Journal of Pathology and Translational Medicine

Original Articles

Association of Ubiquitin-Positive Neuritic Threads in the CA 2-3 Region of the Hippocampus with Cortical Lewy Bodies.: Ki Hwa Yang, Ki Seung Yang, Choong Gu Kang, Joo Ho Sung; Korean J Pathol. 1995;29(5):660-668.

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Abstract: Ubiquitin-positive neuritic threads (UNTS) in the hippocampal CA 2-3 region are reported to occur exclusively in association with so-called diffuse Lewy body disease (DLBD). hi order to assess the association between the occurrence of Lewy bodies (LBs) and that of the UNTs, an immunohistochemical study on the hippocampus including the parahippocampal gyrus with antiubiquitin antibody (Chemicon Co., California, U.S.A.) was perfon-ned in four groups of patient's brains. All brains were selected from the large pool of brains referred to the Neuropadiology Laboratory of the University of Minnesota for studies of Alzheimer's disease. Group 1 consisted of 34 cases (20 male and 14 female) with LBs widespread in the frontal and temporal cortex and the brain stem nuclei (basal nucleus, substantia nigra, locus ceruleus and dorsal vagal nucleus) associated with varying degrees of degeneration of the substantia nigra; 21 (11 male and 10 female) combined with and 13 (9 male and 4 female) without Alzheimer's disease (AD) pathology. Group 2 included 12 cases (9 male and 3 female) in which LBs were observed only in the brain stem nuclei; 7 with and 4 without AD pathology. Group 3 consisted of 30 cases (9 male and 21 female) without LBs but with AD pathology and degeneration of the substantia nigra. Group 4 included 23 cases (11 male and 12 female) with neither LBs nor AD pathology but with degeneration of the substantia nigra. Ages of the patients varied among the groups. In the 46 cases in the first two groups with LBs. The mean age in the 28 cases with AD pathology was 77.3+/-8.9 and in the 18 cases without AD pathology it was 71.6+/-8.8 (P<0.05). In the 53 cases in groups 3 and 4 without LBs, which served as the controls, the mean ages were 80.8+/-7.7 and 74.0+/-9.7 respectively. UNTs were encountered in all (100%) of 34 cases of group I with widespread LBs which met the histological criteria of DLBD regardless of combined AD pathology. In 12 cases of group 2 with LBs confined to the brain stem, UNTs occurred in 3 (25%), 1 with and 2 without AD pathology. hi the group 3 cases with only AD pathology, UNTs occurred in 4 (13%) of 30 cases, while no UNTs were encountered in the 23 cases of group 4 without AD pathology or LBs. In conclusion, UNTs in the hippocampal CA 2-3 region occur invariably but not exclusively in association with widespread LBs, frequently when LBs are confined to the brain stem, and infrequently with AD pathology. It seems, therefore, that the UNTs are closely related to LBs and increase in ftequency as LBs spread beyond the brain stem with time, but the pathogenesis of the UNTs is little understood.

Expression of c-fos, p53, Transforming Growth Factor-beta1 and Glial Fibrillary Acidic Protein in Hippocampus Following Transient Forebrain Ischemia in Mongolian Gerbil.: Jae Hwa Lee, Bang Hur; Korean J Pathol. 2001;35(1):60-70.

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Abstract PDF: BACKGROUND
Recent studies have shown that delayed neuronal death is closely associated with early gene (c-fos or c-jun)-related apoptosis in addition to hypoxia-induced energy deficiency in the hippocampus.
METHODS
To elucidate the role of c-fos, p53, TGF-1 and glial fibrillary acidic protein (GFAP) and their interactions, cellular expression with immunohistochemistry was examined during the time period of 10-minute hypoxia with variable reperfusion intervals in the mongolian gerbil hippocampus.
RESULTS
Hippocampal CA1 shows progressive and delayed neuronal damage beginning from the 24-hour reperfusion, while CA2-3 reveals non-progressive, eosinophilic inclusion body within the neuron throughout the time period. CA1 neurons show short-term expressions of c-fos prior to significant cellular damage. However, CA2-3 neurons show persistent expressions by 3-day reperfusion. In both CA1 and CA2-3, p53 is expressed for the short-term period of the early time points. However, its intensity and duration are much less in CA2-3 than in CA1. While TGF-1 is transiently expressed at 24-hour reperfusion in CA1, its expression in CA2-3 is persistent in late time points. Early expression of GFAP is observed in the pyramidal layer of CA1 prior to neuronal damage and progressively increased in the late time points.
CONCLUSION
These results suggest that c-fos and TGF-1 may play a role in neuronal viability in the early- and late time points. Astrocytes may also be responsible for the active protective mechanism to neuronal death, as well as reactive gliosis. The hypoxia-induced neuronal damage is, in part, a p53-dependent process in the CA1 neurons.

Expression of Tumor Necrosis Factor-alpha, Interleukin-1beta and Inducible Nitric Oxide Synthase after Stereotaxic Injection of Lipopolysaccharide in Rat Hippocampus.: Hoon Kyu Oh, Ku Seong Kang, Ji Yeon Kim, Eun Kyoung Kwak, Jung Wan Kim, Ji Young Park, Yoon Kyung Sohn; Korean J Pathol. 2004;38(3):157-164.

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Abstract PDF: BACKGROUND
Brain inducible nitric oxide synthase (iNOS) might be detectable in several pathologic conditions, and it is thought to play an important role in their pathophysiology. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta are believed to be essential factors of iNOS induction of the brain.
METHODS
After intrahippocampal stereotaxic injection of lipopoly-saccharide (LPS), the rat brains were removed at 6, 12 and 24 h. The rat brain tissues were examined to clarify the expression patterns of TNF-alpha, IL-1beta and iNOS.
RESULTS
The inflammatory cells which were stained with anti-TNF-alpha antibody, appeared in 6 h and increased for 24 h after LPS injection. The iNOS positive cells appeared after 12 h of LPS injection. A semiquantitative analysis of reverse transcription-polymerase chain reaction (RT-PCR) revealed that the TNF-alpha and IL-1beta mRNA arose at 1 h, peaked at 6 h and then declined until 48 h after LPS injection. The iNOS mRNA arose after 6 h, peaked at 12 h, and declined until 48 h after LPS injection.
CONCLUSIONS
We conclude that the induction of inflammatory events by intrahippocampal injection of LPS activates TNF-alpha and IL-1beta secretion, and this is followed by an induction of iNOS expression. TNF-alpha and IL-1beta seem to be related with iNOS expression in brain inflammation.

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