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Phentermine 37.5 mg benefits and does not appear to enhance performance in this study. Discussion The current study confirms previously reported benefits of Methylphenidate on working memory, attention and psychomotor speed. These findings are consistent with prior studies demonstrating improvements short-acting methylphenidate (up to 25 mg) in ADHD[26,27] and cognitive function, both laboratory studies involving attention and working memory as well a randomized controlled for sale phentermine hydrochloride 37.5 mg trial. Although in the acute dose-response study, Methylphenidate did not exhibit clinically significant benefit compared to placebo, the effect size was not small and likely to have an impact on future studies. Although the Methylphenidate benefits were primarily seen with short-acting methylphenidate, this is likely not a true reflection of the drug's half-life. In fact, when using the same doses of methylphenidate for a longer period of time (3–6 weeks) and assessing the long-term effects, Methylphenidate still showed positive effects. Thus, the effects may be due to the longer-duration of study compared to short-acting methylphenidate and the longer time frame over which cognitive and psychomotor performance was tested. We also compared methylphenidate's benefits in the acute and delayed doses when evaluated separately for their effects on cognition and psychomotor speed. In previous work on ADHD,[4–6] we found that methylphenidate's acute benefits are likely due to its effects on prefrontal alpha-2 neurotransmission, and as such, do not need to last for long on their own to have positive clinical effects. In contrast, our findings on the delayed dose of methylphenidate showed that also increased cerebral blood flow. Hence, despite the fact that both methylphenidate and placebo showed positive effects on attention and working memory in phentermine k 25 37.5 mg the acute and delayed periods, enhanced cognition observed in the delayed period could be due to the effects of methylphenidate's attention raising properties. The acute and delayed doses of methylphenidate showed similar beneficial psychomotor benefits. These findings are of interest because, although the mechanisms of action methylphenidate are still unknown, we believe that these findings give credence to the claim that acute and delayed effects of methylphenidate in ADHD may result from the improved attention afforded through its alpha-2 agonism. While the mechanisms of action Methylphenidate (and other cognitive enhancers) remain unknown, the positive effect observed when administered in the acute phase may be associated with multiple mechanisms. By increasing alpha-2 neurotransmission, methylphenidate may increase the activity of both fast and slow, in the brain[29–31]. Increased alpha-2 neurotransmission was also shown to enhance the ability of dopamine to enter the presynaptic neuron. Therefore, Methylphenidate's attention-producing effects may be due to the increased alpha-2 neurotransmission associated with amphetamine. Alternatively, Methylphenidate may show a direct anxiolytic effect. In recent study, an anxiolytic (anxiety reliever) was shown to have positive and dose-related neuroprotective (enhanced neurotransmission) effects on spatial cognition using the Wisconsin card sorting task in young adults. Methylphenidate at doses up to 30 mg also displayed a direct anxiolytic effect when administered at 50 mg . While Methylphenidate's increased cognitive effects cannot be explained simply by its anxiolytic properties, the direct and effects are likely due to the same mechanisms of action. ability Methylphenidate to enhance dopamine function may also be indicative of its alpha-2 agonist effects.
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