TY - JOUR
T1 - Clusterin/apolipoprotein J is associated with cortical Lewy bodies
T2 - Immunohistochemical study in cases with α-synucleinopathies
AU - Sasaki, Kensuke
AU - Doh-ura, Katsumi
AU - Wakisaka, Yoshinobu
AU - Iwaki, Toru
N1 - Funding Information:
Acknowledgements We are grateful to Dr. T. Iwatsubo for his generous gift of anti-α-synuclein antibody. We wish to express our appreciation to Ms. Kazue Hatanaka for her excellent technical assistance. Part of this study was carried out at the Morphology Core, Graduate School of Medical Sciences, Kyushu University. The English used in this manuscript was revised by Miss K. Miller (Royal English Language Centre, Fukuoka, Japan). This work was supported by grants from the Japan Intractable Disease Research Foundation and the Japanese Ministry of Health, Labour and Welfare to K. Doh-ura
PY - 2002
Y1 - 2002
N2 - Clusterin/apolipoprotein J protein expression in cases with "α-synucleinopathies", such as Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA), was investigated using an immunohistochemical method for the labeling of multiple antigens. About 50% of the cortical Lewy bodies in the cases with DLB were immunoreactive for clusterin, whereas brain-stem Lewy bodies in PD and DLB were rarely associated with clusterin. Clusterin was also immunopositive in around 10% of the glial cytoplasmic inclusions (GCIs) in the cases with MSA. Colocalization of clusterin with α-synuclein in such bodies or inclusions was clearly correlated with the immunostaining pattern of α-synuclein. Subcellular localization of clusterin was almost completely overlapped with the homogeneous immunoreaction of α-synuclein in the cortical Lewy bodies; however, clusterin immunoreactivity was not detected in the halo or ring-like structures of the brain-stem Lewy bodies. Furthermore, some Lewy bodies with intense immunoreactivity for clusterin showed only a weak signal for α-synuclein. These results suggest that clusterin may modify the formation of α-synuclein-positive inclusion bodies such as Lewy bodies and GCIs, through a previously proposed chaperone property of clusterin.
AB - Clusterin/apolipoprotein J protein expression in cases with "α-synucleinopathies", such as Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA), was investigated using an immunohistochemical method for the labeling of multiple antigens. About 50% of the cortical Lewy bodies in the cases with DLB were immunoreactive for clusterin, whereas brain-stem Lewy bodies in PD and DLB were rarely associated with clusterin. Clusterin was also immunopositive in around 10% of the glial cytoplasmic inclusions (GCIs) in the cases with MSA. Colocalization of clusterin with α-synuclein in such bodies or inclusions was clearly correlated with the immunostaining pattern of α-synuclein. Subcellular localization of clusterin was almost completely overlapped with the homogeneous immunoreaction of α-synuclein in the cortical Lewy bodies; however, clusterin immunoreactivity was not detected in the halo or ring-like structures of the brain-stem Lewy bodies. Furthermore, some Lewy bodies with intense immunoreactivity for clusterin showed only a weak signal for α-synuclein. These results suggest that clusterin may modify the formation of α-synuclein-positive inclusion bodies such as Lewy bodies and GCIs, through a previously proposed chaperone property of clusterin.
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U2 - 10.1007/s00401-002-0546-4
DO - 10.1007/s00401-002-0546-4
M3 - Article
C2 - 12172907
AN - SCOPUS:0036934473
SN - 0001-6322
VL - 104
SP - 225
EP - 230
JO - Acta neuropathologica
JF - Acta neuropathologica
IS - 3
ER -