ArticleBiomedicines2024
Tau Protein and β-Amyloid Associated with Neurodegeneration in Myelin Oligodendrocyte Glycoprotein-Induced Experimental Autoimmune Encephalomyelitis (EAE), a Mouse Model of Multiple Sclerosis.
Article in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Baseline Findings from Dual-Phase Amyloid PET Study in Newly Diagnosed Multiple Sclerosis: Exploring Its Potential as a Biomarker of Myelination and Neurodegeneration.Journal of personalized medicine · 2025Article
- The IL-12 family cytokines in neurodegenerative diseases: dual roles in neurotoxicity and neuroprotection.Inflammopharmacology · 2025Review
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5 authors.
Funding
Abstract
backgroundThe levels of β-amyloid precursor protein (β-APP), tau protein, and phosphorylation of tau (p-tau) protein were examined by quantitative immunohistochemistry in the spinal cord sections of mice suffering from experimental autoimmune encephalomyelitis (EAE) in the successive phases of the disease: onset, peak, and chronic.
methodsEAE was induced in C57BL/6 mice by immunization with MOG35-55 peptide. The degree of pathological changes was assessed in cross-sections of the entire spinal cord.
resultsβ-APP expression was observed in the white matter and colocalized with some Iba-1-positive macrophages/microglia. It increased in the peak phase of EAE and remained at the same level in the chronic phase. During the onset and peak phases of EAE, expression of tau protein was observed in nerve fibers and nerve cell perikaryons, with a predominance of nerve fibers, whereas in the chronic phase, tau was labeled mainly in the perikaryons of nerve cells, with its content significantly decreased. P-tau immunostaining was seen only in nerve fibers.
conclusionsThe expression of p-tau increased with the progression of EAE, reaching the maximum in the chronic phase. The correlation between these proteins and neurodegeneration/neuroinflammation highlights their potential roles in the progression of neurodegenerative mechanisms in MS.
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