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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depression is a multifarious disease, having an impact on most aspects of everyday life. Cognitive deficits cause considerable impairments and restraints in performance and have become one of the major clinical and research foci in recent years. According to previous work, deficits in executive functioning seem to be particularly prominent. At present only a few functional neuroimaging studies investigated the neurofunctional correlates aimed at these deficits by using specific activation tasks. These findings are somewhat controversial, revealing prefrontal hypo- as well as hyperactivation as a substrate of executive performance. This paper reviews current functional neuroimaging findings within a framework of depression as a dysfunction in limbic-cortical circuits. As a conclusion, the concept of "simple" hypofrontality does not offer a satisfactory explanation. Rather, a more dynamic model will be necessary in order to achieve a more realistic concept of executive deficits in depression.
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PMID:[Executive functions in patients with depression. The role of prefrontal activation]. 1727 98

Emerging epidemiological data indicates that diabetes is a potential predisposing factor for neuropsychiatric deficits as stroke, cerebrovascular diseases, diabetic encephalopathy, depression and anxiety. Diabetic encephalopathy, characterized by impaired cognitive functions and neurochemical and structural abnormalities, involves direct neuronal damage caused by intracellular glucose. Curcumin, a well-established phenolic antioxidant and anti-inflammatory molecule, is capable of playing an important role against amyloid and dendritic pathology and thus has neuroprotective properties. The aim of the present study was to explore the effect of curcumin (60 mg/kg; p.o.) on cognitive functions, oxidative stress and inflammation in diabetic rats. Learning and memory behaviors were investigated using a spatial version of the Morris water maze test. Acetylcholinesterase activity, a marker of cholinergic dysfunction, was increased by 80% in the cerebral cortex of diabetic rats. There was 107% and 121% rise in thiobarbituric acid reactive substance levels in cerebral cortex and hippocampus of diabetic rats, respectively. Reduced glutathione level and enzymatic activities of superoxide dismutase and catalase were decreased in both cerebral cortex and hippocampal regions of diabetic rat brain. Nitrite levels in cerebral cortex and hippocampus were increased by 112% and 94% respectively. Serum TNF-alpha, a marker for inflammation, was found to increase by 1100% in diabetic rats. Chronic treatment with curcumin (60 mg/kg; p.o.) significantly attenuated cognitive deficit, cholinergic dysfunction, oxidative stress and inflammation in diabetic rats. The results emphasize the involvement of cholinergic dysfunction, oxidative stress and inflammation in the development of cognitive impairment in diabetic animals and point towards the potential of curcumin as an adjuvant therapy to conventional anti-hyperglycemic regimens for the prevention and treatment of diabetic encephalopathy.
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PMID:Curcumin attenuates diabetic encephalopathy in rats: behavioral and biochemical evidences. 1782 93

Emerging epidemiologic data indicates that diabetes is a potential predisposing factor for neuropsychiatric deficits as stroke, cerebrovascular diseases, diabetes-associated cognitive decline, depression and anxiety. Diabetes-associated cognitive decline, characterized by impaired cognitive functions and neurochemical and structural abnormalities, involves direct neuronal damage caused by intracellular glucose. The present study was designed to investigate the effect of sesamol (3,4-methylenedioxyphenol), a phenolic antioxidant and anti-inflammatory molecule, on cognitive functions, oxidative stress and inflammation in diabetic rats. Learning and memory behaviors were investigated using a spatial version of the Morris water maze test. Acetylcholinesterase activity, a marker of cholinergic dysfunction, was increased by 80% in the cerebral cortex of diabetic rats. There was 107 and 121% rise in thiobarbituric acid reactive substance levels in cerebral cortex and hippocampus of diabetic rats, respectively. Reduced glutathione levels and enzymatic activities of superoxide dismutase and catalase were decreased in both cerebral cortex and hippocampal regions of diabetic rat brain. Nitrite levels in cerebral cortex and hippocampus was increased by 138 and 109%, respectively. Serum tumor necrosis factor-alpha, a marker for inflammation, was found to increase by 1,100% in diabetic rats. Chronic treatment with sesamol (2, 4 and 8 mg/kg; p.o.) significantly and dose-dependently attenuated cognitive deficit, reduced acetylcholinesterase, oxidative stress and inflammation in diabetic rats. The results emphasize the involvement of oxidative stress and inflammation in the development of cognitive impairment in diabetic animals and point towards the therapeutic potential of sesamol in diabetes-associated cognitive decline.
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PMID:Effect of sesamol on diabetes-associated cognitive decline in rats. 1795 23

