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)

The term mild cognitive impairment (MCI) is used to identify individuals with worse cognitive performance than those with normal aging, and who are at risk of dementia, especially Alzheimer's disease (AD). Although the MCI concept is based on the presence of specific cognitive deficits, several studies have shown that these subjects can develop depression, disruptive behaviors (e.g., agitation, aggression), and psychosis. In this study, we examined the baseline psychiatric characteristics of 228 MCI (Mean age: 71.2, Mini-mental State Examination [MMSE] score: 25.9) and 427 mildly demented Probable AD (Mean age: 73.2; Mean MMSE score: 23.5) subjects from a referral dementia clinic. The psychiatric assessment was conducted by geriatric psychiatrists using semi-structured interviews. The proportion of subjects with major depression (MCI: 7.5% vs. Probable AD: 8%) and aggression (MCI: 10% vs. Probable AD: 12.5%) was similar in the two groups. There were more Probable AD patients with psychomotor agitation (52% vs. 38%), delusions (29% vs. 14%), and hallucinations (9% vs. 4%) than MCI subjects. Within MCI groups, we did not observe any differences between MCI subjects with amnesic syndrome versus MCI subjects with a much broader cognitive deficit. These results showed that the MCI syndrome is not circumscribed to a neuropsychological definition, but occurs with a wide range of psychiatric syndromes. Furthermore, it is possible that the development of disruptive behaviors and psychosis, in MCI subjects with no previous history of psychiatric illness, constitutes a strong indication that there is an underlying neurodegenerative disorder.
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PMID:Non-cognitive symptoms in mild cognitive impairment subjects. 1580 26

Hepatic encephalopathy is characterized by disturbances of motor and cognitive functions involving the basal ganglia. So far no standards for assessment of neuropsychiatric abnormalities (disorders of sleep, mood, anxiety and personality) in subclinical hepatic encephalopathy have been defined. Using an animal model of mild (subclinical) hepatic encephalopathy we investigated now striatum-related behaviors and cortico-striatal synaptic plasticity in rats 2 months after introduction of a portacaval shunt and sham-operated matched controls. In a novel open field portacaval shunt rats displayed less locomotor activity; unlike controls they also showed no habituation to the field and no recall of the field environment after 24 h, indicative of cognitive deficit. The elevated-plus maze test indicated no differences in fear/anxiety in the portacaval shunt animals. Tetanic stimulation of cortical afferents in magnesium-free solution evoked an N-methyl-D-aspartate-dependent long-term potentiation in sham-operated animals. In portacaval shunt animals long-term potentiation was significantly impaired. Histamine, a potent modulator of cortico-striatal transmission, induced a larger long-term depression of field potentials in control compared with portacaval shunt rats. In conclusion, a combination of electrophysiological and behavioral approaches has revealed functional changes in cortico-striatal transmission. These data are relevant for understanding the mechanisms of motor and cognitive dysfunctions in hepatic encephalopathy patients and for the development of precise psychometric tests, evaluating cognitive deficits in subclinical hepatic encephalopathy.
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PMID:Deficits in cortico-striatal synaptic plasticity and behavioral habituation in rats with portacaval anastomosis. 1603 90

Cognitive deficits related to executive functioning have been previously identified in anorexia nervosa (AN). Currently, there is limited knowledge about the degree to which other variables related to AN or executive function may influence the observed relationships. The present study examined three groups of participants, women with AN (n=22), and two control groups: women who were high in obessionality (n=20) and women who were low in obsessionality (n=21). Women reporting disordered eating over the previous 4 weeks were screened out of the control groups. Executive function was measured using the Wisconsin card sorting test (WCST) and the uses of common objects test (UCOT). In addition, depression, obsessionality and body mass index were measured. Initial analyses showed no significant differences between the groups on executive function, but moderate effect sizes were obtained for performance on UCOT total perseverations and WCST total trials. When controlling for either depression or obsessionality, the group differences on the UCOT total perseverations became significant and in the case of depression attained a large effect size. Both the AN and high obsessional groups showed significantly more perseverations than the low obsessional group. Depression appeared to suppress variance that was irrelevant to the prediction of perseverance thus enhancing the importance of group membership. It is recommended that variables strongly associated with AN be investigated in future research as this may clarify the relationship between AN and executive function.
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PMID:Executive functioning in anorexia nervosa: exploration of the role of obsessionality, depression and starvation. 1633 55

