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Glial involvement in diffuse Lewy body disease.
Acta Neuropathol. 2003 Feb; 105(2):163-9.AN

Abstract

Diffuse Lewy body disease (DLBD) is characterized by the presence of Lewy bodies (LB) in the neurons and neurites of cortical, subcortical, and brain stem structures. Recently, alpha-synuclein (alphaS) has been found to be a central constituent of LB. In DLBD, abnormal accumulation of alphaS has been reported in both neurons and glia, but studies on glial lesions in DLBD have been limited. We examined in detail the constituents and distribution of glial lesions in eight patients with DLBD and report the pathogenesis of the glial lesions. alphaS-positive neuronal cytoplasmic inclusions (NI), neuropil threads (NT), and coiled bodies (CB) showed similar immunostaining profiles. Without pretreatment, NI, NT, and CB were detected by all antibodies against alphaS. The immunostaining profile of star-like astrocytes (SLA) was quite different from those of NI, NT, and CB. A few SLA were stained by an antibody against the non-Abeta component portion of alphaS without pretreatment, but formic acid pretreatment dramatically enhanced SLA immunoreactivity. SLA and CB were found in all eight brains with DLBD. SLA were scarce in the brain stem, but there were hundreds of SLA per visual field at x100 magnification in the temporal cortex of most cases, while CB were found diffusely in both the cerebral cortex and brain stem, similar to NI. This suggests that the pathogenesis of SLA is different from those of NI and CB.

Authors+Show Affiliations

Department of Neuropsychiatry, Okayama Graduate School of Medicine and Dentistry, Okayama University, 2-5-1 Shikata-cho, Japan. terada_1@cc.okayama-u.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12536227

Citation

Terada, Seishi, et al. "Glial Involvement in Diffuse Lewy Body Disease." Acta Neuropathologica, vol. 105, no. 2, 2003, pp. 163-9.
Terada S, Ishizu H, Yokota O, et al. Glial involvement in diffuse Lewy body disease. Acta Neuropathol. 2003;105(2):163-9.
Terada, S., Ishizu, H., Yokota, O., Tsuchiya, K., Nakashima, H., Ishihara, T., Fujita, D., Uéda, K., Ikeda, K., & Kuroda, S. (2003). Glial involvement in diffuse Lewy body disease. Acta Neuropathologica, 105(2), 163-9.
Terada S, et al. Glial Involvement in Diffuse Lewy Body Disease. Acta Neuropathol. 2003;105(2):163-9. PubMed PMID: 12536227.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Glial involvement in diffuse Lewy body disease. AU - Terada,Seishi, AU - Ishizu,Hideki, AU - Yokota,Osamu, AU - Tsuchiya,Kuniaki, AU - Nakashima,Hanae, AU - Ishihara,Takeshi, AU - Fujita,Daisuke, AU - Uéda,Kenji, AU - Ikeda,Kenji, AU - Kuroda,Shigetoshi, Y1 - 2002/10/25/ PY - 2002/06/04/received PY - 2002/08/25/revised PY - 2002/08/26/accepted PY - 2003/1/22/pubmed PY - 2003/4/24/medline PY - 2003/1/22/entrez SP - 163 EP - 9 JF - Acta neuropathologica JO - Acta Neuropathol VL - 105 IS - 2 N2 - Diffuse Lewy body disease (DLBD) is characterized by the presence of Lewy bodies (LB) in the neurons and neurites of cortical, subcortical, and brain stem structures. Recently, alpha-synuclein (alphaS) has been found to be a central constituent of LB. In DLBD, abnormal accumulation of alphaS has been reported in both neurons and glia, but studies on glial lesions in DLBD have been limited. We examined in detail the constituents and distribution of glial lesions in eight patients with DLBD and report the pathogenesis of the glial lesions. alphaS-positive neuronal cytoplasmic inclusions (NI), neuropil threads (NT), and coiled bodies (CB) showed similar immunostaining profiles. Without pretreatment, NI, NT, and CB were detected by all antibodies against alphaS. The immunostaining profile of star-like astrocytes (SLA) was quite different from those of NI, NT, and CB. A few SLA were stained by an antibody against the non-Abeta component portion of alphaS without pretreatment, but formic acid pretreatment dramatically enhanced SLA immunoreactivity. SLA and CB were found in all eight brains with DLBD. SLA were scarce in the brain stem, but there were hundreds of SLA per visual field at x100 magnification in the temporal cortex of most cases, while CB were found diffusely in both the cerebral cortex and brain stem, similar to NI. This suggests that the pathogenesis of SLA is different from those of NI and CB. SN - 0001-6322 UR - https://www.unboundmedicine.com/medline/citation/12536227/Glial_involvement_in_diffuse_Lewy_body_disease_ L2 - https://dx.doi.org/10.1007/s00401-002-0622-9 DB - PRIME DP - Unbound Medicine ER -