Detailed neuropsychological assessment was performed in 86 women (48 patients with stable relapsing-remitting multiple sclerosis (MS) and 38 matched healthy controls (HC)). Patients were categorized into patients without (EDSS < or =1, n = 26) and with physical disability (EDSS > or =2, n = 22). Patients with EDSS > or =2 scored significantly (P < 0.05) higher in Beck's depression inventory (BDI) and depression scores (DS) compared to HC and patients with EDSS < or =1. No significant differences were found with respect to the use of specific coping strategies between the patient groups, who preferred active (EDSS < or =1) or distracting (EDSS > or =2) strategies. Cognitive deficits were significantly increased in MS with EDSS > or =2 with regard to visuo-construction and visual memory, in particular with respect to geometric figures, compared to MS with EDSS < or =1. Significant positive correlations of depression variables (BDI, DS and BL) and depressive as well as denying coping strategies were found. Our results showed increased depression scores and increased cognitive deficits in advanced physically disabled patients, without selection of specific coping strategies. This supports an individual MS-specific neuropsychological therapeutic approach in order to improve disease related deficits together with social functioning.
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PMID:Neuropsychological deficits but not coping strategies are related to physical disability in multiple sclerosis. 1799 54

The serotonin 5-HT(6) receptor has become a promising target for the treatment of neuropsychological diseases, such as affective disorders. Increasing evidence implicates stress and its effector system, the hypothalamic-pituitary-adrenal (HPA) axis, in the neurobiology of depression. In addition, there are important memory disturbances in stress-related psychiatric disorders that have been associated to an impairment of the HPA axis reactivity. The aim of the present work is to study the functional interactions between 5-HT(6) receptors and HPA axis. In a situation of increased HPA axis responsiveness (maternal separation, MS) no differences were found in the expression of 5-HT(6) gene in the hippocampus or frontal cortex, although serotonin levels were higher in the frontal cortex of MS rats. 5-HT(6) receptor mRNA expression increased significantly in the hippocampus in a situation of decreased glucocorticoid levels, such as adrenalectomy. Cognitive deficits associated to HPA dysfunction, such those found in the MS model, were fully reversed by administration of SB271046, a selective 5-HT(6) receptor antagonist. A chronic treatment with SB271046 did not modify CRF mRNA levels in the hypothalamus, but there was a higher glucocorticoid receptor density in the hippocampus compared to control. In contrast, in the frontal cortex, treatment with SB271046 induced a significant decrease in glucocorticoid receptor density. These data suggest that expression of 5-HT(6) receptors might be differentially regulated depending on levels of circulating adrenal corticoids. These results are discussed in terms of therapeutical approaches to the treatment of behavioral (depressive-like) and cognitive disturbances associated to an altered response to stress.
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PMID:Functional interaction between 5-HT(6) receptors and hypothalamic-pituitary-adrenal axis: cognitive implications. 1820 83

Medication nonadherence is a key clinical concern in bipolar disorder (BD) across the life span. Cognitive deficits in older adults with BD may hinder medication management ability, which, in turn, may lead to nonadherence. Using an innovative performance-based measure of medication management ability, the Medication Management Ability Assessment (MMAA), we compared performance of 29 middle-aged older community-dwelling outpatients with BD who were clinically stable (mean age, 61 years; SD, 11 years; range, 45-86 years) with those of 59 normal control subjects (NCs) and 219 outpatients with schizophrenia. The MMAA is a role-play task that simulates a medication regimen likely to be encountered by older adults. Within the BD group, we examined the relationships of MMAA scores to demographic, psychiatric symptoms severity, and the Mattis Dementia Rating Scale (DRS) scores. The BD group made 2.8 times the errors on the MMAA than NCs (BD group, 6.2; SD, 5.5 vs NCs, 2.2; SD, 2.5) and did not significantly differ from the Schizophrenia group in errors on the MMAA. Errors in the BD group were more likely to be taking in too few medications as taking in too many. Within the BD group, a significant correlation was seen between MMAA scores and the DRS Total score, but not with age, education, Brief Psychiatric Rating Scale, Hamilton Depression Rating Scale, number of psychiatric medications, or medical conditions. Among DRS subscales, the Memory Subscale correlated most strongly with MMAA errors. This small cross-sectional study suggests that deficits in medication management ability may be present in later-life BD. Neurocognitive deficits may be important in understanding problems with unintentional nonadherence.
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PMID:Assessment of medication management ability in middle-aged and older adults with bipolar disorder. 1834 36