Improvement of cardiosurgery treatment and perioperative care of CABG (coronary artery bypass grafting) patients has been associated with essential reduction of early mortality. Nevertheless neurological complications have not changed. Cerebrovascular death, stroke, encephalopathy and cognitive decline remain the most common disturbances. Cognitive impairment after CABG seems to be a multifactorial problem. Demographic, medical history and perioperative factors strongly influence cognitive outcome. Incidence of decline is common immediately after surgery (53-79%), less frequent after 6 months (10-30%) and it depends on cardiosurgery method (on-pump > off-pump surgery). Early impairment is the predictor of late cognitive deficit in the 5-year follow-up. Microembolic signals, cerbral hypoperfusion and systemic inflammatory response are the main reasons of damage. Neuropsychological tests consist of verbal and non-verbal memory, visuo-spatial and construction abilities, motor speed, language and executive functions evaluation. It is proposed to perform examinations before the operation and at least 3 months after CABG Twenty per cets or 1 SD decline in at least 20% of tests will be significant. Anxiety and depression signs should be taken into consideration as well.
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PMID:[Cognitive impairment after coronary artery bypass grafting surgery]. 1642 95

Many researchers have questioned whether new potential therapies aimed at reversing Alzheimer's disease (AD) are indeed scientifically feasible. A number of approved therapies already exist for Alzheimer's disease, yet these drugs only slow the disease progression for a period of time and treat the symptoms of this devastating disease. New therapies intended to reverse the disease would necessarily need to replace dead, dying and dysfunctional neurons in affected regions of the brain. This complex drug discovery problem is further complicated by the knowledge that AD is mainly an aging disorder and that aging, though not considered a disease, causes biological changes that may also need to be overcome [1]. The requirement for new, functional neurons under neurodegenerative diseases, as seen in AD and stroke suggests that an inhibitor of neuronal death, like Memantine, is insufficient to reverse the cognitive and physical loss. New neurons, or neurogenesis, may be required for real improvement or reversal of the cognitive deficit. Adult neurogenesis, first described by Altman in the early 1960s [2, 3], has more recently been observed as a response to injury or disease. Of interest was the finding that new neurons appear to migrate to disease/injury-affected areas in the brain not normally neurogenic in the adult. This pathological-stimulation of neurogenesis does not appear sufficient to stave off the disease and subsequent behavioral decline. Therefore, the desire to amplify and improve upon the neurogenesis-response to neurodegenerative disease appears warranted, if not yet feasible. The key to doing so lies in identifying what signals are required to promote neurogenesis and neuron survival, either in injury and disease or under environmental stimuli. This could provide clues for how to pharmacologically induce neurogenesis under neurodegenerative conditions. Currently, progress in identifying therapeutics that appear to promote ameliorative neurogenesis for AD is lagging behind the pharmacological induction of neurogenesis as a therapy for depression.
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PMID:Discovery of neurogenic, Alzheimer's disease therapeutics. 1647 4

Cognitive deficits are associated with nonadherence to HIV medications. HIV-positive injecting drug users (IDUs) are at particular risk for nonadherence and cognitive barriers to adherence specific to this population should therefore be identified. The present study assessed the relation of three domains of cognitive functioning, executive functions, memory, and psychomotor speed, to self-reported antiretroviral adherence in a sample of HIV-positive IDUs. Depression, use of alcohol, heroin, cocaine/crack, or marijuana in the last week were also included in the models. Logistic regression analyses showed that only psychomotor slowing was significantly associated with nonadherence. Executive functions, memory, depression, and active alcohol and substance use were unrelated to adherence. No other studies to date have exclusively linked psychomotor slowing to nonadherence in HIV infection. Psychomotor slowing among our study sample was severe and suggests that when evident, such slowing may be a valuable determinant for antiretroviral adherence among IDUs.
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PMID:Neurocognitive aspects of medication adherence in HIV-positive injecting drug users. 1648 72

