Complement 3 and factor h in human cerebrospinal fluid in Parkinson's disease, Alzheimer's disease, and multiple-system atrophy.
Identifieur interne : 000080 ( PubMed/Checkpoint ); précédent : 000079; suivant : 000081Complement 3 and factor h in human cerebrospinal fluid in Parkinson's disease, Alzheimer's disease, and multiple-system atrophy.
Auteurs : Yu Wang [États-Unis] ; Aneeka. Hancock ; Joshua Bradner ; Kathryn. Chung ; Joseph. Quinn ; Elaine. Peskind ; Douglas Galasko ; Joseph Jankovic [États-Unis] ; Cyrus. Zabetian ; Hojoong. Kim ; James. Leverenz ; Thomas. Montine ; Carmen Ginghina ; Karen. Edwards ; Katherine. Snapinn ; David. Goldstein ; Min Shi ; Jing ZhangSource :
- The American journal of pathology ; 2011.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Alzheimer Disease (cerebrospinal fluid), Amyloid beta-Peptides (cerebrospinal fluid), Case-Control Studies, Cohort Studies, Complement C3 (cerebrospinal fluid), Complement Factor H (cerebrospinal fluid), Female, Humans, Inflammation, Male, Middle Aged, Multiple System Atrophy (cerebrospinal fluid), Parkinson Disease (cerebrospinal fluid), Peptide Fragments (cerebrospinal fluid), Quality Control, Regression Analysis.
- MESH :
- chemical , cerebrospinal fluid : Amyloid beta-Peptides, Complement C3, Complement Factor H, Peptide Fragments.
- cerebrospinal fluid : Alzheimer Disease, Multiple System Atrophy, Parkinson Disease.
- Adult, Aged, Aged, 80 and over, Case-Control Studies, Cohort Studies, Female, Humans, Inflammation, Male, Middle Aged, Quality Control, Regression Analysis.
Abstract
Complement activation, a key component of neuroinflammation, has been reported in both Parkinson's disease (PD) and Alzheimer's disease (AD). However, it is unclear whether complement activation and neuroinflammation in general are distinctly different from each another in major neurodegenerative disorders. In the present study, cerebrospinal fluid complement 3 (C3) and factor H (FH) were measured and evaluated together with amyloid-β(42) (Aβ(42)), which in recent investigations was decreased in patients with PD, in particular those with cognitive impairment. The study included 345 participants: 126 patients with PD at various stages with or without cognitive impairment, 50 with AD, and 32 with multiple-system atrophy, and 137 healthy control individuals. In addition to changes in Aβ(42) concentrations, there were clear differences in the patterns of complement profiles among neurodegenerative disorders. The C3/FH ratio demonstrated high sensitivity and specificity in differentiating patients with multiple-system atrophy from those with AD or PD and control individuals. In addition, the C3/Aβ(42) and FH/Aβ(42) ratios not only correlated with PD severity approximated using the Unified Parkinson's Disease Rating Scale but also with the presence of cognitive impairment or dementia in PD. Both C3 and FH correlated with the severity of impairment in AD as indicated using Mini-Mental State Examination scores.
DOI: 10.1016/j.ajpath.2011.01.006
PubMed: 21435440
Affiliations:
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pubmed:21435440Le document en format XML
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<term>Amyloid beta-Peptides (cerebrospinal fluid)</term>
<term>Case-Control Studies</term>
<term>Cohort Studies</term>
<term>Complement C3 (cerebrospinal fluid)</term>
<term>Complement Factor H (cerebrospinal fluid)</term>
<term>Female</term>
<term>Humans</term>
<term>Inflammation</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Multiple System Atrophy (cerebrospinal fluid)</term>
<term>Parkinson Disease (cerebrospinal fluid)</term>
<term>Peptide Fragments (cerebrospinal fluid)</term>
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<term>Regression Analysis</term>
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<term>Peptide Fragments</term>
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<front><div type="abstract" xml:lang="en">Complement activation, a key component of neuroinflammation, has been reported in both Parkinson's disease (PD) and Alzheimer's disease (AD). However, it is unclear whether complement activation and neuroinflammation in general are distinctly different from each another in major neurodegenerative disorders. In the present study, cerebrospinal fluid complement 3 (C3) and factor H (FH) were measured and evaluated together with amyloid-β(42) (Aβ(42)), which in recent investigations was decreased in patients with PD, in particular those with cognitive impairment. The study included 345 participants: 126 patients with PD at various stages with or without cognitive impairment, 50 with AD, and 32 with multiple-system atrophy, and 137 healthy control individuals. In addition to changes in Aβ(42) concentrations, there were clear differences in the patterns of complement profiles among neurodegenerative disorders. The C3/FH ratio demonstrated high sensitivity and specificity in differentiating patients with multiple-system atrophy from those with AD or PD and control individuals. In addition, the C3/Aβ(42) and FH/Aβ(42) ratios not only correlated with PD severity approximated using the Unified Parkinson's Disease Rating Scale but also with the presence of cognitive impairment or dementia in PD. Both C3 and FH correlated with the severity of impairment in AD as indicated using Mini-Mental State Examination scores.</div>
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<Abstract><AbstractText>Complement activation, a key component of neuroinflammation, has been reported in both Parkinson's disease (PD) and Alzheimer's disease (AD). However, it is unclear whether complement activation and neuroinflammation in general are distinctly different from each another in major neurodegenerative disorders. In the present study, cerebrospinal fluid complement 3 (C3) and factor H (FH) were measured and evaluated together with amyloid-β(42) (Aβ(42)), which in recent investigations was decreased in patients with PD, in particular those with cognitive impairment. The study included 345 participants: 126 patients with PD at various stages with or without cognitive impairment, 50 with AD, and 32 with multiple-system atrophy, and 137 healthy control individuals. In addition to changes in Aβ(42) concentrations, there were clear differences in the patterns of complement profiles among neurodegenerative disorders. The C3/FH ratio demonstrated high sensitivity and specificity in differentiating patients with multiple-system atrophy from those with AD or PD and control individuals. In addition, the C3/Aβ(42) and FH/Aβ(42) ratios not only correlated with PD severity approximated using the Unified Parkinson's Disease Rating Scale but also with the presence of cognitive impairment or dementia in PD. Both C3 and FH correlated with the severity of impairment in AD as indicated using Mini-Mental State Examination scores.</AbstractText>
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