It is well established that cognitive deficits are an almost invariable component of the schizophrenia syndrome. Much less is known about the association of cognitive deficits and the range of psychiatric disorders. The current study made use of a Swedish conscript cohort which included an IQ assessment and full psychiatric evaluation at conscription of all 18- to 19-year-old males. It was found that reduced intellectual functioning was found in association with psychosis and neurotic disorders including depression, personality disorders, alcoholism, and drug dependence. The effect was particularly strong for alcoholism. This presumably represents a combination of premorbid deficits (as demonstrated in those who developed schizophrenia some years later) plus coincident impairments. The direction of causality of this latter association is likely to be both forward and reverse. Different cognitive subtests showed varied strengths of association: "mechanical ability/knowledge," which might reflect planning and reasoning more than the other subtests, had the strongest effect. Cognitive deficits are widespread in psychiatric disorders and should be taken into account in clinical interactions.
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PMID:Impairments in cognition across the spectrum of psychiatric disorders: evidence from a Swedish conscript cohort. 1844 31

Cognitive deficits are well documented in psychiatric disorders, particularly in schizophrenia and depression. Cognitive activity roots in perceptions. However, research on sensorial alterations in psychiatric conditions has mainly focused on visual or auditory processes and less on olfaction. Here, we examine data on olfactory deficits in psychiatric patients using a systematic review of recent publications. Schizophrenic patients are mainly characterized by no reliable change in odour sensitivity and by a deficit in odour identification, recognition and discrimination. Depressed patients principally exhibit a deficit in the hedonic aspects of this perception, even if, in some case, alterations in sensitivity or identification are also found. Changes in odour perception are also found in dementia and in some neurodegenerative disease, but in this case alterations concern all aspects of the sensorial experience (detection threshold, identification and recognition). Taken together, these data indicate that olfactory abnormalities might be a marker of psychiatric conditions, with a specific pattern for each disease.
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PMID:Olfaction: a potential cognitive marker of psychiatric disorders. 1855 28

Studies were carried out using the mini mental state examination (MMSE) and the geriatric depression scale (GDS) in 71 elderly patients, in order to establish eventual correlations between cognitive deficit, depression and multiple pathologies. This examination was part of a multidimensional evaluation involving patients over 65 years of age hospitalized in the Department of Clinical Medicine. The patients were divided into 5 grades on the basis of the extent ot functional impairments (from Grade 0 to Grade IV) (British Columbia Classification). Mean MMSE and GDS scores, as well as the mean of the multiple pathologies were calculated in each group. As all the MMSE items could not always be applied, we used a score obtained by dividing the maximum score accomplished by the maximum score applicable. No MMSb impairment was present in 94.11% of the Grade 0 patients, in 57.14% of the Grade I, in 37.5% of the Grade II, and in 40% of the Grade III patients. However, impairment was present in all the Grade IV patients. GDS analysis revealed no depression in 82.35% of Grade 0 patients, in 21.43% Grade I, in 50% Grade II, in 16% Grade III patients. However, some degree of depression was present in all Grade IV patients. The occurrence of patients affected by multiple pathologies was as follows: 1-2 pathologies were recorded in 47.06% of Grade 0 patients, in 57.14% Grade I, in 37.5% Grade II, in 36% Grade III, and in 57.14% of Grade IV patients.
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PMID:Cognitive and affective assessment and multiple pathologies in institutionalized elderly. 1865 4

Interactions between brain, psyche and thyroid are known from historical descriptions of thyroidectomy (Kocher) and hyperthyroidism. However, their importance is often underscored in clinical routine. Thyroid hormone deficiency during pregnancy may result in irreversible mental retardation and requires levothyroxine substitution. TSH screening after delivery must identify newborns with congenital hypothyroidism: An early levothyroxine substitution and long term therapy control are required. Hypothyroidism and depression have many symptoms in common. Cognitive deficits and depressive states are often found in overt hypothyroidism, psychotic derangements are rare. Levothyroxine improves hypothyroid symptoms and mental performance, mood and motivation. Psychic symptoms of hyperthyroidism include agitation, irritability, mood disturbances, hyperactivity, anxiousness and even panic attacks. Manic and delusional states are rare. In geriatric patients hyperthyroidism may be oligosymptomatic. In psychiatric patients more frequent but unspecific disturbances of thyroid laboratory values being reversible without specific therapy have to be distinguished from rather rare but causative organic thyroid diseases with therapeutic consequences. Some psychiatric drugs influence thyroid laboratory results. Hypothyroidism in depressive patients is a negative prognostic parameter and requires therapy. Psychiatric symptoms associated with hypothyroidism are usually reversible under levothyroxine within 4-8 weeks. The standard for hypothyroidism is mono-levothyroxine therapy.
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PMID:[Interactions between brain, psyche and thyroid]. 1905 95


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