Blood-brain barrier dysfunction in Binswanger's disease; An immunohistochemical study

Ichiro Akiguchi, Hidekazu Tomimoto, Toshihiko Suenaga, Hideaki Wakita, Herbert Budka

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Abstract

Binswanger's disease is pathologically characterized by a combination of diffuse cerebrovascular white matter lesions and lacunar infarcts in the basal ganglia and white matter. Although a blood-brain barrier (BBB) dysfunction has been implicated in the pathogenesis of these white matter (WM) lesions, few authors have addressed this problem. In the present study, we describe BBB dysfunction and its regional differences in the brains of Binswanger's disease patients. Twelve brains from Binswanger's disease patients (group III) were examined and compared with those from five patients with non-neurological disease (group I) and five cortical infarct patients without significant WM lesions (group II). Immunohistochemistry was performed for glial fibrillary acidic protein and vimentin as astroglial cell markers, and for immunoglobulins, complements and fibrinogen as extravasated serum protein markers. The grading scores for IgG extravasation were significantly higher in group III as compared to group I, in both the periventricular WM and the subcortical WM (P < 0.01). In group III, the scores in the periventricular WM and subcortical WM were significantly higher than in the subcortical U fibers and cerebral cortex (P < 0.01 for the periventricular WM; P < 0.001 for the subcortical WM), respectively. Clasmatodendritic astroglia, which had swollen cell bodies and large cytoplasmic vacuoles with disintegrated processes, incorporated the serum components IgG, IgM, C3d, C1q and fibrinogen, both in the periventricular WM and subcortical WM in 5 out of 12 (42%) Binswanger's disease brains. These results indicate that WM lesions in Binswanger's disease are accompanied by BBB dysfunction, although it remains uncertain whether BBB dysfunction is secondary to either chronic cerebral ischemia or arterial hypertension.

Original languageEnglish
Pages (from-to)78-84
Number of pages7
JournalActa Neuropathologica
Volume95
Issue number1
DOIs
Publication statusPublished - 27-02-1998

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Vascular Dementia
Blood-Brain Barrier
Brain Diseases
White Matter
Fibrinogen
Immunoglobulin G
Lacunar Stroke
Glial Fibrillary Acidic Protein
Vimentin
Vacuoles
Basal Ganglia
Brain Ischemia
Astrocytes
Cerebral Cortex
Immunoglobulin M
Immunoglobulins
Blood Proteins

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

Cite this

Akiguchi, Ichiro ; Tomimoto, Hidekazu ; Suenaga, Toshihiko ; Wakita, Hideaki ; Budka, Herbert. / Blood-brain barrier dysfunction in Binswanger's disease; An immunohistochemical study. In: Acta Neuropathologica. 1998 ; Vol. 95, No. 1. pp. 78-84.
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abstract = "Binswanger's disease is pathologically characterized by a combination of diffuse cerebrovascular white matter lesions and lacunar infarcts in the basal ganglia and white matter. Although a blood-brain barrier (BBB) dysfunction has been implicated in the pathogenesis of these white matter (WM) lesions, few authors have addressed this problem. In the present study, we describe BBB dysfunction and its regional differences in the brains of Binswanger's disease patients. Twelve brains from Binswanger's disease patients (group III) were examined and compared with those from five patients with non-neurological disease (group I) and five cortical infarct patients without significant WM lesions (group II). Immunohistochemistry was performed for glial fibrillary acidic protein and vimentin as astroglial cell markers, and for immunoglobulins, complements and fibrinogen as extravasated serum protein markers. The grading scores for IgG extravasation were significantly higher in group III as compared to group I, in both the periventricular WM and the subcortical WM (P < 0.01). In group III, the scores in the periventricular WM and subcortical WM were significantly higher than in the subcortical U fibers and cerebral cortex (P < 0.01 for the periventricular WM; P < 0.001 for the subcortical WM), respectively. Clasmatodendritic astroglia, which had swollen cell bodies and large cytoplasmic vacuoles with disintegrated processes, incorporated the serum components IgG, IgM, C3d, C1q and fibrinogen, both in the periventricular WM and subcortical WM in 5 out of 12 (42{\%}) Binswanger's disease brains. These results indicate that WM lesions in Binswanger's disease are accompanied by BBB dysfunction, although it remains uncertain whether BBB dysfunction is secondary to either chronic cerebral ischemia or arterial hypertension.",
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Blood-brain barrier dysfunction in Binswanger's disease; An immunohistochemical study. / Akiguchi, Ichiro; Tomimoto, Hidekazu; Suenaga, Toshihiko; Wakita, Hideaki; Budka, Herbert.

In: Acta Neuropathologica, Vol. 95, No. 1, 27.02.1998, p. 78-84.

Research output: Contribution to journalArticle

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