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Abstract: Aggregated amyloid-β causes pathological changes in mixed cultures of neurons and astrocytes such as sporadic cytoplasmic intracellular Ca2+-signalling, increase in reactive oxygen species production and cell death. Some of the toxic effects of amyloid-β are mediated through the interaction of the peptide with α7-type nicotinic acetylcholine receptors at the cell surface. Here we demonstrated that affinity purified antibodies to synthetic fragment 173–193 of the α7-subunit of the nAChR are able to protect cells from amyloid-β induced cell death. The antibodies had no effect on the amyloid-β induced calcium signal in astrocytes. However, they significantly reduced amyloid-β induced and NADPH oxidase mediated ROS production. Modulation of the NADPH oxidase activity by either the antibodies, the receptor agonist acetylcholine or the antagonist of the α7-type nicotinic acetylcholine receptors α-bungarotoxin was vital in inhibiting both amyloid-β induced ROS production, caspase 3 cleavage as well as cell death. The uncovered details of the mechanism underlying the action of antibodies to α7-type nicotinic acetylcholine receptors gives additional insight into the involvement of this receptor in Alzheimer''s disease pathology and provides a new approach to anti-Alzheimer''s disease vaccine design. [Copyright &y& Elsevier]