ArticleBrain communications2022
Tau propagation is dependent on the genetic background of mouse strains.
Article in Brain communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Pathological tau alters head direction signaling and induces spatial disorientation.Cell reports · 2025Article
- Analysis of Oral Microbiota in Elderly Thai Patients with Alzheimer's Disease and Mild Cognitive Impairment.International journal of environmental research and public health · 2024Article
- Aqueous extractable nonfibrillar and sarkosyl extractable fibrillar Alzheimer's disease tau seeds have distinct properties.Acta neuropathologica communications · 2024Article
- Inhibitory Roles ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Article
- Network analysis identifies strain-dependent response to tau and tau seeding-associated genes.The Journal of experimental medicine · 2023Article
- Rate of tau propagation is a heritable disease trait in genetically diverse mouse strains.iScience · 2023Article
- Neuropathology-Independent Association BetweenNeurology. Genetics · 2023Article
- Brain sciences and the R words.Brain communications · 2023Article
- Apolipoprotein E isoform does not influence trans-synaptic spread of tau pathology in a mouse model.Brain and neuroscience advancesArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Progressive cognitive decline in Alzheimer's disease correlates closely with the spread of tau protein aggregation across neural networks of the cortical mantle. We tested the hypothesis that heritable factors may influence the rate of propagation of tau pathology across brain regions in a model system, taking advantage of well-defined genetically diverse background strains in mice. We virally expressed human tau locally in the hippocampus and the entorhinal cortex neurons and monitored the cell-to-cell tau protein spread by immunolabelling. Interestingly, some strains showed more tau spreading than others while tau misfolding accumulated at the same rate in all tested mouse strains. Genetic factors may contribute to tau pathology progression across brain networks, which could help refine mechanisms underlying tau cell-to-cell transfer and accumulation, and potentially provide targets for understanding patient-to-patient variability in the rate of disease progression in Alzheimer's disease.
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Registered trials
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