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. Author manuscript; available in PMC: 2011 Mar 10.
Published in final edited form as: Arch Neurol. 2009 Mar;66(3):352–361. doi: 10.1001/archneurol.2008.588

Figure 2.

Figure 2

Increased concentration of glucose inhibits peroxisome proliferator–activated receptor γ coactivator 1α (PGC-1α) expression and promotes β-amyloid (Aβ) generation in Tg2576 neurons, which is prevented by exogenous viral expression of PGC-1α. A and B, Culturing Tg2576 neurons with 91, 182, and 273 mg/dL of glucose (to convert to millimoles per liter, multiply by 0.055) for 24 hours resulted in a dose-dependent inhibition of PGC-1α protein expression (A) as assessed by Western blot analysis and a dose-dependent promotion of Aβ generation (B) as detected by enzyme-linked immunosorbent assay (ELISA). C and D, Adenovirus-mediated overexpression of PGC-1α in primary neuron cultures prevents 273-md/dL glucose–mediated induction of Aβ1-40 and Aβ1-42 contents released into the culture media, assessed by ELISA 24 hours postinfection (10 multiplicities of infection). Western blot analysis of PGC-1α expression in parts A and C used an anti–PGC-1α antibody. Results are expressed as a percentage of its own control. Values represent mean (SEM) of determinations made in 3 separate culture preparations; n=3 per culture preparation. *P<.05 and †P<.01 vs control group by t test.