ArticleNeuroscience2019
Cre-inducible Adeno Associated Virus-mediated Expression of P301L Mutant Tau Causes Motor Deficits and Neuronal Degeneration in the Substantia Nigra.
Article in Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Microglial-Targeted nSMase2 Inhibitor Fails to Reduce Tau Propagation in PS19 Mice.Pharmaceutics · 2023Article
- Influence of Host Age on Intracranial AAV9 TauP301L Induced Tauopathy.Journal of Alzheimer's disease : JAD · 2023Article
- Wolframin-1-expressing neurons in the entorhinal cortex propagate tau to CA1 neurons and impair hippocampal memory in mice.Science translational medicine · 2021Article
- Sex-Related Motor Deficits in the Tau-P301L Mouse Model.Biomedicines · 2021Article
- Postganglionic sympathetic neurons, but not locus coeruleus optostimulation, activates neuromuscular transmission in the adult mouse in vivo.Molecular and cellular neurosciences · 2020Article
- Sowing the Seeds of Discovery: Tau-Propagation Models of Alzheimer's Disease.ACS chemical neuroscience · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Accumulation of microtubule associated protein tau in the substantia nigra is associated with several tauopathies including progressive supranuclear palsy (PSP). A number of studies have used mutant tau transgenic mouse model to mimic the neuropathology of tauopathies and disease phenotypes. However, tau expression in these transgenic mouse models is not specific to brain subregions, and may not recapitulate subcortical disease phenotypes of PSP. It is necessary to develop a new disease modeling system for cell and region-specific expression of pathogenic tau for modeling PSP in mouse brain. In this study, we developed a novel strategy to express P301L mutant tau to the dopaminergic neurons of substantia nigra by coupling tyrosine hydroxylase promoter Cre-driver mice with a Cre-inducible adeno-associated virus (iAAV). The results showed that P301L mutant tau was successfully transduced in the dopaminergic neurons of the substantia nigra at the presence of Cre recombinase and iAAV. Furthermore, the iAAV-tau-injected mice displayed severe motor deficits including impaired movement ability, motor balance, and motor coordination compared to the control groups over a short time-course. Immunochemical analysis revealed that tau gene transfer significantly resulted in loss of tyrosine hydroxylase-positive dopaminergic neurons and elevated phosphorylated tau in the substantia nigra. Our development of dopaminergic neuron-specific neurodegenerative mouse model with tauopathy will be helpful for studying the underlying mechanism of pathological protein propagation as well as development of new therapies.
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Registered trials
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