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Vascular cell components of the medullary arteries in Binswanger's disease brains: a morphometric and immunoelectron
J X Lin1, H Tomimoto, I Akiguchi
1Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
Background And Purpose:
It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger's disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique.
Methods:
A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin.
Results:
The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for collagen type I and type IV to the cross-sectional area was 2-fold higher in the BD patients than in the control patients, regardless of the vessel caliber (P<0.005). Although the ratio for smooth muscle actin in the BD brains was increased in arteries of <100 microm (P<0.0001), there was no corresponding increase in the arteries of >100 microm. However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by proliferated fibrils. The basal lamina appeared multilayered, and the endothelial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the BD brains.
Conclusions:
The proliferation of collagen fibrils in the media and adventitia of the blood vessels in BD brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sclerosis, smooth muscle cell proliferation in the terminal arterioles, and their morphological transformation in the proximal arteries may alter the shear rates and thus cause profound microcirculatory disturbances in BD brains.
Insights
Binswanger's disease (BD) involves fibrohyalinosis and collagen proliferation in medullary arteries, leading to white matter lesions. These vascular changes, including smooth muscle cell alterations, cause microcirculatory disturbances in BD brains.
Area of Science:
- Neuropathology
- Vascular Biology
- Neurodegenerative Diseases
Background:
- Binswanger's disease (BD) is characterized by white matter lesions.
- The role of fibrohyalinosis in medullary arteries and its impact on vascular cell components in BD remains unclear.
- Previous studies show inconsistent findings regarding pathological alterations in BD-affected vessels.
Purpose of the Study:
- To quantitatively examine vasculopathy in defined caliber medullary arteries in Binswanger's disease (BD) brains.
- To investigate the alterations in vascular cell components, including collagen and smooth muscle actin.
- To correlate vascular changes with white matter lesions in BD.
Main Methods:
- Quantitative immunohistochemistry and immunoelectron microscopy were used.
- Twenty brains (10 BD, 10 controls) were analyzed.
- Vascular cell components, collagen, and smooth muscle actin were quantified.
Main Results:
- Patients with BD showed marked white matter lesions and fibrohyalinosis of medullary arteries.
- Collagen type I and IV were significantly increased in BD arteries compared to controls.
- Smooth muscle actin increased in smaller arteries (<100 microm) in BD, with cellular hypertrophy and fibril proliferation observed ultrastructurally.
- Collagen also proliferated in the pericapillary space in BD brains.
Conclusions:
- Binswanger's disease (BD) exhibits widespread collagen fibril proliferation in blood vessels and pericapillary spaces.
- Smooth muscle cell proliferation and morphological changes in arterioles and arteries contribute to microcirculatory disturbances in BD.
- These vascular pathologies are strongly associated with white matter lesions observed in Binswanger's disease.
