title: Topographical and cytopathological lesion analysis of the white matter in Binswanger's disease brains.
abstract: The purpose of the present study was to document the topographical and cytopathological lesions in the white matter (WM) of Binswanger's disease (BD) brains. Subcortical WM lesions in each lobe and fiber bundle lesions related to the medial thalamic and hippocampal structures in clinicopathologically proven BD brains were evaluated by Klüver-Barrera staining using a grading score. Lesions in the frontal subcortical WM of BD brains, brains from non-neurological patients, and brains with cerebral hemorrhage or large cortical infarcts were also examined immunohistochemically using molecular markers for axonal flow damage: amyloid precursor protein (APP); and for demyelinating axonopathy: encephalitogenic peptide (EP). Our results indicated that the WM lesions in BD were significantly more prominent in the frontal periventricular and subcortical regions as compared with other subcortical WM lesions, in the order of the parietal, occipital and temporal lobes. Fiber bundle lesions in the capsular genu, including the anterior thalamic peduncle, were also significantly more prominent in BD brains as compared with the other bundle lesions. Furthermore, the frequency of damaged nerve fibers labeled by the EP antiserum and APP immunoreactive fibers was significantly higher in BD brains as compared with the control brains. The grading scores for the WM damage correlated significantly with those for the APP and EP immunoreactive fibers in all brains, including the control brains. The axonal damage in the frontal WM lesions of the BD brains was clearly revealed in our study using immunohistochemistry for APP and EP.
authors.affiliation: Department of Neurology, Faculty of Medicine, Kyoto University, Japan. akiguchi@kuhp.kyoto-u.ac.jp
authors.forename: Ichiro
authors.initials: I
authors.lastname: Akiguchi
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Tomimoto
authors.forename: Hideaki
authors.initials: H
authors.lastname: Wakita
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Kawamoto
authors.forename: Akinori
authors.initials: A
authors.lastname: Matsuo
authors.forename: Katsunori
authors.initials: K
authors.lastname: Ohnishi
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Watanabe
authors.forename: Herbert
authors.initials: H
authors.lastname: Budka
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D015140:Dementia, Vascular / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D008875:Middle Aged; D004676:Myelin Basic Protein / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism
chemical_list: D016564:Amyloid beta-Protein Precursor; D004676:Myelin Basic Protein; D010446:Peptide Fragments; C110235:myelin basic protein 68-86