title: Regressive changes of astroglia in white matter lesions in cerebrovascular disease and Alzheimer's disease patients.
abstract: The pathogenesis of white matter lesions, which are frequently found in ischemic cerebrovascular disease and Alzheimer's disease, remains unclear. Using light and electron microscopic immunohistochemistry for glial fibrillary acidic protein (GFAP) as a marker, the present study focused on the role of astroglia which show characteristic morphological alterations. Of 29 brains of patients with cerebrovascular disease and Alzheimer's disease, 4 brains showed extensive swelling and vacuolation of white matter astroglia with their processes disintegrated and beaded (termed clasmatodendrosis). No such cells were observed in 6 control patients. Clasmatodendritic astroglia were not intensely eosinophilic using hematoxylin and eosin staining and included large lipophilic granules in their perikarya. These astroglia were immunoreactive for serum proteins such as immunoglobulins, fibrinogen and complement C3, C1q and C3d, as well as for proteins which are known to increase in reactive astroglia, such as vimentin, alpha-B crystallin, apolipoprotein-E and laminin. Double labeling for GFAP and microglial cell markers indicated that these cells were of astroglial lineage. Immunoelectron microscopy for GFAP revealed that clasmatodendritic astroglia had condensed chromatin, lysosomes and large membrane-bound osmiophilic cytoplasmic inclusions, which corresponded to the lipophilic granules observed with light microscopy. These cytochemical features collectively suggest that clasmatodendritic astroglia incorporate edema fluid and phagocytose cellular debris, and eventually degenerate as a result of cerebral edema.
authors.affiliation: Department of Neurology, Faculty of Medicine, Kyoto University, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Tomimoto
authors.forename: I
authors.initials: I
authors.lastname: Akiguchi
authors.forename: H
authors.initials: H
authors.lastname: Wakita
authors.forename: T
authors.initials: T
authors.lastname: Suenaga
authors.forename: S
authors.initials: S
authors.lastname: Nakamura
authors.forename: J
authors.initials: J
authors.lastname: Kimura
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000503:physiopathology*; D001253:Astrocytes / Q000276:immunology / Q000378:metabolism* / Q000648:ultrastructure; D001798:Blood Proteins / Q000276:immunology; D001921:Brain / Q000473:pathology* / Q000503:physiopathology; D001927:Brain Diseases / Q000209:etiology; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology; D002561:Cerebrovascular Disorders / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D005904:Glial Fibrillary Acidic Protein; D006048:Gold Colloid, Radioactive; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008853:Microscopy; D016253:Microscopy, Immunoelectron; D008875:Middle Aged; D009457:Neuroglia / Q000378:metabolism; D014018:Tissue Distribution
chemical_list: D001798:Blood Proteins; D005904:Glial Fibrillary Acidic Protein; D006048:Gold Colloid, Radioactive