Amyloid Beta Peptide (Aβ_1-42) Reverses the Cholinergic Control of Monocytic IL-1β Release.

ABSTRACT: Amyloid-β peptide (Aβ_1-42), the cleavage product of the evolutionary highly conserved amyloid precursor protein, presumably plays a pathogenic role in Alzheimer's disease. Aβ_1-42 can induce the secretion of the pro-inflammatory cytokine intereukin-1β (IL-1β) in immune cells within and out of the nervous system. Known interaction partners of Aβ_1-42 are α7 nicotinic acetylcholine receptors (nAChRs). The physiological functions of Aβ_1-42 are, however, not fully understood. Recently, we identified a cholinergic mechanism that controls monocytic release of IL-1β by canonical and non-canonical agonists of nAChRs containing subunits α7, α9, and/or α10. Here, we tested the hypothesis that Aβ_1-42 modulates this inhibitory cholinergic mechanism.

SUBMITTER: Richter K 

PROVIDER: S-EPMC7564705 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature