153 results match your criteria: "Clinical Neuroscience Research Center[Affiliation]"

A sleep diary and questionnaire study of naturally short sleepers.

J Sleep Res

September 2001

Clinical Neuroscience Research Center, Western Psychiatric Institute and Clinic, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA.

Whereas most people require more than 6 h of sleep to feel well rested, there appears to be a group of people who can function well on between 3 and 6 h of sleep. The aims of the present study were to compare 12 naturally short (3-6 h) sleepers (9 males 3 females, mean age 39.6 years, SD age 10.

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Three new cholinesterase inhibitors, donepezil, rivastigmine, and galantamine, all inhibit the enzyme AChE. Rivastigmine also inhibits BuChE, which could lead to additional benefits in late-stage Alzheimer's disease, but also cause more GI side effects at initiation of therapy. Galantamine is also an allosteric modulator of nicotinic receptors, which could lead to additional efficacy for attention and for behaviors mediated by neurotransmitters other than ACh.

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The highly effective psychopharmacologist will develop the habit of "sharpening the saw" by clever selection of unbiased and efficient CME programs that incorporate the most thoughtful applications of the principles of adult education to enhance retention rates after a single exposure.

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Neurotransmitters activate genes in their target neurons by precipitating a molecular cascade, which may be the ultimate consequence of chemical neurotransmission. When this transfer is aberrant, a mental disorder may be manifest. When drugs act upon neurons to change gene expression, this could lead to therapeutic actions, side effects, and the long-term consequences of drug abuse.

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One of the most important advances in molecular neurobiology of relevance to the practicing psychiatrist is how an intracellular second messenger can "turn on" genes by activating first a protein kinase enzyme and then a transcription factor. Failure to turn on the right genes may lead to psychiatric illnesses. Causing the appropriate genes to turn on may be the therapeutic mechanism of action of many current and future psychotropic drugs.

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Chemical neurotransmission begins when receptor occupancy by a neurotransmitter is converted into an intracellular second messenger that carries the information from the neurotransmitter deep into the target neuron. For clinicians, it is this transfer of neurotransmitter information all the way to the genome that hypothetically explains the therapeutic actions of many psychotropic drugs. This also accounts for why drugs that modify neurotransmission may take time to fully develop their clinical actions.

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Antipsychotic polypharmacy is a surprisingly frequent occurrence that can be both justified and unjustifed, depending on how it is used. To the extent that this phenomenon has been unrecognized and is not being studied, it is a "dirty little secret." To the extent that careful clinicians have uncovered a useful strategy for boosting the effectiveness of available antipsychotic monotherapies, it represents an opportunity to improve the outcomes of patients with psychotic illnesses.

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Three atypical antipsychotics are currently considered to be first-line therapies for schizophrenia, namely risperidone, olanzapine, and quetiapine. Deciding which one of these agents to choose for any given patient can be a daunting task because head-to-head comparisons of these 3 agents are just beginning, and most published trials are comparisons with typical antipsychotics, not with another atypical antipsychotic. Furthermore, results from clinical trials often do not match findings from clinical practice.

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Serotonin selective reuptake inhibitors (SSRIs) are currently among the most frequently prescribed therapeutic agents in all of medicine. Their therapeutic actions are diverse, ranging from efficacy in depression to obsessive-compulsive disorder, panic disorder, bulimia and other conditions as well. The plethora of biological substrates, receptors and pathways for serotonin are candidates to mediate not only the therapeutic actions of SSRIs, but also their side effects.

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