ArticleBrain structure & function2016
Transgene expression in the Nop-tTA driver line is not inherently restricted to the entorhinal cortex.
Article in Brain structure & function, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- A mouse model of early sporadic tau pathology induces neurogenic plasticity in the hippocampus.PloS one · 2025Article
- Potential Mechanisms of Tunneling Nanotube Formation and Their Role in Pathology Spread in Alzheimer's Disease and Other Proteinopathies.International journal of molecular sciences · 2024Review
- Spreading of Tau Protein Does Not Depend on Aggregation Propensity.Journal of molecular neuroscience : MN · 2023Article
- Article
- Targeting tau only extracellularly is likely to be less efficacious than targeting it both intra- and extracellularly.Seminars in cell & developmental biology · 2022Review
- Does proteopathic tau propagate trans-synaptically in the brain?Molecular neurodegeneration · 2022Article
- Bridging Scales in Alzheimer's Disease: Biological Framework for Brain Simulation With The Virtual Brain.Frontiers in neuroinformatics · 2021Review
- Protein transmission in neurodegenerative disease.Nature reviews. Neurology · 2020Review
- From the prion-like propagation hypothesis to therapeutic strategies of anti-tau immunotherapy.Acta neuropathologica · 2020Review
- Brain-wide distribution of reporter expression in five transgenic tetracycline-transactivator mouse lines.Scientific data · 2019Article
- Propagation and spread of pathogenic protein assemblies in neurodegenerative diseases.Nature neuroscience · 2018Review
- Patterns of Invasive Growth in Malignant Gliomas-The Hippocampus Emerges as an Invasion-Spared Brain Region.Neoplasia (New York, N.Y.) · 2018Article
- Prion-like Spreading in Tauopathies.Biological psychiatry · 2018Review
- Prion-like mechanisms in Alzheimer disease.Handbook of clinical neurology · 2018Review
- What is the evidence that tau pathology spreads through prion-like propagation?Acta neuropathologica communications · 2017Review
- Trans-Synaptic Spread of Amyloid-Neural plasticity · 2017Review
- Impaired Recall of Positional Memory following Chemogenetic Disruption of Place Field Stability.Cell reports · 2016Article
- A critical appraisal of the pathogenic protein spread hypothesis of neurodegeneration.Nature reviews. Neuroscience · 2016Review
- A local insult of okadaic acid in wild-type mice induces tau phosphorylation and protein aggregation in anatomically distinct brain regions.Acta neuropathologica communications · 2016Article
- Prions and Protein Assemblies that Convey Biological Information in Health and Disease.Neuron · 2016Review
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5 authors.
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Abstract
The entorhinal cortex (EC) plays a central role in episodic memory and is among the earliest sites of neurodegeneration and neurofibrillary tangle formation in Alzheimer's disease. Given its importance in memory and dementia, the ability to selectively modulate gene expression or neuronal function in the EC is of widespread interest. To this end, several recent studies have taken advantage of a transgenic line in which the tetracycline transactivator (tTA) was placed under control of the neuropsin (Nop) promoter to limit transgene expression within the medial EC and pre-/parasubiculum. Although the utility of this driver is contingent on its spatial specificity, no detailed neuroanatomical analysis of its expression has yet been conducted. We therefore undertook a systematic analysis of Nop-tTA expression using a lacZ reporter and have made the complete set of histological sections available through the Rodent Brain Workbench tTA atlas, www.rbwb.org . Our findings confirm that the highest density of tTA expression is found in the EC and pre-/parasubiculum, but also reveal considerable expression in several other cortical areas. Promiscuous transgene expression may account for the appearance of pathological protein aggregates outside of the EC in mouse models of Alzheimer's disease using this driver, as we find considerable overlap between sites of delayed amyloid deposition and regions with sparse β-galactosidase reporter labeling. While different tet-responsive lines can display individual expression characteristics, our results suggest caution when designing experiments that depend on precise localization of gene products controlled by the Nop-tTA or other spatially restrictive transgenic drivers.
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