ArticleAging cell2017
Accelerated aging exacerbates a pre-existing pathology in a tau transgenic mouse model.
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Understanding Tau pathology: Insights from animal models.Zoological research · 2025Review
- Autophagy and Cellular Senescence in Alzheimer's Disease: Key Drivers of Neurodegeneration.CNS neuroscience & therapeutics · 2025Review
- Non-Drug and Non-Invasive Therapeutic Options in Alzheimer's Disease.Biomedicines · 2025Review
- Immunoproteasome deficiency results in age-dependent development of epilepsy.Brain communications · 2024Article
- Long term high fat diet induces metabolic disorders and aggravates behavioral disorders and cognitive deficits in MAPT P301L transgenic mice.Metabolic brain disease · 2022Article
- Neuropathological and behavioral features of an APP/PS1/MAPT (6xTg) transgenic model of Alzheimer's disease.Molecular brain · 2022Article
- An early proinflammatory transcriptional response to tau pathology is age-specific and foreshadows reduced tau burden.Brain pathology (Zurich, Switzerland) · 2022Article
- Aging, Cellular Senescence, and Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Sex-Related Motor Deficits in the Tau-P301L Mouse Model.Biomedicines · 2021Article
- Altered ribosomal function and protein synthesis caused by tau.Acta neuropathologica communications · 2021Article
- Diffusion Tensor Imaging Detects Acute Pathology-Specific Changes in the P301L Tauopathy Mouse Model Following Traumatic Brain Injury.Frontiers in neuroscience · 2021Article
- Differential compartmental processing and phosphorylation of pathogenic human tau and native mouse tau in the line 66 model of frontotemporal dementia.The Journal of biological chemistry · 2020Article
- Synergy between amyloid-β and tau in Alzheimer's disease.Nature neuroscience · 2020Review
- Article
- Decreased synthesis of ribosomal proteins in tauopathy revealed by non-canonical amino acid labelling.The EMBO journal · 2019Article
- Rodent models for Alzheimer disease.Nature reviews. Neuroscience · 2018Review
- The ProNGF/p75NTR pathway induces tau pathology and is a therapeutic target for FTLD-tau.Molecular psychiatry · 2018Article
- Amyloid-β and tau complexity - towards improved biomarkers and targeted therapies.Nature reviews. Neurology · 2018Review
Corrections and comments
- Erratum issuedCorrigendum.2018
Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age is a critical factor in the prevalence of tauopathies, including Alzheimer's disease. To observe how an aging phenotype interacts with and affects the pathological intracellular accumulation of hyperphosphorylated tau, the tauopathy mouse model pR5 (expressing P301L mutant human tau) was back-crossed more than ten times onto a senescence-accelerated SAMP8 background to establish the new strain, SApT. Unlike SAMP8 mice, pR5 mice are characterized by a robust tau pathology particularly in the amygdala and hippocampus. Analysis of age-matched SApT mice revealed that pathological tau phosphorylation was increased in these brain regions compared to those in the parental pR5 strain. Moreover, as revealed by immunohistochemistry, phosphorylation of critical tau phospho-epitopes (P-Ser202/P-Ser205 and P-Ser235) was significantly increased in the amygdala of SApT mice in an age-dependent manner, suggesting an age-associated effect of tau phosphorylation. Anxiety tests revealed that the older cohort of SApT mice (10 months vs. 8 months) exhibited a behavioural pattern similar to that observed for age-matched tau transgenic pR5 mice and not the SAMP8 parental mice. Learning and memory, however, appeared to be governed by the accelerated aging background of the SAMP8 strain, as at both ages investigated, SAMP8 and SApT mice showed a decreased learning capacity compared to pR5 mice. We therefore conclude that accelerated aging exacerbates pathological tau phosphorylation, leading to changes in normal behaviour. These findings further suggest that SApT mice may be a useful novel model in which to study the role of a complex geriatric phenotype in tauopathy.
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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.