Abstract
Background: Neuro-inflammation, triggered by β-amyloid peptide, is implicated as one of the primary contributors to Alzheimer's disease (AD) pathogenesis, and several cytokines were identified as key instigating factors. Methods: To reveal the inflammatory response of lymphocytes to the neuro-toxic β-amyloid peptide, we evaluated the release of several cytokines from peripheral blood mononuclear cells with immuno-assays (ELISA). From hyper-acute to chronic effects of β-amyloid peptide were assessed at a wide range of concentrations. Results: The pro-inflammatory interleukin (IL)-1β, tumor necrosis factor-α, monocyte chemotactic protein-1, and Rantes (acronym for regulated on activation, normal T-cell expressed and secreted) as well as the pleiotropic IL-6 showed a biphasic release pattern over time in both low and high doses of amyloid treatment: after an initial increase, their concentration gradually fell to the baseline. The suppressors IL-4 and IL-10 had a sinus-like secretion panel: an acute increase in their levels turned to a depression and later followed by their over-secretion. Interestingly, β-amyloid below 10-8 mol/L produced no effect at all, but any molarity above this threshold caused the very same cytokine secretion pattern, the mark of an all-or-nothing response of β-amyloid peptide. Conclusions: These results delineate a highly organized pro- and anti-inflammatory response of cells to the neuro-toxic peptide. This is the first study to describe how the β-amyloid-induced inflammatory processes in Alzheimer's dementia are regulated.
Original language | English (US) |
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Pages (from-to) | 891-895 |
Number of pages | 5 |
Journal | Biological Psychiatry |
Volume | 64 |
Issue number | 10 |
DOIs | |
State | Published - Nov 15 2008 |
Externally published | Yes |
Keywords
- β-amyloid peptide
- Alzheimer's disease
- cytokine
- interleukin
- lymphocyte
ASJC Scopus subject areas
- Biological Psychiatry