title: Chronic alcoholics have substantial glial pathology in the forebrain and diencephalon.
abstract: We have analyzed glial changes in forebrain and diencephalic regions in 19 alcoholics with different histories of chronic alcohol consumption and related medical complications including Wernicke's encephalopathy and alcoholic liver disease. Cases with postmortem evidence of hepatic encephalopathy were excluded. Two of the alcoholic patients had ceased drinking for several years prior to death. Brains were obtained postmortem and fixed in formalin. Serial 50 microns sections of the forebrain and diencephalon at 750 microns intervals were stained with standard histochemical stains (haematoxylin and eosin, luxol fast blue, cresyl violet and silver), as well as immunohistochemically for glial fibrillary acidic protein (GFAP). In control tissue, GFAP-positive astrocytes were intimately associated with ependymal, pial, and vascular surfaces. In alcoholic cases, the morphology of these cells was markedly changed showing enlargement of the cell bodies and beading of the cellular processes. In contrast to controls, GFAP-positive astrocytes were seen within and surrounding clusters of magnocellular neurons in the basal forebrain and hypothalamus. In thiamine-deficient alcoholics, glial scarring in the vicinity of the large branches of the cerebral arteries disrupted the normal forebrain architecture. A patchy loss of GFAP immunostaining was seen in most severe cases. A remarkable number of corpora amylacea also rimmed blood vessels, pial and ependymal surfaces in all alcoholics compared to controls. The beaded fibers were seen in alcoholics drinking at the time of death as well as in those who had ceased drinking alcohol several years prior to death. These results indicate that chronic alcoholics have prominent glial changes which persist despite the cessation of alcohol consumption and are not exclusive to alcoholics with liver pathology.
authors.affiliation: Department of Pathology, University of Sydney, Australia.
authors.forename: K M
authors.initials: KM
authors.lastname: Cullen
authors.forename: G M
authors.initials: GM
authors.lastname: Halliday
mesh_terms: D000328:Adult; D000368:Aged; D000437:Alcoholism / Q000378:metabolism / Q000473:pathology*; D016022:Case-Control Studies; D004027:Diencephalon / Q000378:metabolism / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008108:Liver Diseases, Alcoholic / Q000378:metabolism / Q000473:pathology; D008875:Middle Aged; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology*; D016548:Prosencephalon / Q000378:metabolism / Q000473:pathology*; D013695:Temperance; D014899:Wernicke Encephalopathy / Q000378:metabolism / Q000473:pathology
chemical_list: D005904:Glial Fibrillary Acidic Protein