ArticleJournal of neuropathology and experimental neurology2020
Mechanisms of Cerebral Microbleeds.
Article in Journal of neuropathology and experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Newly identified cerebral microbleeds in patients on anticoagulation for secondary stroke prevention.Medicine · 2025Observational
- Erythrocyte-brain endothelial interactions induce microglial responses and cerebral microhemorrhages in vivo.Journal of neuroinflammation · 2023Article
- De novo appearance of cerebral microbleeds in community-dwelling older adults. Neuroimaging and clinical correlates.The neuroradiology journal · 2023Article
- Neuropathology of microbleeds in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).Journal of neuropathology and experimental neurology · 2023Article
- Chronic kidney disease promotes cerebral microhemorrhage formation.Journal of neuroinflammation · 2023Article
- Arteriolar neuropathology in cerebral microvascular disease.Neuropathology and applied neurobiology · 2023Review
- Correlation of lipoprotein-associated phospholipase A2 and cerebral microbleeds in patients with acute ischaemic stroke.BMC neurology · 2022Article
- Insights Into the Mechanisms of Brain Endothelial Erythrophagocytosis.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Cerebral microbleeds (CMB) are a common MRI finding, representing underlying cerebral microhemorrhages (CMH). The etiology of CMB and microhemorrhages is obscure. We conducted a pathological investigation of CMH, combining standard and immunohistological analyses of postmortem human brains. We analyzed 5 brain regions (middle frontal gyrus, occipital pole, rostral cingulate cortex, caudal cingulate cortex, and basal ganglia) of 76 brain bank subjects (mean age ± SE 90 ± 1.4 years). Prussian blue positivity, used as an index of CMH, was subjected to quantitative analysis for all 5 brain regions. Brains from the top and bottom quartiles (n = 19 each) were compared for quantitative immunohistological findings of smooth muscle actin, claudin-5, and fibrinogen, and for Sclerosis Index (SI) (a measure of arteriolar remodeling). Brains in the top quartile (i.e. with most extensive CMH) had significantly higher SI in the 5 brain regions combined (0.379 ± 0.007 vs 0.355 ± 0.008; p < 0.05). These findings indicate significant coexistence of arteriolar remodeling with CMH. While these findings provide clues to mechanisms of microhemorrhage development, further studies of experimental neuropathology are needed to determine causal relationships.
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