http://www.cnr.it/ontology/cnr/individuo/prodotto/ID11349
Plasma alpha-1 antichymotrypsin in Alzheimer's disease; relationships with APOE genotypes. (Articolo in rivista)
- Type
- Label
- Plasma alpha-1 antichymotrypsin in Alzheimer's disease; relationships with APOE genotypes. (Articolo in rivista) (literal)
- Anno
- 2001-01-01T00:00:00+01:00 (literal)
- Alternative label
Scacchi R. 1, Ruggeri M. 2, Gambina G. 3, Marini M.C. 3, Ferrari G. 3, Corbo R.M. 1,4 (2001)
Plasma alpha-1 antichymotrypsin in Alzheimer's disease; relationships with APOE genotypes.
in Neurobiology of aging
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- Scacchi R. 1, Ruggeri M. 2, Gambina G. 3, Marini M.C. 3, Ferrari G. 3, Corbo R.M. 1,4 (literal)
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- R.M. Corbo è a disposizione dell'IBPM (literal)
- Note
- ISI Web of Science (WOS) (literal)
- Titolo
- Plasma alpha-1 antichymotrypsin in Alzheimer's disease; relationships with APOE genotypes. (literal)
- Abstract
- Inflammatory processes are thought to be important contributors to the pathogenesis of Alzheimers disease (AD). Alpha1-antichymotrypsyn (ACT) is a proteinase inhibitor characteristic of acute-phase inflammation and has been identified in amyloid plaques. We analysed the plasma ACT levels in a sample of subjects with late-onset AD and correspondent controls. Plasma ACT was higher in AD patients (62.8 ± 20.2 mg/dl) than in controls (58.8 ± 18.1 mg/dl), but not significantly (p= 0.13). In the AD patients regression analysis showed a positive linear relationship between ACT levels and duration of the disease (p= 0.037). Increased ACT concentrations (64.6 ± 21.2 mg/dl) were also found in patients with greater cognitive impairment (MMSE scores < 20), but since this factor depends on the duration of the disease as well, our present data seem to indicate a complex relationship involving elevated ACT levels, disease duration and cognitive impairment. Plasma ACT was found to differ significantly according to APOE genotypes (p=0.017), the highest levels being associated to E3-E3 homozygotes (66.1±17.8 mg/dl) and the lowest to E4-E3 subjects (53.1±18.2 mg/dl). In patients not carrying APOE*4 allele the ACT levels were higher than in controls (p=0.014), and the relationship between ACT and disease duration was stronger than that observed in the total AD sample (p= 0.003), but it was absent in those carrying APOE*4 (p= 0.67). Taken together our results seem to suggest that inflammation is a relevant factor in AD pathogenesis for subjects with E3-E3 and E3-E2 genotypes but less important for APOE*4 carrying subjects. (literal)
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