ArticleJournal of neuroinflammation2010
Genetic background modifies neurodegeneration and neuroinflammation driven by misfolded human tau protein in rat model of tauopathy: implication for immunomodulatory approach to Alzheimer's disease.
Article in Journal of neuroinflammation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Current updates on latest basic research of scientific relevance in hypertensive dementia.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- Myeloid antigen-presenting cells in neurodegenerative diseases: a focus on classical and non-classical MHC molecules.Frontiers in neuroscience · 2024Review
- Association of modified dementia risk score with cerebrospinal fluid biomarkers and cognition in adults without dementia.Frontiers in aging neuroscience · 2024Article
- Rate of tau propagation is a heritable disease trait in genetically diverse mouse strains.iScience · 2023Article
- sTREM2 is associated with amyloid-related p-tau increases and glucose hypermetabolism in Alzheimer's disease.EMBO molecular medicine · 2023Article
- Plasma Leptin Reflects Progression of Neurofibrillary Pathology in Animal Model of Tauopathy.Cellular and molecular neurobiology · 2022Article
- Tau Protein and Its Role in Blood-Brain Barrier Dysfunction.Frontiers in molecular neuroscience · 2020Review
- Intersection of pathological tau and microglia at the synapse.Acta neuropathologica communications · 2019Review
- Article
- Genetic Background Influences the Propagation of Tau Pathology in Transgenic Rodent Models of Tauopathy.Frontiers in aging neuroscience · 2019Article
- Distinct Microglial Responses in Two Transgenic Murine Models of TAU Pathology.Frontiers in cellular neuroscience · 2018Article
- Stress-Induced Alterations of Immune Profile in Animals Suffering by Tau Protein-Driven Neurodegeneration.Cellular and molecular neurobiology · 2018Article
- Ten Years of Tau-Targeted Immunotherapy: The Path Walked and the Roads Ahead.Frontiers in neuroscience · 2018Review
- Metabolic status of CSF distinguishes rats with tauopathy from controls.Alzheimer's research & therapy · 2017Article
- Long-term trihexyphenidyl exposure alters neuroimmune response and inflammation in aging rat: relevance to age and Alzheimer's disease.Journal of neuroinflammation · 2016Article
- Characterization of neuropathology in the HIV-1 transgenic rat at different ages.Journal of neuroimmunology · 2016Article
- Tauopathy in transgenic (SHR72) rats impairs function of central noradrenergic system and promotes neuroinflammation.Journal of neuroinflammation · 2016Article
- Article
- Microglia display modest phagocytic capacity for extracellular tau oligomers.Journal of neuroinflammation · 2014Article
- Modeling Alzheimer's disease in transgenic rats.Molecular neurodegeneration · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNumerous epidemiological studies demonstrate that genetic background modifies the onset and the progression of Alzheimer's disease and related neurodegenerative disorders. The efficacious influence of genetic background on the disease pathway of amyloid beta has been meticulously described in rodent models. Since the impact of genetic modifiers on the neurodegenerative and neuroinflammatory cascade induced by misfolded tau protein is yet to be elucidated, we have addressed the issue by using transgenic lines expressing the same human truncated tau protein in either spontaneously hypertensive rat (SHR) or Wistar-Kyoto (WKY) genetic background.
methodsBrains of WKY and SHR transgenic rats in the terminal stage of phenotype and their age-matched non-transgenic littermates were examined by means of immunohistochemistry and unbiased stereology. Basic measures of tau-induced neurodegeneration (load of neurofibrillary tangles) and neuroinflammation (number of Iba1-positive microglia, their activated morphology, and numbers of microglia immunoreactive for MHCII and astrocytes immunoreactive for GFAP) were quantified with an optical fractionator in brain areas affected by neurofibrillary pathology (pons, medulla oblongata). The stereological data were evaluated using two-way ANOVA and Student's t-test.
resultsTau neurodegeneration (neurofibrillary tangles (NFTs), axonopathy) and neuroinflammation (microgliosis, astrocytosis) appeared in both WKY and SHR transgenic rats. Although identical levels of transgene expression in both lines were present, terminally-staged WKY transgenic rats displayed significantly lower final NFT loads than their SHR transgenic counterparts. Interestingly, microglial responses showed a striking difference between transgenic lines. Only 1.6% of microglia in SHR transgenic rats expressed MHCII in spite of having a robust phagocytic phenotype, whereas in WKY transgenic rats, 23.2% of microglia expressed MHCII despite displaying a considerably lower extent of transformation into phagocytic phenotype.
conclusionsThese results show that the immune response represents a pivotal and genetically variable modifying factor that is able to influence vulnerability to neurodegeneration. Therefore, targeted immunomodulation could represent a prospective therapeutic approach to Alzheimer's disease.
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