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)

A double-blind, intra-individual cross-over comparison of the effect of piracetam on retrograde memory impairement as measured by the KS memory test battery was performed in connection with second and third Bi-ECT in 18 patients diagnosed as suffering from depression. The seizure duration and the post-ECT EGG patterns were examined visually and the post-ECT confusion time was measured. Piracetam was given orally in the dose of 4.8 g/day for 3 days. No significant effects were obtained on memory scores, electrical stimulus duration, EEG pattern or post-ECT confusion time. The findings may indicate that the protective effect of piracetam shown in animal electroconvuslive stimulation (ECS) is due to a counteraction of the disturbing effect of hypoxia on memory functions. It is concluded that more information is needed as regards the pharmacokinetics and the mode of action of the drug.
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PMID:Does piracetam counteract the ECT-induced memory dysfunctions in depressed patients? 109 38

The effect of Piracetam (UCB 6215, 2-pyrrolidoneacetamide) on learning mediated by transcommissural information flow was studied in hooded rats. Acquisition of monocular pattern discrimination was faster in drug-treated rats (100 mg/kg, 30 min before training) than in untreated controls. Subsequent relearning with one hemisphere functionally eliminated by cortical spreading depression showed that the strength of the primary engram formed under Piracetam in the hemisphere contralateral to the trained eye remained unaffected but that the secondary trace (in the ipsilateral hemisphere) was considerably improved and almost equalled the primary one (savings increased from 20-30% to 50-60%). Learning with uncrossed optic fibers was unaffected by the drug. Interhemispheric transfer of lateralized visual engrams acquired during functional hemidecortication was facilitated by Piracetam administration preceding the five transfer trials performed with the untrained eye open (imperative transfer). Piracetam was ineffective when the trained eye was open during transfer trials (facultative transfer). After a visual engram had been lateralized by 5 days of monocular overtraining, Piracetam facilitated formation of the secondary engram induced by 3 interocular transfer trials. It is concluded that Piracetam enhances transcommissural encoding mechanisms activated in the initial stage of monocular learning and in some forms of interhemispheric transfer, but does not affect the transcommissural readout. This effect is interpreted as a special case of the Piracetam-induced facilitation of the phylogenetically old mechanisms of redundant information storage which improve liminal or subnormal learning.
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PMID:Piracetam-induced facilitation of interhemispheric transfer of visual information in rats. 125 71

The effect of piracetam on the electrophysiological and biochemical characteristics of the GABA system was studied and compared to that of cethyl ether of GABA (CEGABA). It was shown that piracetam (250-500 mg/kg) enhances the test response depression in the primary response recovery cycle and produces synchronization of the ECoG of the sensomotor cortex similarly to the previously described GABA-positive substances. The synchronizing effects of piracetam are retained upon isolation of the cortex and can be removed by bicucullin (rather than by strychnine) applied to the cortex. Piracetam decreases the GABA content in the brain cortex and inhibits the activity of glutamate decarboxylase. Analogous effect is exerted by CEGABA. A conclusion is drawn that GABA-ergic processes get potentiated under the effect of both the drugs. The selectivity of piracetam effects as to the cortical GABA-ergic inhibitory systems is likely to be the reason for the absence in the drug of anticonvulsant effect inherent in GABA mimetics with more generalized effects (CEGABA, muscimol).
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PMID:[GABA-ergic cortical component in the action of piracetam and cetyl GABA]. 708 5

Sixty patients with disabling myoclonus excluding mainly spinal myoclonus were treated by piracetam as an open-labeled study, and myoclonus score, neurological symptoms, functional disability, and intensity of myoclonus were scored before and after treatment, including a blinded video inspection. Electrophysiological correlation also was investigated before and after treatment. Piracetam was effective in myoclonus, especially that of cortical origin, in both monotherapy and polytherapy. Piracetam also had positive benefits on gait ataxia and convulsions but not on dysarthria, and feeding and hand writing improved much more significantly. Psychologically significant improvement was seen in decreased motivation, sleep disturbance, attention deficit, and depression, all of which might be possibly secondary benefits associated with improvement of myoclonus. There was no positive correlation between clinical and electrophysiological improvement. Tolerance was good, and side effects were transient. However, hematological abnormalities observed in at least two patients in the present study should be kept in mind when relatively large doses of piracetam are administered, especially in combination with other antimyoclonic drugs.
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PMID:Clinical trial of piracetam in patients with myoclonus: nationwide multiinstitution study in Japan. The Myoclonus/Piracetam Study Group. 891 96

Electroconvulsive therapy (ECT) is still the fastest, most effective, and frequently life-saving therapeutic intervention in several forms of depression and some other psychiatric disorders. Transient memory disturbances are frequent after ECT. A randomized, double-blind, placebo-controlled study was conducted to investigate the effects of piracetam on ECT-induced confusion and memory disturbances. Thirty-eight consecutively admitted patients with depressive illness or schizophrenia requiring ECT were given either piracetam or an identical-looking placebo during the period of ECT treatment and for 2 weeks afterward. Daily dosage of piracetam was 7.2 g, given orally for the first 2 weeks while patients underwent ECT (loading phase), followed by 4.8 g for the rest of the study period. Participants were evaluated by standardized clinical rating scales and cognitive psychologic tests 1 to 2 days before ECT, 1 day after their third and sixth ECT treatments, and 2 weeks after they had completed their ECT courses. Piracetam had no significant effect in preventing ECT-induced memory disturbances. All clinical ratings were consistently, albeit not significantly, better in the piracetam group, suggesting that piracetam may have augmented the effects of ECT.
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PMID:Effect of piracetam on ECT-induced cognitive disturbances: a randomized, placebo-controlled, double-blind study. 1279 65

