Neuronal loss in the hippocampus in Huntington's disease: a comparison with HIV infection.
نویسندگان
چکیده
The hippocampus is usually affected in primary dementias and the pathological changes may be severe. Knowledge of hippocampal pathology in HIV infection and Huntington's disease (HD), however, is extremely limited. A stereological technique (the optical "disector") has been used to assess neuronal populations in four areas of the hippocampus in 11 patients with HIV infection and in nine patients with HD. The HIV patients died without opportunistic infections or neoplasms affecting the brain; they had HIV encephalitis or minimal changes. The HD cases were all clinically diagnosed, had a positive family history and showed the characteristic lesions in the caudate nucleus. The neuronal counts were compared with those in nine controls. In the granule cell layer of the dentate, CA3 and CA4, there was no significant difference in the neuronal numerical density between the three groups. A striking difference between the HIV and HD groups was seen in the CA1 region. The neuronal numerical density in the CA1 area was significantly lower in the HD patients than in either the HIV patients or the controls (mean (SD) 37.5 (5.0); 70.1 (13.4); 57.9 (15.4) x 10(3) per mm3, p < 0.001 (Students' t test)). This difference represents a neuronal loss of 35%. In all four hippocampal areas the neuronal density was higher in the HIV group than in the controls but the differences were not significant and can be explained by the higher average age of the control group. These findings contribute to the understanding of the mechanism of dementia in both AIDS and in Huntington's disease.
منابع مشابه
The Lentiviral Vector Pseudotyped by Modified Rabies Glycoprotein Does Not Cause Reactive Gliosis and Neurodegeneration in Rat Hippocampus
Background: A human immunodeficiency virus type 1 (HIV-1)-based lentiviral vector (LV) pseudotyped by a variant of rabies envelope glycoprotein, FUG-B2, has previously been prepared and used in transfection of hippocampal CA1 ("Cornu Ammonis" area 1) neurons. This study aimed to verify reactive gliosis and neuronal damage after injection of the vector into the rat hippocampus. Methods: HEK 293T...
متن کاملNeuropathological Changes in Brain Cortex and Hippocampus in a Rat Model of Alzheimer’s Disease
Background: Alzheimer’s disease (AD) is a neurodegenerative disorder with progressive loss of cognitive abilities and memory loss. The aim of this study was to compare neuropathological changes in hippocampus and brain cortex in a rat model of AD. Methods: Adult male Albino Wistar rats (weighing 250-300 g) were used for behavioral and histopathological studies. The rats were randomly assigned t...
متن کاملIs Mitochondria Biogenesis and Neuronal Loss Prevention in Rat Hippocampus Promoted by Apigenin?
In this Correspondence, a comment to a recent paper by Nikbakht et al., published in the latest ssu of this Journal is reported. The flavone apigenin can exert both its anti-oxidant potetial via the usual enzymatic ROS scavenging system and the mitochondria biogenesis via the PGC-1α/ TFAM/NRF-1 pathway. The very interesting paper by Nikbakht et al, may earn more insighful clues about the activi...
متن کاملThe effect of hydroalcoholic extract of Ziziphora clinopodioides L. on spatial memory and neuronal density of hippocampal CA1 region in rats with sporadic Alzheimer's disease
Objective: Alzheimer's disease is a neurodegenerative disorder associated with gradual loss of cognitive and memory abilities. It was shown that the hippocampus is one of the first structures in the brain that is affected by the disease. Ziziphora clinopodioides<span style="font-size: mediu...
متن کاملBehavioral study of effects of mesenchymal stem cells transplant on motor deficits improvement in animal model of Huntington\'s disease
Introduction: As an inherited neurodegenerative disease, Huntington's disease is accompanied with wide neuronal degeneration in neostriatum and neocortex. Progress of the disease causes disabling clinical effects on movements, recognition and physiology of the body, and finally results in death. At this stage of knowledge we are, there is no effective therapeutic strategy for diminishing the mo...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Journal of neurology, neurosurgery, and psychiatry
دوره 56 5 شماره
صفحات -
تاریخ انتشار 1993