CHRONIC ALCOHOL-CONSUMPTION DOES NOT CAUSE HIPPOCAMPAL NEURON LOSS INHUMANS

Citation
Aj. Harding et al., CHRONIC ALCOHOL-CONSUMPTION DOES NOT CAUSE HIPPOCAMPAL NEURON LOSS INHUMANS, Hippocampus, 7(1), 1997, pp. 78-87
Citations number
53
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
10509631
Volume
7
Issue
1
Year of publication
1997
Pages
78 - 87
Database
ISI
SICI code
1050-9631(1997)7:1<78:CADNCH>2.0.ZU;2-A
Abstract
High alcohol consumption for long periods of time causes significant h ippocampal neurodegeneration in rodents. A single study using neuronal density measures has reported similar findings in humans. The present study aims to substantiate these findings in human alcoholics using u nbiased stereological techniques. Both amnesic (n = 5) and nonamnesic (n = 7) chronic alcoholics were selected and compared with nonalcoholi c controls (n = 8) and patients with marked memory loss and hippocampa l neurodegeneration caused by Alzheimer's disease (n = 4). Hippocampal volume was significantly reduced in the alcoholics and in patients wi th Alzheimer's disease. However, in alcoholics the volume reduction oc curred exclusively in the white matter, whereas both the gray and whit e matter were reduced in the patients with Alzheimer's disease. Neuron loss occurred exclusively from the CA1 and subiculum subregions of th e hippocampus in Alzheimer's disease. No neuron loss occurred from any subregion of the hippocampus in alcoholics. There were no correlation s with age and any of the volume or neuron number measures. Hippocampa l volume correlated with brain volume and with the regional gray and w hite matter volumes within the hippocampus. In addition, hippocampal g ray matter volume correlated with the number of CA1 pyramidal neurons. These results do not support the theory that chronic alcohol consumpt ion is neurotoxic to hippocampal pyramidal neurons in humans. Further, the present results suggest that changes observed in rodent models of alcoholism do not parallel those observed in humans, questioning the validity of such models. (C) 1997 Wiley-Liss, Inc.