The Hordaland Homocysteine Study (HHS) is a population-based study of more than 18,000 men and women in the county of Hordaland in Western Norway. The first investigation (HHS-I) took place in 1992-93, when the subjects were aged 40-67 y. In 1997-99, a follow-up study (HHS-II) of 7,053 subjects was carried out. In this large population, plasma levels of total homocysteine (tHcy) are associated with several physiologic and lifestyle factors and common diseases. Increasing age, male sex, smoking, coffee consumption, high blood pressure, unfavorable lipid profile, high creatinine, and the MTHFR 677C > T polymorphism are among the factors associated with increased tHcy levels; physical activity, moderate alcohol consumption, and a good folate or vitamin B-12 status are associated with lower tHcy levels. Subjects with raised tHcy levels have increased risk of cardiovascular morbidity, cardiovascular and noncardiovascular mortality, and are more likely to suffer from depression and from cognitive deficit (elderly). Among women, raised tHcy levels are associated with decreased bone mineral density and increased risk of osteoporosis. Women with raised tHcy levels also have an increased risk of having suffered from pregnancy complications and an adverse pregnancy outcome. Significant associations between tHcy and clinical outcomes are usually observed for tHcy levels > 15 micromol/L, but for most conditions, there is a continuous concentration-response relation with no apparent threshold concentration. Overall, the findings from HHS indicate that a raised tHcy level is associated with multiple clinical conditions, whereas a low tHcy level is associated with better physical and mental health.
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PMID:The Hordaland Homocysteine Study: a community-based study of homocysteine, its determinants, and associations with disease. 1670 48

Depression is a frequent and important complication after stroke. The occurrence of a post-stroke-depression (PSD) has a significant impact on the functional and cognitive deficit, on mortality and on quality of life after stroke. In contrast to the clinical importance, PSD is often ignored in routine management of stroke patients and remains often untreated if diagnosed. The diagnostic uncertainty is aggravated by the lack of appropriate diagnostic criteria for PSD in the International Classification of Diseases (ICD-10) used in Germany. For the first time, we present an algorithm, which allows for a standardized examination of stroke patients on the presence of PSD. All stroke patients should be examined initially by a short and simple screening tool and are subjected to more extensive procedures only if PSD is assumed based on the screening result. Furthermore potentials and limitations to convert the diagnosis of PSD into a diagnostic related group (DRG) that is used to calculate the hospital's reimbursement are highlighted. Finally pharmacological treatment options for PSD are discussed.
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PMID:[Post-stroke-depression. Algorithm for a standardized diagnostic approach in clinical routine]. 1675 37

Prenatal stress can cause long-term effects on cognitive functions in offspring. Hippocampal synaptic plasticity, believed to be the mechanism underlying certain types of learning and memory, and known to be sensitive to behavioral stress, can be changed by prenatal stress. Whether enriched environment treatment (EE) in early postnatal periods can cause a recovery from these deficits is unknown. Experimental animals were Wistar rats. Prenatal stress was evoked by 10 foot shocks (0.8 mA for 1s, 2-3 min apart) in 30 min per day at gestational day 13-19. After weaning at postnatal day 22, experimental offspring were given the enriched environment treatment through all experiments until tested (older than 52 days age). Electrophysiological and Morris water maze testing was performed at 8 weeks of age. The results showed that prenatal stress impaired long-term potentiation (LTP) but facilitated long-term depression (LTD) in the hippocampal CA1 region in the slices. Furthermore, prenatal stress exacerbated the effects of acute stress on hippocampal LTP and LTD, and also impaired spatial learning and memory in the Morris water maze. However, all these deficits induced by prenatal stress were recovered by enriched environment treatment. This work observes a phenomenon that may contribute to the understanding of clinically important interactions among cognitive deficit, prenatal stress and enriched environment treatment. Enriched environment treatment on early postnatal periods may be one potentially important target for therapeutic interventions in preventing the prenatal stress-induced cognitive disorders.
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PMID:Enriched environment treatment restores impaired hippocampal synaptic plasticity and cognitive deficits induced by prenatal chronic stress. 1704 88

Cognitive deficits are increasingly considered as essential in schizophrenic disorders. Positive symptoms and cognitive deficits have been found to be independent, whereas negative symptoms show only weak correlations to cognitive impairment. However, the relationship to a third symptom dimension, disorganization, is yet unclear. In a sample of n = 151 schizophrenia inpatients (DSM-IV/SCID) we assessed cognitive impairment using a comprehensive neuropsychological test battery and symptoms of schizophrenia applying the Positive and Negative Syndrome Scale (PANSS). Factor analyses resulted in three neuropsychological (attention, memory, abstraction) and five symptom factor scores (negative, impulsiveness, positive, disorganization, depression). The disorganization factor did not correlate significantly with any of the neuropsychological factor scores. Even after controlling for different demographic and clinical variables partial correlation coefficients did not reach a significant level. Thus, we could not confirm the previously reported associations between disorganization and measures of cognitive impairment. Despite a considerable conceptual overlap between interview based symptom ratings and classic neuropsychological tests the empirical association is limited. Our results suggest that disorganization and cognitive impairment represent different symptom dimensions.
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PMID:Disorganization and cognitive impairment in schizophrenia: independent symptom dimensions? 1716 77


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