ArticleFrontiers in aging2026
Increased neurotoxic gliosis and blood-brain barrier dysregulation in canine cognitive dysfunction syndrome (CCD).
Article in Frontiers in aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: As Alzheimer's Disease (AD) and related dementias (ADRD) prevalence is projected to double by 2050, the urgency for relevant models to study its pathology intensifies. Aging is the primary risk factor for AD development and influenced by a myriad of factors including neurotoxic glial activation and BBB degradation; however, historically AD models consist of transgenic mouse Methods/Results: We utilized immunohistochemistry (IHC), morphological analyses, and immunofluorescence to investigate CCD pathology comparing CCD negative and CCD positive dogs. In this study we see glial morphology consistent with those seen in neurotoxic glia in neurodegenerative disease, increased S100β/C3 astrocyte activation, decreased claudin-5 expression, and region-dependent perivascular AQP4 expression modulation in dogs with CCD, compared to those without CCD. Conclusion: Our results further characterize glial and BBB roles in CCD pathogenesis and reinforces the strengths of modeling AD/ADRD in aging dogs.
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