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Adenosine schizophrenia sleep

Zsolt Kovács, Gábor Juhász, Miklós Palkovits, Arpád Dobolyi, Katalin A Kékesi
Nucleosides, such as uridine, inosine, guanosine and adenosine, may participate in the regulation of sleep, cognition, memory and nociception, the suppression of seizures, and have also been suggested to play a role in the pathophysiology of some neurodegenerative and neuropsychiatric diseases. Under pathological conditions, levels of nucleosides change extremely in the brain, indicating their participation in the pathophysiology of disorders like Alzheimer's disease, Parkinson's disease and schizophrenia. These findings have resulted in an increasing attention to the roles of nucleosides in the central nervous system...
2011: Current Topics in Medicinal Chemistry
Detlev Boison
Nucleoside receptors are known to be important targets for a variety of brain diseases. However, the therapeutic modulation of their endogenous agonists by inhibitors of nucleoside metabolism represents an alternative therapeutic strategy that has gained increasing attention in recent years. Deficiency in endogenous nucleosides, in particular of adenosine, may causally be linked to a variety of neurological diseases and neuropsychiatric conditions ranging from epilepsy and chronic pain to schizophrenia. Consequently, augmentation of nucleoside function by inhibiting their metabolism appears to be a rational therapeutic strategy with distinct advantages: (i) in contrast to specific receptor modulation, the increase (or decrease) of the amount of a nucleoside will affect several signal transduction pathways simultaneously and therefore have the unique potential to modify complex neurochemical networks; (ii) by acting on the network level, inhibitors of nucleoside metabolism are highly suited to fine-tune, restore, or amplify physiological functions of nucleosides; (iii) therefore inhibitors of nucleoside metabolism have promise for the "soft and smart" therapy of neurological diseases with the added advantage of reduced systemic side effects...
2011: Current Topics in Medicinal Chemistry
Joaquim A Ribeiro, Ana M Sebastião
Caffeine causes most of its biological effects via antagonizing all types of adenosine receptors (ARs): A1, A2A, A3, and A2B and, as does adenosine, exerts effects on neurons and glial cells of all brain areas. In consequence, caffeine, when acting as an AR antagonist, is doing the opposite of activation of adenosine receptors due to removal of endogenous adenosinergic tonus. Besides AR antagonism, xanthines, including caffeine, have other biological actions: they inhibit phosphodiesterases (PDEs) (e.g., PDE1, PDE4, PDE5), promote calcium release from intracellular stores, and interfere with GABA-A receptors...
2010: Journal of Alzheimer's Disease: JAD
Diogo R Lara
1. Current evidence strongly supports the idea of an inhibitory deficit as a central pathophysiological mechanism in schizophrenia. This deficit has been well documented in sensory gating and paired-pulse studies and may be related to decreases in inhibitory interneurons found in schizophrenic patients. 2. The GABAergic system has been repeatedly postulated to mediate this deficit, but the findings are controversial, at least in some areas, and mostly negative regarding treatment with drugs enhancing GABAergic activity...
June 2002: Cellular and Molecular Neurobiology
U Baumann, J Angst
The psychopathologic and somatic state of 681 psychiatric patients were investigated in longitudinal studies within the scope of different psychopharmacologic trials. Most psychologic symptoms occur less frequently, whereas somatic symptoms are found to increase, which suggests side effects from psychotropic drugs. The analyses show that the AMP-system can be reduced by 49 (possibly 45) symptoms, as initial findings and developments show that these symptoms are rare, and do not allow of differentiation between diagnostic groups...
May 16, 1977: Archiv Für Psychiatrie und Nervenkrankheiten
J C Gilbert
No abstract text is available yet for this article.
April 10, 1976: British Medical Journal (1857-1980)
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