Affiliations: [a] International Biotechnological Center, M.V. Lomonosov Moscow State University, Department of Biochemistry, 119992 Moscow, Russia | [b] Department of Medical Biochemistry, University of the People Friendship, Moscow, Russia | [c] School of Public Health, University at Albany, SUNY, Albany, NY, USA
Correspondence:
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Corresponding author: Professor Alexander Boldyrev, Department of Biochemistry, School of Biology (Room 141), M.V. Lomonosov Moscow State University, Lenin's Hills, Moscow 119992, Russia. Tel./Fax: +7 095 939 1398; E-mail: [email protected].
Abstract: Acutely dissociated rat cerebellar granule cell neurons were incubated with amyloid-β (1–42) and studied by flow cytometry. Amyloid-β caused a dose-dependent loss of viability, as determined by intracellular accumulation of propidium iodide (PI),and that was not accompanied by significant elevation of intracellular calcium, measured by Fluo-3 or reactive oxygen species (ROS), measured by 2',7'-dihydro-dichlorfluorescein diacetate (DCF). Carnosine, a ROS scavenger and an inhibitor of non-enzymatic glycosylation, partially reduced cell death caused by amyloid-β. We conclude that amyloid-β causes a relatively acute loss of cell viability in cerebellar granule cell neurons, which does not result from either elevation of intracellular calcium concentration or generation of ROS.
