TY - JOUR
T1 - Alpha-synuclein-immunoreactive cortical Lewy bodies are associated with cognitive impairment in Parkinson's disease
AU - Mattila, P. M.
AU - Rinne, J. O.
AU - Helenius, H.
AU - Dickson, D. W.
AU - Röyttä, M.
N1 - Funding Information:
Acknowledgements We thank Ms. Toini Vieno, Ms. Sisko Lilja and the personnel in the Department of Pathology for their assistance in the preparation and staining of specimens. Financial support from Turku University Foundation, the Päivikki and Sakari Sohlberg Foundation, Turku University Hospital (EVO grant) and the Finnish Parkinson Foundation is gratefully acknowledged.
PY - 2000/9
Y1 - 2000/9
N2 - Amygdala, hippocampus and six cortical gyri were examined for the Lewy body (LB) degeneration and Alzheimer's disease (AD) type changes in 45 patients with Parkinson's disease (PD). For detection of LBs, the brain areas were stained with an antibody against alpha-synuclein. The extent of neuropathological lesions was investigated in relation to cognitive dysfunction and apolipoprotein E (apoE) ε4 allele dosage. At least one cortical LB was found in 95% of cases (43/45). Furthermore, 40% of cases (18/45) had histological findings of definite AD (CERAD class C). Those PD cases with the apoE ε4 allele had a significantly greater number of cortical LBs than those without the apoE ε4 allele, but this was statistically significant only in precentral, angular and temporal gyri. The LB density correlated better with the number of plaques than with the density of tangles. The number of LBs in several cortical areas correlated significantly with the cognitive impairment. In stepwise linear regression analysis, the number of LBs in the cingulate gyrus and the amount of tangles in the temporal cortex remained statistically significant. When the CERAD class C was excluded, the correlation between cognitive decline and the number of LBs in cortical areas became even more pronounced. A stepwise linear regression analysis in these cases found the number of LBs in the frontal gyrus to be the statistically most significant predictor of cognitive impairment. This study shows, for the first time, that in PD, alpha-synuclein-positive cortical LBs are associated with cognitive impairment independent of AD-type pathology.
AB - Amygdala, hippocampus and six cortical gyri were examined for the Lewy body (LB) degeneration and Alzheimer's disease (AD) type changes in 45 patients with Parkinson's disease (PD). For detection of LBs, the brain areas were stained with an antibody against alpha-synuclein. The extent of neuropathological lesions was investigated in relation to cognitive dysfunction and apolipoprotein E (apoE) ε4 allele dosage. At least one cortical LB was found in 95% of cases (43/45). Furthermore, 40% of cases (18/45) had histological findings of definite AD (CERAD class C). Those PD cases with the apoE ε4 allele had a significantly greater number of cortical LBs than those without the apoE ε4 allele, but this was statistically significant only in precentral, angular and temporal gyri. The LB density correlated better with the number of plaques than with the density of tangles. The number of LBs in several cortical areas correlated significantly with the cognitive impairment. In stepwise linear regression analysis, the number of LBs in the cingulate gyrus and the amount of tangles in the temporal cortex remained statistically significant. When the CERAD class C was excluded, the correlation between cognitive decline and the number of LBs in cortical areas became even more pronounced. A stepwise linear regression analysis in these cases found the number of LBs in the frontal gyrus to be the statistically most significant predictor of cognitive impairment. This study shows, for the first time, that in PD, alpha-synuclein-positive cortical LBs are associated with cognitive impairment independent of AD-type pathology.
KW - Alpha-synuclein
KW - Cognitive impairment
KW - Cortical Lewy bodies
KW - Parkinson's disease
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U2 - 10.1007/s004019900168
DO - 10.1007/s004019900168
M3 - Article
C2 - 10965798
AN - SCOPUS:0033923545
SN - 0001-6322
VL - 100
SP - 285
EP - 290
JO - Acta neuropathologica
JF - Acta neuropathologica
IS - 3
ER -