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H Haug

Publications and source records attributed to H Haug.

At least 37 records · Page 2Linked to original sources
PubMed1993

Neuronal damage in the cerebral cortex of AIDS brains: a morphometric study.

Using stereological methods, two cerebral cortical areas from AIDS brains were investigated. Neuronal density, profile area of neurons, and perikaryon volume fraction were measured and compared to age-matched control brains. In the fronto-orbital cortex (area 11) of AIDS brains, a significant loss of neurons was seen. The perikaryon volume fraction was likewise decreased. The size of neurons did not differ between control and AIDS brains. In patients with clinical signs of progressive dementia and in brains with human immunodeficiency virus (HIV)-specific neuropathology (HIV-leukoencephalopathy and/or HIV-encephalitis) as compared to patients lacking these features, a small decrease in neuronal density was noted but this difference did not reach the level of statistical significance (P = 0.16). In the superior parietal lobule (area 7) of AIDS brains, no loss of nerve cells was noted. AIDS patients with progressive dementia and brains with HIV-specific neuropathology showed no difference in neuronal densities as compared to those without such features. We conclude that the fronto-orbital cortex, in contrast to the parietal cortex, is mainly damaged in AIDS brains. Neuronal loss was not significantly correlated with development of dementing symptoms and of HIV-specific neuropathology.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Astroglial changes in the cerebral cortex of AIDS brains: a morphometric and immunohistochemical investigation.

Astroglial changes in the cerebral cortex of AIDS brains were analysed by means of morphometry. Astrocytes with and without immunoreactivity for glial acidic protein (GFAP) were counted and their size was measured. In the two investigated cortical areas (frontal and parietal), a similar reaction pattern of astroglia was observed. The total number of astrocytes (i.e. GFAP-positive and GFAP-negative astrocytes) did not differ between control and AIDS brains. However, the number of GFAP-positive astrocytes was significantly increased in AIDS brains, while the number of GFAP-negative cells was significantly reduced. Nuclear size of GFAP-negative and GFAP-positive astrocytes was significantly increased. The reaction pattern of cortical astrocytes in AIDS seems to be characterized by GFAP production in protoplasmic astroglia as well as by hypertrophy of all astrocytes.

AIDS Dementia Complex↗
PubMed1992

[The effect of cyclooxygenase inhibitors on the course of hereditary retinal dystrophy in RCS rats].

Daily administration of acetyl salicylic acid (ASA) and ibuprofen leads to an appreciable retardation in the process of retinal degeneration in the RCS rat which is dependent on the dosage given. The photoreceptor cell nuclei and inner segments are relatively well preserved in all regions of the retina. While the outer nuclear layer of 32 day old RCS rats is usually composed of only 3-4 rows, we found 8-9 nuclear rows exhibiting minimal pyknotic change in animals which had been treated with higher doses of ASA. These differences in layer thickness could be confirmed using morphometric analysis. The outer segments show evidence of degenerative change although they are in a clearly better condition than those found in untreated animals and in those animals treated at lower dose. Phagolysosomal structures which are not otherwise apparent in this strain of rat are detected only in the RPE cells of animals treated with higher dose. The animals treated with ibuprofen show essentially the same morphological changes although a corresponding effect in regard to the thickness of the outer nuclear layer was only achieved after a high dose. The determined dose for the optimal preservation (thickness) of the outer nuclear layer lies around 160 mg/kg body weight for acetyl salicylic acid and at 400 mg/kg body weight for ibuprofen.

Animals↗
PubMed1991

Prominent cortical atrophy with neuronal loss as correlate of human immunodeficiency virus encephalopathy.

A 25-year-old homosexual AIDS patient presented with progressive cognitive, motor and behavioral disturbances consistent with HIV encephalopathy. CT scans demonstrated progressive diffuse brain atrophy. Neuropathology showed predominant cortical changes including severe neuronal loss corroborated by morphometry. Only minimal changes were found in the white matter and basal ganglia. Immunocytochemistry for HIV stained occasional microglial cells more markedly in the cerebral cortex. This suggests that HIV infection of the brain may cause predominant cortical nerve cell loss, and that HIV encephalopathy is not necessarily due to white matter lesions.

AIDS Dementia Complex↗
PubMed1990

Loss of neurons in the frontal cortex in AIDS brains.

Neurons of Area 11 in the fronto-orbital cortex of 18 unselected AIDS brains are analyzed by means of stereology. Neurological abnormalities including dementing symptoms were described in eight patients. Neuropathology diagnosed human immunodeficiency virus (HIV)-specific changes in four, and diffuse poliodystrophy in eight brains. The majority (71.4%) of these brains was immunoreactive for HIV antigens when tested by immunocytochemistry. A significant loss of neurons is found as compared to normal controls. Neuronal density in AIDS brains is reduced by 18%, and the perikaryon volume fractions is reduced by 31%. Although only speculation on pathogenesis of this neuronal loss is possible at present, it may represent a part of the pathomorphological substrate of AIDS-related dementia. Moreover, it confirms by quantitative means damage to the cerebral cortex in AIDS which has been described only qualitatively as diffuse poliodystrophy.

Acquired Immunodeficiency Syndrome↗