ArticleSynapse (New York, N.Y.)2017
Spread of tau down neural circuits precedes synapse and neuronal loss in the rTgTauEC mouse model of early Alzheimer's disease.
Article in Synapse (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 72 citations in OpenAlex.
- IgLON5 autoimmune antibodies activate Tau via neuronal hyperactivity.Science advances · 2026Article
- Extracellular Vesicles in Tauopathies: Mechanisms and Applications.International journal of molecular sciences · 2026Review
- Therapeutic Potential of Naive Hair Follicle Stem Cells in Alzheimer's Disease: A Comprehensive Evaluation of Neuroprotection and Neurogenesis.Neuropsychiatric disease and treatment · 2026Article
- Polygenic pathways shape white matter vulnerability to Alzheimer's disease-related pathophysiological changes.Alzheimer's research & therapy · 2025Article
- Evidence for trans-synaptic propagation of oligomeric tau in human progressive supranuclear palsy.Nature neuroscience · 2025Article
- Insights into pathophysiology, biomarkers, and therapeutics in tauopathies: Proceedings of the Tau2024 Global Conference.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Tau pathology is associated with postsynaptic metabotropic glutamate receptor 5 (mGluR5) in early Alzheimer's disease in a sex-specific manner.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
- Developing diagnostic biomarkers for Alzheimer's disease based on histone lactylation-related gene.Heliyon · 2024Article
- Entorhinal cortex vulnerability to human APP expression promotes hyperexcitability and tau pathology.Nature communications · 2024Article
- Synaptopathy: presynaptic convergence in frontotemporal dementia and amyotrophic lateral sclerosis.Brain : a journal of neurology · 2024Review
- The Enigma of Tau Protein Aggregation: Mechanistic Insights and Future Challenges.International journal of molecular sciences · 2024Review
- Delivering synaptic protein mRNAs via extracellular vesicles ameliorates cognitive impairment in a mouse model of Alzheimer's disease.BMC medicine · 2024Article
- Article
- DnaJs are enriched in tau regulators.International journal of biological macromolecules · 2023Article
- Oligomeric, phosphorylated, and truncated tau and spliceosome pathology within the entorhinal-hippocampal connectome across stages of Alzheimer's disease.The Journal of comparative neurology · 2023Article
- Entorhinal cortex vulnerability to human APP expression promotes hyperexcitability and tau pathology.Research square · 2023Article
- Implication of tau propagation on neurodegeneration in Alzheimer's disease.Frontiers in neuroscience · 2023Review
- Accumulation of pTau231 at the Postsynaptic Density in Early Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- A luminescence-based reporter to study tau secretion reveals overlapping mechanisms for the release of healthy and pathological tau.Frontiers in neuroscience · 2023Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Synaptic dysfunction and loss is the strongest pathological correlate of cognitive decline in Alzheimer's disease (AD) with increasing evidence implicating neuropathological tau protein in this process. Despite the knowledge that tau spreads through defined synaptic circuits, it is currently unknown whether synapse loss occurs before the accumulation of tau or as a consequence. To address this, we have used array tomography to examine an rTgTauEC mouse model expressing a P301L human tau transgene and a transgene labeling cytoplasm red (tdTomato) and presynaptic terminals green (Synaptophysin-EGFP). All transgenes are restricted primarily to the entorhinal cortex using the neuropsin promotor to drive tTA expression. It has previously been shown that rTgTauEC mice exhibit neuronal loss in the entorhinal cortex and synapse density loss in the middle molecular layer (MML) of the dentate gyrus at 24 months of age. Here, we observed the density of tau-expressing and total presynapses, and the spread of tau into the postsynapse in the MML of 3-6, 9, and 18 month old red-green-rTgTauEC mice. We observe no loss of synapse density in the MML up to 18 months even in axons expressing tau. Despite the maintenance of synapse density, we see spread of human tau from presynaptic terminals to postsynaptic compartments in the MML at very early ages, indicating that the spread of tau through neural circuits is not due to the degeneration of axon terminals and is an early feature of the disease process.
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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.