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The following antibodies were used in this experiment: SMA (MX097), Desmin (MX046), Caldesmon (h-CALD), ER (SP1), PR (SP2), CD10 (MX002), P16 (MX007), CyclinD1 (SP4), SMARB1(MRQ-27), FH (J-13), SDHB (MX096), CD31 (MX032), CD34 (QBEnd/10), and KI67(MX006)

Post-mortem analysis of human brains from AD patients showed that that A 40 discriminated between AD patients and high pathology controls more readily than A 42 (Gao et al., 40 oligomers have been shown to induce neurotoxicity and disrupt brain lipid bilayers while other amyloid species do not (Bode et al., 40 is induced by an increase in intracellular Ca 2+ , and this has led to the hypothesis that the accumulation of intracellular A may occur as an early event in the pathogenesis of AD (Itkin et al., 2+ ] i and may enhance Ca 2+ -mediated excitotoxicity, which may induce progressive memory loss and cognitive deficits and enhance neuronal cell apoptosis

5, when glucose is high inside a cell, most of that glucose is metabolized through glycolysis, going first to glucose-6 phosphate, then fructose-6 phosphate, and then on through the rest of the glycolytic pathway

[145] incorporated a diethylaminocoumarin (DEACM) cage into an estrogen-related receptor (ERR)-targeting PROTAC, producing photocaged PROTAC 5 (Fig