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)

Cognitive deficits, including memory deficiencies, are currently deemed one of key symptoms of psychopathologic mental disorders or epilepsy. The impairment of neurocognitive processes could be due to the administered therapy, in particular combined therapy or therapy using antiepileptics of older type. Gabapentin (GBP) is one of new antiepileptics with normothymic properties. It is known that epileptic patients run a significant risk of developing depression and mood changes. Smoking may also have a negative effect on memory processes and efficacy of administered drugs. Note that smoking in pregnant women also leads to neurobehavioral changes in their children. The objective of our research was to evaluate the effect of GBP on memory functions and antidepressant effect in rats not exposed and exposed to tobacco smoke in fetal life. We were also intent on finding whether GBP has an anticonvulsant effect in contact and without contact with tobacco smoke, and whether it affects motor coordination in animals if administered in the dose of 25 mg/kg. Spatial memory of the animals was assessed in the Morris test and the antidepressant effect in the Porsolt test. The ED(50) value was determined in the Swinyard maximum electric shock test, and the effect on motor coordination was assessed in the chimney test. GBP administered in the dose of 25 mg/kg intraperitoneal (i.p.) significantly reduced the immobility time on days 1 and 7 of the test in animals exposed to tobacco smoke, and on days 7 and 14 of the test in rats not exposed to tobacco smoke. Upon single and multiple administration of GBP to animals not exposed to tobacco smoke, the spatial memory improved, whereas in animals exposed to tobacco smoke in fetal life tolerance for procognitive effect was observed on day 21 of the test. It has been found that in rats not exposed to tobacco smoke, ED(50) of GBP was 28.73 mg/kg, whereas in animals exposed to tobacco smoke in fetal life, ED(50) was 46.2 mg/kg. Upon 14 and 21 days of drug administration, motor coordination was impaired in both GBP receiving animal groups. In conclusion, GBP beside its anticonvulsant efficacy also improves memory processes and has antidepressant effect. We also proved that GBP may reverse cognitive deficits concerning working memory induced by prenatal exposure to tobacco smoke and may have antidepressant effect in rats exposed to tobacco smoke.
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PMID:Effect of gabapentin on cognitive processes in rats not exposed and exposed to tobacco smoke during fetal life. 1927 43

A 69-year-old man presented with Cotard's delusions, insomnia, profound depression, amnesia, difficulty concentrating, and cognitive deficit after two different surgical interventions. Brain imaging showed frontotemporal-subcortical atrophy and lateral ventricular enlargement. He responded poorly to a combination of sertraline, amisulpride and mirtazapine, with modest benefit on insomnia, and developed hypotension. After 18 days he was switched to olanzapine and venlafaxine, but his cognition worsened. He underwent bilateral electroconvulsive therapy (ECT). His mood improved, cognitive performance increased and anxiety symptoms remitted. This improvement persisted through the one-month post-discharge follow-up and depression eventually remitted.
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PMID:Improvement of cognition in a patient with Cotard's delusions and frontotemporal atrophy receiving electroconvulsive therapy (ECT) for depression. 1936 57

Macrophagic myofasciitis (MMF) is an emerging condition, characterized by specific muscle lesions assessing long-term persistence of aluminum hydroxide within macrophages at the site of previous immunization. Affected patients mainly complain of arthromyalgias, chronic fatigue, and cognitive difficulties. We designed a comprehensive battery of neuropsychological tests to prospectively delineate MMF-associated cognitive dysfunction (MACD). Compared to control patients with arthritis and chronic pain, MMF patients had pronounced and specific cognitive impairment. MACD mainly affected (i) both visual and verbal memory; (ii) executive functions, including attention, working memory, and planning; and (iii) left ear extinction at dichotic listening test. Cognitive deficits did not correlate with pain, fatigue, depression, or disease duration. Pathophysiological mechanisms underlying MACD remain to be determined. In conclusion, long-term persistence of vaccine-derived aluminum hydroxide within the body assessed by MMF is associated with cognitive dysfunction, not solely due to chronic pain, fatigue and depression.
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PMID:Long-term persistence of vaccine-derived aluminum hydroxide is associated with chronic cognitive dysfunction. 1974 79

Cognitive deficits are common in patients with multiple sclerosis (MS) and may be observed early in the course of the disease. Current knowledge about the association between cognitive impairment and health-related quality of life (HQOL) in patients with early MS is limited. We used a well-established battery of cognitive tests and standardized HQOL measures to examine the associations between overall and domain-specific cognitive performance and quality of life in patients with early MS. Ninety-two patients with CIS or MS diagnosed in the previous three years participating in the CLIMB Natural History Study underwent a neurologic examination, neuropsychological evaluation and quality of life assessment. Associations between cognitive scores and HQOL measures were examined. There were no differences between cognitively impaired versus unimpaired subjects on any of the HQOL measures. After controlling for depression, scores on tests of information processing speed were significantly associated with several measures of HQOL including physical well-being, fatigue, and social support. In all cases, correlations between HQOL and cognitive measures were mild. These findings were observed in patients with limited cognitive impairment and minimal physical disability. Our results suggest that cognitive remediation programs aimed at improving cognitive skills may also improve quality of life for patients with early MS.
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PMID:The association between cognitive impairment and quality of life in patients with early multiple sclerosis. 1994 29

