(2013) makes a strong case for excess glutamate to be a pathogeni

(2013) makes a strong case for excess glutamate to be a pathogenic click here driver, use of antipsychotic drugs may hasten the transition to psychosis and, therefore, should be avoided during the prodromal stage of the illness. Prevention strategies are now commonplace in most fields of medicine. This includes neurology, where dietary and other lifestyle recommendations have become mainstream for prevention or reduction of

illness progression for brain disorders such as Alzheimer’s disease. Early identification of individuals who are at high risk to develop schizophrenia holds the promise of advancing preventive treatment to psychiatry, and in particular to prevention of schizophrenia. Research so far indicates that pathophysiological changes in the prodrome and first-episode patients may be distinct from that observed in chronic patients (Kaur and Cadenhead, 2010) and that early intervention with traditional antipsychotic drugs may signaling pathway not only be ineffective, but may actually worsen the outcome. This makes longitudinal and mechanistically oriented translational approaches such as that applied by Schobel et al. (2013) especially critical for the design of prevention strategies to prevent psychosis in individuals

at high clinical risk for schizophrenia. “
“For years, it was routine that each new generation of microtubule researchers would learn to make tubulin preps from bovine or porcine brain (Miller and Wilson, 2010). This would involve regular trips to a slaughterhouse, waiting for the brains to become available so that they could

immediately be put on ice and rushed back to the lab, minced, and then put into a blender with cold buffer. From there, the strategy was based on the simple principle that microtubules would disassemble into soluble tubulin found in the cold and reassemble into microtubules when the prep was warmed. Through cycles of warming and cooling, the prep would become progressively more enriched for tubulin. For most microtubule labs, those days are gone, because molecular approaches can now accomplish what used to require this tedious procedure. Reminiscing about those earlier days brings to mind a fundamental issue about tubulin and microtubules. The initial huge pellet produced by spinning down the brain homogenate was normally washed down the drain without further consideration—but this pellet actually contained a significant amount of tubulin that was not soluble in the cold. Although this was long known, the cold-stable tubulin fraction was given little attention by most investigators—one notable exception being Scott Brady. Nearly three decades ago, Brady et al. (1984) compared the biochemical properties of tubulin in the cold-stable fraction with the properties of the temperature-cycled tubulin. Much of the tubulin in the cold-stable fraction was shown to be extremely basic in charge, as assessed by two-dimensional electrophoresis.

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