Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arundic acid (ONO-2506) is believed to be neuroprotective because of its actions on glia cells; i.e., its inhibitory effects on the synthesis of a calcium-binding protein S100B. ONO-2506 is undergoing clinical trials for the treatment of patients with stroke and Alzheimer's disease. Recent clinical studies point to a pervasive comorbidity of depression with stroke and Alzheimer's disease. Previously, S100B has been implicated in the pathobiological mechanisms of depression. Preclinical studies have shown that antidepressant treatment significantly increases brain S100B. Here we hypothesize that available data that link S100B with depression, along with the proposed inhibitory action of ONO-2506 on S100B synthesis, indicate that this compound could increase vulnerability for depression in patients at risk for this disorder, and we propose that evaluation of patients with stroke and Alzheimer's disease for the presence of depression should be routine in clinical trials employing ONO-2506. Although it may be open for discussion whether the neuroprotective effects of ONO-2506 are exclusively due to its inhibition of S100B synthesis, the latter action of ONO-2506 warrants studies of the effects of this drug in the pathobiology of depression.
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PMID:Could treatment with arundic acid (ONO-2506) increase vulnerability for depression? 1679 59

Mild hypoxia increases ventilation, but severe hypoxia depresses it. The mechanism of hypoxic ventilatory depression, in particular, the functional role of the cerebrum, is not fully understood. Recent progress in glial physiology has provided evidence that astrocytes play active roles in information processing in various brain functions. We investigated the hypothesis that astrocytic activation is necessary to maintain the cerebral function and ventilation in hypoxia, by examining the responses of EEG and ventilation to severe hypoxia before and after administration of a modulator of astrocytic function, arundic acid, in unanesthetized mice. Ventilatory parameters were measured by whole body plethysmography. When hypoxic ventilatory depression occurred, gamma frequency band of EEG was suppressed. Arundic acid further suppressed ventilation, and the EEG power was suppressed in a dose-dependent manner. Arundic acid also suppressed hypoxia-induced c-Fos expression in the hypothalamus. We conclude that severe hypoxia suppresses the cerebral function which could reduce the stimulus to the brainstem resulting in ventilatory depression. Astrocytic activation in hypoxia may counteract both cerebral and ventilatory suppression.
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PMID:Effects of arundic acid, an astrocytic modulator, on the cerebral and respiratory functions in severe hypoxia. 2659 45