ArticleNeuroscience2014
Neuronal degeneration, synaptic defects, and behavioral abnormalities in tau₄₅₋₂₃₀ transgenic mice.
Article in Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- The role of Annexin A2 in Alzheimer's disease: From cellular functions to therapeutic potential.The FEBS journal · 2026Review
- Complicated Role of Post-translational Modification and Protease-Cleaved Fragments of Tau in Alzheimer's Disease and Other Tauopathies.Molecular neurobiology · 2024Review
- Death Induced by Survival gene Elimination (DISE) correlates with neurotoxicity in Alzheimer's disease and aging.Nature communications · 2024Article
- Dysregulation of Neuropeptide and Tau Peptide Signatures in Human Alzheimer's Disease Brain.ACS chemical neuroscience · 2022Article
- Therapeutic strategies for tauopathies and drug repurposing as a potential approach.Biochemical pharmacology · 2022Review
- The Role of Extracellular Matrix Components in the Spreading of Pathological Protein Aggregates.Frontiers in cellular neuroscience · 2022Review
- The formation of small aggregates contributes to the neurotoxic effects of tauNeurochemistry international · 2022Article
- Generation and Role of Calpain-Cleaved 17-kDa Tau Fragment in Acute Ischemic Stroke.Molecular neurobiology · 2021Article
- Review
- Human Tau Isoforms and Proteolysis for Production of Toxic Tau Fragments in Neurodegeneration.Frontiers in neuroscience · 2021Review
- Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease.Molecular neurodegeneration · 2020Review
- Alterations in Tau Metabolism in ALS and ALS-FTSD.Frontiers in neurology · 2020Review
- Aβ oligomer induced cognitive impairment and evaluation of ACU193-MNS-based MRI in rabbit.Alzheimer's & dementia (New York, N. Y.) · 2020Article
- Altered Cytoskeletal Composition and Delayed Neurite Elongation in tauNeuroscience · 2019Article
- Neurological alterations induced by formulated imidacloprid toxicity in Japanese quails.Metabolic brain disease · 2019Article
- Annexins A2 and A6 interact with the extreme N terminus of tau and thereby contribute to tau's axonal localization.The Journal of biological chemistry · 2018Article
- Tau Proteolysis in the Pathogenesis of Tauopathies: Neurotoxic Fragments and Novel Biomarkers.Journal of Alzheimer's disease : JAD · 2018Review
- The Molecular Chaperone Artemin Efficiently Blocks Fibrillization of TAU Protein In Vitro.Cell journal · 2018Article
- TauNeuroscience · 2017Article
- Roles of tau protein in health and disease.Acta neuropathologica · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The complement of mechanisms underlying tau pathology in neurodegenerative disorders has yet to be elucidated. Among these mechanisms, abnormal tau phosphorylation has received the most attention because neurofibrillary tangles present in Alzheimer's disease (AD) and related disorders known as tauopathies are composed of hyperphosphorylated forms of this microtubule-associated protein. More recently, we showed that calpain-mediated cleavage leading to the generation of the 17kDa tau₄₅₋₂₃₀ fragment is a conserved mechanism in these diseases. To obtain insights into the role of this fragment in neurodegeneration, we generated transgenic mice that express tau₄₅₋₂₃₀ and characterized their phenotype. Our results showed a significant increase in cell death in the hippocampal pyramidal cell layer of transgenic tau₄₅₋₂₃₀ mice when compared to wild-type controls. In addition, significant synapse loss was detected as early as six months after birth in transgenic hippocampal neurons. These synaptic changes were accompanied by alterations in the expression of the N-methyl-d-aspartate glutamate (NMDA) receptor subunits. Furthermore, functional abnormalities were detected in the transgenic mice using Morris Water Maze and fear conditioning tests. These results suggest that the accumulation of tau₄₅₋₂₃₀ is responsible, at least in part, for neuronal degeneration and some behavioral changes in AD and other tauopathies. Collectively, these data provide the first direct evidence of the toxic effects of a tau fragment biologically produced in the context of these diseases in vertebrate neurons that develop in situ.
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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.