UMLS:C0011570 - FACTA Search

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 present study explores neuropsychological functioning in patients with depression with reference to key clinical, etiological and genetic features. In comparison to healthy volunteers, patients with severe depression demonstrated poorer performance on all neuropsychological tests except for WAIS-R Vocabulary and a 64-item computerized version of the Wisconsin Card Sorting Test. On average, patients exhibited significant impairments (greater than -2 standard deviation units) on tests of simple reaction time, Part B of the Trail Making Test and Raven's Colored Progressive Matrices. When performance decrements were analyzed with reference to key clinical features, patients with melancholia performed more poorly on WAIS-R Vocabulary, semantic fluency and choice reaction time than those with nonmelancholic depression. After controlling for age, those patients with late-onset depression (i.e., age of onset > or =50 years) exhibited poorer performance on a computerized version of the Tower of London test in comparison to those with an early onset. While there was no relationship between neuropsychological test scores and summed vascular risk factors or apolipoprotein E genotypes, presence of the methylenetetrahydrofolate reductase gene mutation was associated with slowed reaction time. The differential relationships between clinical, etiological and genetic risks and neuropsychological performance supports the presence of unique pathophysiological mechanisms in distinct subgroups of patients. These findings underscore the need to consider subtypes when investigating neuropsychological deficits in patients with depression.
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PMID:Neuropsychological performance in patients with depression is associated with clinical, etiological and genetic risk factors. 1368 Apr 63

The epsilon4 allele of apolipoprotein E (APOE), and the plasma levels of APOE, amyloid beta-protein precursor, amyloid beta1-40 (Abeta40) and homocysteine (Hcy) have all been correlated with the presence of dementia. Mutations in the methylnetetrahydrofolate reductase enzyme (MTHFR) have been associated with elevated levels of Hcy. This study explored the association of these factors with cognition and depression in community dwelling older men. Two hundred and ninety-nine men, mean age 78.9 years (SD 2.8), were studied in this cross-sectional survey. Mean plasma Hcy was 13.5 (SD 5.3) micromol/L. The MTHFR genotype had no obvious impact on Hcy levels. Ln Hcy and Ln Abeta40 were both inversely correlated with calculated glomerular filtration rate (cGFR), r = -0.41 (p < 0.001) and r = -0.28 (p < 0.001), respectively. There was a positive correlation between Ln Hcy and Ln Abeta40, r = 0.19 (p < 0.001), which remained significant after adjusting for cGFR, with a doubling of Hcy associated with a 24% increase of Abeta40. The e4 allele was associated with increased depressive symptoms as measured by the Geriatric Depression Scale-15, Odds ratio (OR) = 2.59 (95%CI 1.06-6.34) and poorer performance on the Clock Drawing Test, OR = 2.32 (95% CI: 1.25-4.29). There was a positive association between Abeta40 and Hcy, even after adjustment for cGFR in this sample of well, community dwelling older men. This association may help elucidate the link between elevated levels of Hcy and Alzheimer's disease.
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PMID:Homocysteine, Alzheimer genes and proteins, and measures of cognition and depression in older men. 1520 87

The apolipoprotein E (APOE) polymorphism is associated with neurodegenerative diseases. Its role regarding psychiatric disorders is controversial. It has been suggested to affect antidepressant treatment response and response to electroconvulsive therapy (ECT). In the present study, the association between APOE polymorphism and response to ECT in 119 patients with major depressive disorder was investigated. Moreover, a relation between APOE polymorphism and the age of onset of depression as well as the cognitive outcome of ECT was studied. In the whole population, no association was found between APOE polymorphism and response to ECT. However, in nonpsychotic patients, the epsilon2 allele tended to be more frequent in responders than nonresponders. Earlier onset of depression was observed in the patients with epsilon4 allele in late-life depression. There was no association between the APOE genotype and the cognitive change caused by ECT in the population as a whole. In women, however, epsilon2 allele may play a protective and epsilon4 allele a deleterious role in cognition during ECT.
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PMID:The apolipoprotein E polymorphism is not associated with response to electroconvulsive therapy in major depressive disorder. 1579 Nov 70

This study investigated the contribution that white matter changes (WMCs) make to clinical and cognitive features in Alzheimer's disease (AD), independently of possible confounders such as cortical atrophy and the apolipoprotein E genotype as well as their relationship to vascular risk factors. We semiquantitatively assessed the degree and location of WMCs (global, periventricular and deep white matter), lacunes and global atrophy on brain MRI scans of 86 AD cases, extensively evaluated from a clinical and neuropsychological point of view. Multivariate logistic and linear regression analysis showed that age was the only significant predictor of all WMC measures and revealed a significant association of periventricular WMCs with performance on executive function tasks as well as of deep WMCs with history of mood depression. Our results underline the significance of WMC location over size in the occurrence of specific cognitive deficits in AD.
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PMID:Alzheimer's disease: role of size and location of white matter changes in determining cognitive deficits. 1619 26