Cognitive deficits are a common feature of major depression (MD), with largely unknown biological underpinnings. In addition to the affective and cognitive symptoms of MD, a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is commonly observed in these patients. Increased plasma glucocorticoid levels are known to render the hippocampus susceptible to neuronal damage. This structure is important for learning and memory, creating a potential link between HPA axis dysregulation and cognitive deficits in depression. In order to further elucidate how altered stress responsiveness may contribute to the etiology of MD, three mouse lines with high (HR), intermediate (IR), or low (LR) stress reactivity were generated by selective breeding. The aim of the present study was to investigate whether increased stress reactivity is associated with deficits in hippocampus-dependent memory tests. To this end, we subjected mice from the HR, IR, and LR breeding lines to tests of recognition memory, spatial memory, and depression-like behavior. In addition, measurements of brain-derived neurotrophic factor (BDNF) in the hippocampus and plasma of these animals were conducted. Our results demonstrate that HR mice exhibit hippocampus-dependent memory deficits along with decreased hippocampal, but not plasma, BDNF levels. Thus, the stress reactivity mouse lines are a promising animal model of the cognitive deficits in MD with the unique feature of a genetic predisposition for an altered HPA axis reactivity, which provides the opportunity to explore the progression of the symptoms of MD, predisposing genetic factors as well as new treatment strategies.
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PMID:Increased stress reactivity is associated with cognitive deficits and decreased hippocampal brain-derived neurotrophic factor in a mouse model of affective disorders. 2003 53

The concept of "mild cognitive impairment" (MCI) refers to alterations in cognition in the transition between normal aging and dementia. However, from a neuropsychological point of view the conventional diagnostic criteria appear not sufficiently valid. In particular, it is still difficult to differentiate between subjects with MCI and subjects with depression plus cognitive deficits on the basis of their neuropsychological profiles. The aim of this study is to compare cognitive deficit patterns of subjects with MCI and with depression. 24 subjects with MCI, 50 subjects with depression (DEP) and 20 healthy control subjects were included (age: 55-74years). The neuropsychological assessment consisted of standardized tests to assess attention, memory, and executive functions. Compared to healthy controls both subject groups showed significantly lower performance in all cognitive domains. However, we did not find significant differences in cognitive performance between MCI and DEP subjects, neither at baseline nor at follow-up. In addition, preliminary results of follow-up assessments after 2 (DEP) and 6months (MCI), respectively, revealed no significant changes in cognition in subjects with depression, regardless of whether depressive symptoms had improved. Subjects with MCI also showed no changes in cognition at follow-up. The comparable neuropsychological patterns identified in the two subject groups may be understood as a consequence of similar alterations in cognitive systems, supporting the idea of a final common pathway disorder. Thus, the cognitive deficits present in a subgroup of subjects with depression may possibly better be understood in the context of MCI.
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PMID:Neuropsychological profiles in MCI and in depression: Differential cognitive dysfunction patterns or similar final common pathway disorder? 2006 Jan 27

From a theoretical point of view it may be hypothezised that cognitive deficits are not uncommon in patients with new-onset epilepsy since causative brain lesions, genetic influences and interictal epileptic activity are likely to exist even before the first unprovoked seizure. We reviewed the literature concerning cognitive deficits in genetically determined epilepsy-syndromes and studies on cognitive and psychiatric deficits in patients with new-onset epilepsy. In several animal models hints of memory deficits or learning disorders even before the manifestation of epileptic seizures were found. Some learning disorders showed characteristics of the human attention-deficit-hyperactivity-disorder. In familial frontal epilepsies specific associations between cognitive deficits as well as psychiatric syndromes and certain mutations were described. Cognitive deficits in adult patients with new-onset epilepsy were described several times with regard to delayed recall in verbal memory, selective attention and psychomotor performance. Depression and suicide attempts were increased before the first seizure. In childhood cognitive deficits were regarded as causative factors for behavioral problems, which sometimes were even found before the first recognized seizure. Verbal memory deficits at the onset of epilepsy seemed to be a risk factor for the development of a therapy refractory course. But on the basis of the published data it is impossible to state whether cognitive deficits after a first unprovoked seizure in adulthood indicate an increased risk of recurrent seizures apart from the results of MRI and EEG studies.
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PMID:[Cognitive deficits and psychiatric disorders in patients with new-onset epilepsy]. 2009 56

