ArticleNeuropathology and applied neurobiology2024
Microglial activation without peripheral immune cell infiltration characterises mouse and human cerebral small vessel disease.
Article in Neuropathology and applied neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Roles of Microglia in Cerebral Small Vessel Disease.CNS neuroscience & therapeutics · 2026Review
- Restoring brain barriers: an innovative approach for treating neurological disorders.Fluids and barriers of the CNS · 2025Review
- Microglial activation without peripheral immune cell infiltration characterises mouse and human cerebral small vessel disease.Neuropathology and applied neurobiology · 2024Article
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9 authors.
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Abstract
aimsCerebral small vessel diseases (SVDs) involve diverse pathologies of the brain's small blood vessels, leading to cognitive deficits. Cerebral magnetic resonance imaging (MRI) reveals white matter hyperintensities (WMHs), lacunes, microbleeds and enlarged perivascular spaces in SVD patients. Although correlations of MRI and histopathology help to understand the pathogenesis of SVD, they do not explain disease progression. Mouse models, both genetic and sporadic, are valuable for studying SVD, but their resemblance to clinical SVD is unclear. The study examined similarities and differences between mouse models of SVDs and human nonamyloid SVD specimens.
methodsWe analysed four mouse models of SVD (hypertensive BPH mice, Col4a1 mutants, Notch3 mutants and Htra1
resultsOnly Notch3 mutant and hypertensive BPH mice showed significant changes in myelin basic protein (MBP) immunostaining, correlating with MRI patterns. These changes were linked to altered microglial morphology and focal plasma protein staining around blood vessels, without peripheral immune cell infiltration. In human specimens, both normal-appearing white matter (NAWM) and WMLs lacked peripheral cell infiltration. However, WMLs displayed altered microglial morphology, reduced myelin staining and occasional fibrinogen staining around arterioles and venules.
conclusionsOur data show that Notch3 mutants and hypertensive BPH/2J mice recapitulate several features of human SVD, including microglial activation, focal sites of demyelination and perivascular plasma protein leakage without peripheral immune cell infiltration.
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