AIDS does not alter the total number of neurons in the hippocampal formation but induces cell atrophy: a stereological study

Citation
Mj. Sa et al., AIDS does not alter the total number of neurons in the hippocampal formation but induces cell atrophy: a stereological study, ACT NEUROP, 99(6), 2000, pp. 643-653
Citations number
51
Categorie Soggetti
Neurosciences & Behavoir
Journal title
ACTA NEUROPATHOLOGICA
ISSN journal
00016322 → ACNP
Volume
99
Issue
6
Year of publication
2000
Pages
643 - 653
Database
ISI
SICI code
0001-6322(200006)99:6<643:ADNATT>2.0.ZU;2-S
Abstract
Although cognitive dysfunction is a common finding in patients with acquire d immunodeficiency syndrome (AIDS) its pathogenesis remains controversial. Given the involvement of the hippocampal formation in the processing of cog nitive information and the scarcity of quantitative studies in this brain r egion, we have examined, using stereological methods, the hippocampal forma tions of AIDS patients. The study was performed in ten AIDS patients and te n age-matched controls. All cases were male. The Principle of Cavalieri was applied to estimate the volume of the layers of the dentate gyrus and of t he CA3 and CA1 hippocampal fields. The fractionator and the nucleator were used as estimators of the total number, and mean somatic and nuclear volume s of the neurons in the cell-containing layers of all hippocampal subdivisi ons. No cell death was detected in AIDS patients but the global volume of t heir hippocampal formations was significantly decreased due to the reduced volume of its layers, mainly the cell-containing layers. Furthermore, the s omatic and nuclear volumes of the neurons in the hippocampal formation were significantly decreased in AIDS patients. No correlation was found between the estimates obtained and the presence or absence of neurological involve ment. Our results show that neurons in the hippocampal formation of AIDS pa tients display marked morphological changes, despite the maintenance of the ir total number. These alterations are likely to lead to dysfunction of the hippocampal circuitries and, thus, might contribute to explaining the deme ntial features which occur in this condition.