Abstract:
BACKGROUND:Inflammation plays a pivotal role in amyloid plaque progression thereby contributing to Alzheimer's disease-related neurodegeneration. We hypothesized that patients with Alzheimer's disease have an innate pro-inflammatory phenotype, as compared to control subjects without dementia. METHODS:Patients with a diagnosis of probable Alzheimer's disease (n=12) and control subjects without signs of dementia (n=18) were enrolled. Whole blood samples were stimulated ex vivo with endotoxin under standard conditions. Cytokine levels were assessed by ELISA and compared by Mann-Whitneyll-test after log transformation. RESULTS:Patients with Alzheimer's disease had seven- to ten-fold higher IL-1beta production relative to the amount of IL-10 both at the low (p=0.006) and high concentration of endotoxin (p=0.007). Subjects who display a pro-inflammatory phenotype as defined by a high IL-1beta/IL-10 ratio had 13.0-fold higher odds (95% CI: 2.1-82) to have dementia. CONCLUSION:The data support the hypothesis that a pro-inflammatory phenotype contributes to the development of Alzheimer's disease.
journal_name
Exp Gerontoljournal_title
Experimental gerontologyauthors
Remarque EJ,Bollen EL,Weverling-Rijnsburger AW,Laterveer JC,Blauw GJ,Westendorp RGdoi
10.1016/s0531-5565(00)00176-5keywords:
subject
Has Abstractpub_date
2001-01-01 00:00:00pages
171-6issue
1eissn
0531-5565issn
1873-6815pii
S0531-5565(00)00176-5journal_volume
36pub_type
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journal_title:Experimental gerontology
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