ArticleThe European journal of neuroscience2021
Human wildtype tau expression in cholinergic pedunculopontine tegmental neurons is sufficient to produce PSP-like behavioural deficits and neuropathology.
Article in The European journal of neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Spontaneous tauopathy with parkinsonism in an aged cynomolgus macaque.Frontiers in aging neuroscience · 2026Article
- Chronic Chemogenetic Activation of Astrocytes in the Murine Mesopontine Region Leads to Disturbances in Circadian Activity and Movement.International journal of molecular sciences · 2025Article
- Tau P301S Transgenic Mice Develop Gait and Eye Movement Impairments That Mimic Progressive Supranuclear Palsy.bioRxiv : the preprint server for biology · 2024Article
- Genetic basis of anatomical asymmetry and aberrant dynamic functional networks in Alzheimer's disease.Brain communications · 2024Article
- Toward an animal model of Progressive Supranuclear Palsy.Frontiers in neuroscience · 2024Review
- The Impact of Muscarinic Antagonism on Psychosis-Relevant Behaviors and Striatal [Biomedicines · 2023Article
- Why Therapeutic Trials Fail in Primary Tauopathies.Movement disorders : official journal of the Movement Disorder Society · 2023Article
- Dystonia-like behaviors and impaired sensory-motor integration following neurotoxic lesion of the pedunculopontine tegmental nucleus in mice.Frontiers in neurology · 2023Article
- Dystonia and the pedunculopontine nucleus: Current evidences and potential mechanisms.Frontiers in neurology · 2022Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Progressive Supranuclear Palsy (PSP) is the most common atypical parkinsonism and exhibits hallmark symptomology including motor function impairment and dysexecutive dementia. In contrast to Parkinson's disease, the underlying pathology displays aggregation of the protein tau, which is also seen in disorders such as Alzheimer's disease. Currently, there are no pharmacological treatments for PSP, and drug discovery efforts are hindered by the lack of an animal model specific to PSP. Based on previous results and clinical pathology, it was hypothesized that viral deposition of tau in cholinergic neurons within the hindbrain would produce a tauopathy along neural connections to produce PSP-like symptomology and pathology. By using a combination of ChAT-CRE rats and CRE-dependent AAV vectors, wildtype human tau (the PSP-relevant 1N4R isoform; hTau) was expressed in hindbrain cholinergic neurons. Compared to control subjects (GFP), rats with tau expression displayed deficits in a variety of behavioural paradigms: acoustic startle reflex, marble burying, horizontal ladder and hindlimb motor reflex. Postmortem, the hTau rats had significantly reduced number of cholinergic pedunculopontine tegmentum and dopaminergic substantia nigra neurons, as well as abnormal tau deposits. This preclinical model has multiple points of convergence with the clinical features of PSP, some of which distinguish between PSP and Parkinson's disease.
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