REGRESSIVE CHANGES OF ASTROGLIA IN WHITE-MATTER LESIONS IN CEREBROVASCULAR-DISEASE AND ALZHEIMERS-DISEASE PATIENTS

The pathogenesis of white matter lesions, which are frequently found i n ischemic cerebrovascular disease and Alzheimer's disease, remains un clear. Using light and electron microscopic immunohistochemistry for g lial fibrillary acidic protein (GFAP) as a marker, the present study f ocused on the role of astroglia which show characteristic morphologica l alterations. Of 29 brains of patients with cerebrovascular disease r ind Alzheimer's disease, 4 brains showed extensive swelling and vacuol ation of white matter astroglia with their processes disintegrated and beaded (termed clasmatodendrosis). No such cells were observed in 6 c ontrol patients. Clasmatodendritic astroglia were nor intensely eosino philic using hematoxylin and eosin staining and included large lipophi lic granules in their perikarya. These astroglia were immunoreactive f or serum proteins such as immunoglobulins, fibrinogen and complement C 3, Clq and C3d, as well as or proteins which rue known to increase in reactive astroglia, such as vimentin, alpha-B crystallin, apolipoprote in-E and laminin. Double labeling for GFAP anti microglial cell marker s indicated that these cells were of astroglial lineage. Immunoelectro n microscopy for GFAP revealed that clasmatodendritic astroglia had co ndensed chromatin, lysosomes and large membrane-bound osmiophilic cyto plasmic inclusions, which corresponded to the lipophilic granules obse rved with light microscopy. These cytochemical features collectively s uggest that clasmatodendritic astroglia incorporate edema fluid and ph agocytose cellular debris, and eventually degenerate as a result of ce rebral edema.