ArticleScientific reports2017
Expression of P301L-hTau in mouse MEC induces hippocampus-dependent memory deficit.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
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- Tau pathology in the dorsal raphe may be a prodromal indicator of Alzheimer's disease.Molecular psychiatry · 2025Article
- Advancing Alzheimer's research by improving disease modeling of secondary tauopathy.NPJ dementia · 2025Review
- Microglial-Targeted nSMase2 Inhibitor Fails to Reduce Tau Propagation in PS19 Mice.Pharmaceutics · 2023Article
- Clinical significance of the cognition-related pathogenic proteins in plasma neuronal-derived exosomes among normal cognitive adults over 45 years old with olfactory dysfunction.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2022Article
- Sowing the Seeds of Discovery: Tau-Propagation Models of Alzheimer's Disease.ACS chemical neuroscience · 2020Article
- Peripheral inflammation promotes brain tau transmission via disrupting blood-brain barrier.Bioscience reports · 2020Article
- AD-Related N-Terminal Truncated Tau Is Sufficient to Recapitulate In Vivo the Early Perturbations of Human Neuropathology: Implications for Immunotherapy.Molecular neurobiology · 2018Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Intracellular accumulation of abnormally phosphorylated tau in different types of neurons is a pathological characteristic of Alzheimer's disease (AD). While tau modification and associated neuronal loss and hypometabolism start in the entorhinal cortex (EC) in early AD patients, the mechanism by which mutant P301L hTau leads to dementia is not fully elucidated. Here, we studied the effects of P301L hTau transduction in the medial EC (MEC) of mice on tau phosphorylation and accumulation, and cognitive deficit. We found that the exogenous mutant tau protein was restricted in MEC without spreading to other brain regions at one month after transduction. Interestingly, expression of the mutant tau in MEC induces endogenous tau hyperphosphorylation and accumulation in hippocampus and cortex, and inhibits neuronal activity with attenuated PP-DG synapse plasticity, leading to hippocampus-dependent memory deficit with intact olfactory function. These findings suggest a novel neuropathological mechanism of early AD, which is initiated by tau accumulation in MEC, and demonstrate a tau pathological model of early stage AD.
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