Cognitive deficits, learning difficulties, and emotional problems occur at significantly higher rates in individuals with phenylketonuria (PKU) than in the general population. The relationship between elevated blood phenylalanine (Phe) levels and the severity of these problems often remain unrecognized. Children and adults with PKU require ongoing screening so that referrals to psychologists or psychiatrists familiar with metabolic disorders can be made when necessary for in-depth evaluation and treatment. To identify screening instruments that can be used by non-psychologists as well as psychologists, a group of 10 psychologists and a psychiatrist in the United States with expertise in neuropsychological assessment and PKU proposed a Uniform Assessment Method for PKU. Questionnaires were selected that reliably detect problems in adaptive behavior, executive function, and emotional well-being, representing the most vulnerable areas for individuals with PKU. These questionnaires are appropriate for individuals from infancy through adulthood, may be administered in less than 1h, have computerized scoring accessibility, have no practice effects, and are available in Spanish and English. In addition to assessing function at a single point in time, the screening measures may be administered at each clinic visit to assess changes in function related to metabolic status or treatment (e.g., Phe-restricted diet, food supplements). The following questionnaires comprise the Uniform Assessment Method for PKU: for 0-2 years, Adaptive Behavior Assessment System-Second Edition (ABAS-II); for 2-17 years, Behavior Rating Inventory of Executive Function (BRIEF) and Behavior Assessment System for Children-Second Edition (BASC-II); and for adults, BRIEF, Beck Anxiety Inventory (BAI), and Beck Depression Inventory-Second Edition (BDI-II). In addition to long-term monitoring of outcomes in PKU, this uniform screening approach facilitates PKU research, as data may be pooled across multiple clinics using a consistent battery of assessment measures.
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PMID:Screening for cognitive and social-emotional problems in individuals with PKU: tools for use in the metabolic clinic. 2012 79

We have previously reported that 14-d chronic intermittent cold (CIC) stress induced a cognitive deficit in reversal learning on the rat attentional set-shifting test. This effect may be related to dysregulation of 5-HT function in orbitofrontal cortex, as a model of cognitive dysfunction in depression. To test the ability of chronic antidepressant drug treatment to reverse the cognitive deficit induced by CIC, it was first necessary to assess the temporal characteristics of the CIC-induced cognitive deficit. Thus, in the first experiment, we assessed the duration of the cognitive deficit following 2-wk CIC stress. Replicating previous experiments, CIC induced a reversal learning deficit tested 3 d after the last cold exposure. However, cognitive performance of CIC-stressed rats was no different from unstressed controls when tested 7, 14 or 21 d after termination of the stress treatment. We next compared behaviour 3 d after 2-wk CIC to that seen 3 d after 5-wk CIC, and found similar deficits in reversal learning. Thus, in the final experiment, antidepressant drug treatment was initiated after 2-wk CIC stress, and was maintained for 3 wk, concurrent with the continuation of CIC stress. Both chronic and acute treatment with the selective serotonin reuptake inhibitor, citalopram, but not the norepinephrine reuptake blocker, desipramine, reversed the cognitive deficit induced by CIC stress. Thus, this stress-induced cognitive deficit may be a useful model for cognitive deficits related to prefrontal cortical hypoactivity in depression, and for investigating neurobiological mechanisms underlying the beneficial effects of chronic antidepressant drug treatment.
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PMID:A cognitive deficit induced in rats by chronic intermittent cold stress is reversed by chronic antidepressant treatment. 2014 67

A large body of documented evidence has found that smoking during pregnancy is harmful to both the mother and the fetus. Prenatal exposure to nicotine in various forms alters neurologic development in experimental animals and may increase the risk for neurologic conditions in humans. There is a positive association between maternal smoking and sudden infant death syndrome (SIDS); however, the connection between nicotine addiction, depression, attention disorders, and learning and behavior problems in humans is not straightforward. Nicotine's action on the production and function of neurotransmitters makes it a prime suspect in the pathology of these diseases. Nicotine accentuates neurotransmitter function in adults but desensitizes these functions in prenatally exposed infants and children. This desensitization causes an abnormal response throughout the lifespan. Furthermore, nicotine use by adolescents and adults can alleviate some of the symptoms caused by these neurotransmitter problems while they increase the risk for nicotine addiction. Although nicotine replacement drugs are used by pregnant women, there is no clear indication that they improve outcomes during pregnancy, and they may add to the damage that occurs to the developing neurologic system in the fetus. Understanding the effects of nicotine exposure is important in providing safe care for pregnant women, children, and families and for developing appropriate smoking cessation programs during pregnancy.
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PMID:The long-term effects of prenatal nicotine exposure on neurologic development. 2018 33


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