The formation of thiobarbituric acid-reactive products was measured as an index of peroxidation by oxygen free radicals in homogenates of frontal cortex and cerebellum from brains taken at autopsy and verified histologically as being Alzheimer's (n = 6) or normal (n = 6). Compared with controls, basal peroxidation is significantly higher in Alzheimer's cortex, and this difference is also evident in the presence of exogenous iron. Peroxidation in cerebellum and levels of total glutathione, RNA, and DNA in cortex and cerebellum do not differ significantly between Alzheimer's brain and controls. Iron-induced peroxidation in cortex is reduced by the lazaroid U-74500A, with calculated IC50 values that are significantly higher in Alzheimer's samples (10 microM) than in controls (2.5 microM). These observations suggest that cerebral cortex from Alzheimer's patients differs from controls with respect to in vitro peroxidation.

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Noradrenaline effects on glucose oxidation were studied in primary cultures of astrocytes. CO2 formation from labeled glucose was enhanced in the presence of noradrenaline. The stimulatory effect by noradrenaline was exerted both on lactate formation (approximately 20%) and on tricarboxylic acid activity (CO2 production from glutamate) (approximately 40%). The effect was, at least partly, exerted on the alpha-ketoglutarate dehydrogenase step. The EC50 value for noradrenaline on lactate formation was significantly lower (60 nM) than that on oxidative metabolism (1,900 nM). Studies with specific adrenergic agonists and antagonists showed that various receptor subtypes are involved. Thus, the effect on lactate formation was mediated exclusively by stimulation of an alpha 1 receptor whereas oxidative metabolism was enhanced by both alpha 1 and alpha 2 receptor stimulation. No effects were exerted by beta receptor agonists or antagonists.