechanisms · 2026Article
- Spinal cord Tau pathology induces tactile deficits and cognitive impairment in Alzheimer's disease via dysregulation of CCK neurons.Nature neuroscience · 2026Article
- Stratification of brain-derived extracellular vesicles of Alzheimer's disease patients indicates a unique proteomic content and a higher seeding capacity of small extracellular vesicles.Translational neurodegeneration · 2025Article
- Seeding Alzheimer's disease-associated tau pathology in MAPT knock-in primary neurons causes early axonopathy and synaptic dysfunction.Scientific reports · 2025Article
- Anti-tau VHH therapy against PHF6: a safe approach to slowing the phenotype of tau pathology.Alzheimer's research & therapy · 2025Article
- Deletion of Murine APP Aggravates Tau and Amyloid Pathologies in the 5xFADXTg30 Alzheimer's Disease Model.Biomolecules · 2025Article
- The lemur tail kinase family in neuronal function and disfunction in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2024Review
- Alteration of gene expression and protein solubility of the PI 5-phosphatase SHIP2 are correlated with Alzheimer's disease pathology progression.Acta neuropathologica · 2024Article
- Behavioral, metabolic, and lipidomic characterization of the 5xFADxTg30 mouse model of Alzheimer's disease.iScience · 2024Article
- Methods for Biochemical Isolation of Insoluble Tau in Rodent Models of Tauopathies.Methods in molecular biology (Clifton, N.J.) · 2024Review
- Behavioral and Neuropathological Phenotyping of the Tau58/2 and Tau58/4 Transgenic Mouse Models for FTDP-17.Life (Basel, Switzerland) · 2023Article
- Loss of forebrain BIN1 attenuates hippocampal pathology and neuroinflammation in a tauopathy model.Brain : a journal of neurology · 2023Article
- Disease-modifying effects of sodium selenate in a model of drug-resistant, temporal lobe epilepsy.eLife · 2023Article
- Review
- Spread of pathological human Tau from neurons to oligodendrocytes and loss of high-firing pyramidal neurons in aging mice.Cell reports · 2022Article
- Inhibition of Tau seeding by targeting Tau nucleation core within neurons with a single domain antibody fragment.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Extracellular vesicles: Major actors of heterogeneity in tau spreading among human tauopathies.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegenerative diseases characterized by brain and spinal cord involvement often show widespread accumulations of tau aggregates. We have generated a transgenic mouse line (Tg30tau) expressing in the forebrain and the spinal cord a human tau protein bearing two pathogenic mutations (P301S and G272V). These mice developed age-dependent brain and hippocampal atrophy, central and peripheral axonopathy, progressive motor impairment with neurogenic muscle atrophy, and neurofibrillary tangles and had decreased survival. Axonal spheroids and axonal atrophy developed early before neurofibrillary tangles. Neurofibrillary inclusions developed in neurons at 3 months and were of two types, suggestive of a selective vulnerability of neurons to form different types of fibrillary aggregates. A first type of tau-positive neurofibrillary tangles, more abundant in the forebrain, were composed of ribbon-like 19-nm-wide filaments and twisted paired helical filaments. A second type of tau and neurofilament-positive neurofibrillary tangles, more abundant in the spinal cord and the brainstem, were composed of 10-nm-wide neurofilaments and straight 19-nm filaments. Unbiased stereological analysis indicated that total number of pyramidal neurons and density of neurons in the lumbar spinal cord were not reduced up to 12 months in Tg30tau mice. This Tg30tau model thus provides evidence that axonopathy precedes tangle formation and that both lesions can be dissociated from overt neuronal loss in selected brain areas but not from neuronal dysfunction.
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