ArticleActa neuropathologica communications2016
Age-dependent neuroinflammation and cognitive decline in a novel Ala152Thr-Tau transgenic mouse model of PSP and AD.
Article in Acta neuropathologica communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27 citing papers in PubMed, 40 citations in OpenAlex.
- Understanding Tau pathology: Insights from animal models.Zoological research · 2025Review
- Limitations and Applications of Rodent Models in Tauopathy and Synucleinopathy Research.Journal of neurochemistry · 2025Review
- Preclinical insights into gamma-tACS: foundations for clinical translation in neurodegenerative diseases.Frontiers in neuroscience · 2025Review
- Profiling the impact of different tau species on glial cell biology.Frontiers in cell and developmental biology · 2025Article
- Effects of Red ginseng on neuroinflammation in neurodegenerative diseases.Journal of ginseng research · 2024Review
- Toward an animal model of Progressive Supranuclear Palsy.Frontiers in neuroscience · 2024Review
- Critical thinking of Alzheimer's transgenic mouse model: current research and future perspective.Science China. Life sciences · 2023Review
- Dementia-related genetic variants in an Italian population of early-onset Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Current and Near-Future Treatment of Alzheimer's Disease.Current neuropharmacology · 2022Article
- Nicotinamide phosphoribosyltransferase inhibitor ameliorates mouse aging-induced cognitive impairment.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- High-content image-based analysis and proteomic profiling identifies Tau phosphorylation inhibitors in a human iPSC-derived glutamatergic neuronal model of tauopathy.Scientific reports · 2021Article
- Inhibition of Tau aggregation with BSc3094 reduces Tau and decreases cognitive deficits in rTg4510 mice.Alzheimer's & dementia (New York, N. Y.) · 2021Article
- Learning from amyloid trials in Alzheimer's disease. A virtual patient analysis using a quantitative systems pharmacology approach.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020Article
- Tau-Mediated Dysregulation of Neuroplasticity and Glial Plasticity.Frontiers in molecular neuroscience · 2020Article
- Passive immunotherapy for N-truncated tau ameliorates the cognitive deficits in two mouse Alzheimer's disease models.Brain communications · 2020Article
- Next Generation Precision Medicine: CRISPR-mediated Genome Editing for the Treatment of Neurodegenerative Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Review
- rAAV-based brain slice culture models of Alzheimer's and Parkinson's disease inclusion pathologies.The Journal of experimental medicine · 2019Article
- Loss of C/EBPδ Exacerbates Radiation-Induced Cognitive Decline in Aged Mice due to Impaired Oxidative Stress Response.International journal of molecular sciences · 2019Article
- Enhanced phosphorylation of T153 in soluble tau is a defining biochemical feature of the A152T tau risk variant.Acta neuropathologica communications · 2019Article
- Extracellular Vesicles Isolated from Familial Alzheimer's Disease Neuronal Cultures Induce Aberrant Tau Phosphorylation in the Wild-Type Mouse Brain.Journal of Alzheimer's disease : JAD · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionMutations of Tau are associated with several neurodegenerative disorders. Recently, the Tau mutation A152T was described as a novel risk factor for frontotemporal dementia spectrum disorders and Alzheimer disease. In vitro Tau-A152T shows a decreased binding to microtubules and a reduced tendency to form abnormal fibers.
resultsTo study the effects of this mutation we generated a mouse model expressing human full-length Tau with this mutation (hTau40(AT)). At young age (2-3 months) immunohistological analysis reveals pathological Tau conformation and Tau-hyperphosphorylation combined with Tau missorting into the somatodendritic compartment of neurons. With increasing age there is Tau aggregation including co-aggregates of endogenous mouse Tau and exogenous human Tau, accompanied by loss of synapses (especially presynaptic failure) and neurons. From ~10 months onwards the mice show a prominent neuroinflammatory response as judged by activation of microglia and astrocytes. This progressive neuroinflammation becomes visible by in vivo bioluminescence imaging after crossbreeding of hTau40(AT) mice and Gfap-luciferase reporter mice. In contrast to other Tau-transgenic models and Alzheimer disease patients with reduced protein clearance, hTau40(AT) mice show a strong induction of autophagy. Although Tau-hyperphosphorylation and aggregation is also present in spinal cord and motor cortex (due to the Thy1.2 promoter), neuromotor performance is not affected. Deficits in spatial reference memory are manifest at ~16 months and are accompanied by neuronal death.
conclusionsThe hTau40(AT) mice mimic pathological hallmarks of tauopathies including a cognitive phenotype combined with pronounced neuroinflammation visible by bioluminescence. Thus the mice are suitable for mechanistic studies of Tau induced toxicity and in vivo validation of neuroprotective compounds.
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