FIG.1.
Amyloid beta peptide (Aβ)1–42 activates astrocytes and alters glucose metabolism. (A and B) Astrocytes were exposed to solvent alone (A), or to 1 µm Aβ1–42 (B) for 24 h and the morphological changes monitored by phase contrast microscopy. (C) Concentration-dependence of Aβ1–42-induced NO accumulation. Cells were exposed to increasing concentrations of Aβ1–42 or scrambled Aβ (AβS), and the accumulation of NO determined at 8 h relative to untreated controls.●–●, Aβ1–42; ○-○, AβS. (D) Aβ alters glucose metabolism. Glial cells were exposed to 1 µm Aβ1–42 or AβS for 24 h and the indicated activities monitored. In each experiment the values are shown as increases or decreases relative to controls (vehicle alone) as the mean plus or minus the standard error of the mean of three independent experiments. The following are the values for the control cells in each: deoxyglucose uptake 7.1 ± 0.5 nmols/min/ 106 cells; glycolysis 5.2 ± 0.2 nmols / min / 106 cells; hexose monophosphate shunt (HMS), 1.4 ± 0.1 nmols/min/106 cells; nicotinamide adenine dinucleotide phosphate (NADPH), 280 ± 20 pmols/mg protein; glucose-6-phosphate dehydrogenase (G6PDH), 124 ± 0.5 nmols/min/mg protein. *P < 0.0003; **P < 0.0001 by two-tailed t-test vs. vehicle (n = 3).