There is an increasing interest in nootropic drugs for the treatment of CNS disorders. Since the last meta-analysis of the clinical efficacy of piracetam, more information has accumulated. The primary objective of this systematic survey is to evaluate the clinical outcomes as well as the scientific literature relating to the pharmacology, pharmacokinetics/pharmacodynamics, mechanism of action, dosing, toxicology and adverse effects of marketed and investigational drugs. The major focus of the literature search was on articles demonstrating evidence-based clinical investigations during the past 10 years for the following therapeutic categories of CNS disorders: (i) cognition/memory; (ii) epilepsy and seizure; (iii) neurodegenerative diseases; (iv) stroke/ischaemia; and (v) stress and anxiety. In this article, piracetam-like compounds are divided into three subgroups based on their chemical structures, known efficacy and intended clinical uses. Subgroup 1 drugs include piracetam, oxiracetam, aniracetam, pramiracetam and phenylpiracetam, which have been used in humans and some of which are available as dietary supplements. Of these, oxiracetam and aniracetam are no longer in clinical use. Pramiracetam reportedly improved cognitive deficits associated with traumatic brain injuries. Although piracetam exhibited no long-term benefits for the treatment of mild cognitive impairments, recent studies demonstrated its neuroprotective effect when used during coronary bypass surgery. It was also effective in the treatment of cognitive disorders of cerebrovascular and traumatic origins; however, its overall effect on lowering depression and anxiety was higher than improving memory. As add-on therapy, it appears to benefit individuals with myoclonus epilepsy and tardive dyskinesia. Phenylpiracetam is more potent than piracetam and is used for a wider range of indications. In combination with a vasodilator drug, piracetam appeared to have an additive beneficial effect on various cognitive disabilities. Subgroup 2 drugs include levetiracetam, seletracetam and brivaracetam, which demonstrate antiepileptic activity, although their cognitive effects are unclear. Subgroup 3 includes piracetam derivatives with unknown clinical efficacies, and of these nefiracetam failed to improve cognition in post-stroke patients and rolipram is currently in clinical trials as an antidepressant. The remaining compounds of this subgroup are at various preclinical stages of research. The modes of action of piracetam and most of its derivatives remain an enigma. Differential effects on subtypes of glutamate receptors, but not the GABAergic actions, have been implicated. Piracetam seems to activate calcium influx into neuronal cells; however, this function is questionable in the light of findings that a persistent calcium inflow may have deleterious impact on neuronal cells. Although subgroup 2 compounds act via binding to another neuronal receptor (synaptic vesicle 2A), some of the subgroup 3 compounds, such as nefiracetam, are similar to those of subgroup 1. Based on calculations of the efficacy rates, our assessments indicate notable improvements in clinical outcomes with some of these agents.
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PMID:Piracetam and piracetam-like drugs: from basic science to novel clinical applications to CNS disorders. 2016 67

There is a strong association between depression and memory impairment. The present study aims to assess the nootropic activity of duloxetine and piracetam combination. Male Swiss Albino mice were divided randomly into 4 groups. Treatment of normal saline (10 ml/kg), duloxetine (10 mg/kg), piracetam (100 mg/kg), and duloxetine (5 mg/kg) plus piracetam (50 mg/kg) were given through intra-peritoneal route to group I-IV, respectively. Transfer latency in elevated plus maze (EPM) and time spent in target quadrant in Morris water maze (MWM) were recorded. Estimation of brain monoamines in hippocampus, cerebral cortex, and whole brain were done using HPLC with fluorescence detector. Piracetam treated group showed significant decrease in transfer latency in EPM and increase in time spent in target quadrant recorded in MWM. Combination treated group failed to produce statistically significant nootropic effect in both EPM and MWM. Combination treated group failed to increase brain monoamine levels when compared against duloxetine and piracetam treated groups, separately. But there was exception of significant increase in norepinephrine levels in hippocampi when compared against duloxetine treated group. Results indicate no cognitive benefits with piracetam plus duloxetine combination. These findings can be further probed with the aim of understanding the interaction between duloxetine and piracetam as a future endeavor.
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PMID:The Combination of Antidepressant Duloxetine with Piracetam in Mice does not Produce Enhancement of Nootropic Activity. 2525 69

Reports on the clinical presentation of adult-onset neuronal ceroid lipofuscinoses (NCL) are scarce compared to infantile- and childhood-onset forms. Here, we aimed to present detailed temporal evolution of clinical and electrophysiological features of two siblings with adult-onset NCL and homozygous mutation in the CLN6 gene. We retrospectively analysed medical records and electrophysiological data in order to delineate evolution of clinical and electrophysiological findings. Electrophysiological studies included routine EEG and video-EEG, as well as polymyographic analysis of myoclonus and brainstem reflex studies. Both patients had seizures and cerebellar signs. Despite the slow progression of ataxia, they developed no mental deterioration, but had severe obsessive compulsive disorder and depression. EEG revealed frequent generalized spikes, polyspikes, and waves, prominent on awakening and during photic stimulation without significant change throughout the clinical course. Abnormalities concerning the blink reflex, auditory startle response, and startle response to somatosensory inputs manifested within four years. The patients underwent transient and mild improvement with valproate, whereas ataxia and seizures were dramatically ameliorated following high-dose piracetam. Patients with adult-onset NCL may present with slowly progressive ataxia, persistent photosensitivity, and seizures without dementia or extrapyramidal findings. Brainstem abnormalities become more evident with time, in line with ataxia. Piracetam is effective for both seizures and ataxia.
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PMID:Long-term follow-up of two siblings with adult-onset neuronal ceroid lipofuscinosis, Kufs type A. 2858 97