We investigated the conversion rate and the risk factors for conversion to dementia from questionable dementia in 124 ethnic Chinese subjects with questionable dementia at a memory clinic of a university hospital. They were evaluated annually based on cognitive testing, the clinical dementia rating scale, and a psychiatrist's interview for depression and anxiety. Apolipoprotein E genotyping was performed on 111 of these questionable dementia subjects. All subjects were evaluated at least twice during the follow-up period of 20.4 +/- 12.4 months. During that period, 42 questionable dementia subjects were diagnosed as having Alzheimer's disease, with an annual conversion rate to dementia of 19.9%. Compared with the 82 nonconverters, the 42 converters were significantly older, had lower cognitive, depression, and anxiety scores, and a higher frequency of the apolipoprotein E epsilon4 allele. Cox regression analysis revealed that the Alzheimer's disease converters had lower scores for orientation, short-term memory, and anxiety, and a higher frequency of the apolipoprotein E epsilon4 allele than the nonconverters.
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PMID:Conversion to dementia from questionable dementia in an ethnic Chinese population. 1754 76

Psychotic symptoms in Parkinson's disease (PD) are relatively common and, in addition to creating a disturbance in patients' daily lives, have consistently been shown to be associated with poor outcome. Our understanding of the pathophysiology of psychosis in PD has expanded dramatically over the past 15 years, from an initial interpretation of symptoms as dopaminergic drug adverse effects to the current view of a complex interplay of extrinsic and disease-related factors.PD psychosis has unique clinical features, namely that it arises within a context of a clear sensorium and retained insight, there is relative prominence of visual hallucinations and progression occurs over time. PD psychosis tends to emerge later in the disease course, and disease duration represents one risk factor for its development. The use of anti-PD medications (particularly dopamine receptor agonists) has been the most widely identified risk factor for PD psychosis. Other risk factors discussed in the literature include older age, disease severity, sleep disturbance, cognitive impairment, dementia and/or depression.Recent efforts have aimed to explore the complex pathophysiology of PD psychosis, which is now known to involve an interaction between extrinsic, drug-related and intrinsic, disease-related components. The most important extrinsic factor is use of dopaminergic medication, which plays a prominent role in PD psychosis. Intrinsic factors include visual processing deficits (e.g. lower visual acuity, colour and contrast recognition deficits, ocular pathology and functional brain abnormalities identified amongst hallucinating PD patients); sleep dysregulation (e.g. sleep fragmentation and altered dream phenomena); neurochemical (dopamine, serotonin, acetylcholine, etc.) and structural abnormalities involving site-specific Lewy body deposition; and genetics (e.g. apolipoprotein E epsilon4 allele and tau H1H1 genotype). Preliminary reports have also shown a potential relationship between deep brain stimulation surgery and PD psychosis.When reduction in anti-PD medications to the lowest tolerated dose does not improve psychosis, further intervention may be warranted. Several atypical antipsychotic agents (i.e. clozapine, olanzapine) have been shown to be efficacious in reducing psychotic symptoms in PD; however, use of clozapine requires cumbersome monitoring and olanzapine leads to motor worsening. Studies of ziprasidone and aripiprazole are limited to open-label trials and case reports and are highly variable; however, it appears that while each may be effective in some patients, both are associated with adverse effects. While quetiapine has not been determined efficacious in two randomized controlled trials, it is a common first-line treatment for PD psychosis because of its tolerability, ease of use and demonstrated utility in numerous open-label reports. Cholinesterase inhibitors currently represent the most promising pharmacological alternative to antipsychotics. Tacrine is rarely tried because of hepatic toxicity, and controlled trials with donepezil have not shown significant reductions in psychotic symptoms, due perhaps to methodological limitations. However, results from an open-label study and a double-blind, placebo-controlled trial involving 188 hallucinating PD patients support the efficacy of rivastigmine. With regard to non-pharmacological interventions, case reports suggest that electroconvulsive therapy has the potential to reduce psychotic symptoms and may be considered in cases involving concurrent depression and/or medication-refractory psychosis. Limited case reports also suggest that specific antidepressants (i.e. clomipramine and citalopram) may improve psychosis in depressed patients. Finally, studies in the schizophrenia literature indicate that psychological approaches are effective in psychosis management but, to date, this strategy has been supported only qualitatively in PD, and further studies are warranted.
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PMID:Pathophysiology and treatment of psychosis in Parkinson's disease: a review. 1866 59

Cognitive and memory complaints were assessed in 100 healthy older adults on two occasions over 2.5 years as part of a 6-year study assessing cognition, mood, and general health factors. Diminished memory for names and actions and lapses in concentration were common complaints, regardless of the individuals' actual cognitive status. No change in cognitive complaints occurred over time, even for individuals whose memory had declined over 6 years. Cognitive complaints correlated with anxiety, depression, and general mental health but not with objectively measured memory or cognition, education or age. Complaints did not differ with gender, apolipoprotein E epsilon4 genotype, cardiovascular risk factors, or intake of sedating medications. Thus, cognitive complaints could not differentiate memory-declining older adults from cognitively normal older adults and were more closely associated with mood and general mental health than actual cognitive status, age, or potential risk factors for Alzheimer's disease. Thus, the evaluation of cognitive complaints must be broad and must consider the correspondence of complaints not only to relevant measurable cognitive abilities but also to the affect of the individual.
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PMID:The nature of cognitive complaints in healthy older adults with and without objective memory decline. 1893 76

Late-onset depression often precedes the onset of dementia associated with the hippocampal degeneration. Using large deformation diffeomorphic metric mapping (LDDMM), we evaluated apolipoprotein E epsilon-4 allele (apoE E4) effects on hippocampal volume and shape in 38 depressed patients without the apoE E4, 14 depressed patients with one apoE E4, and 31 healthy comparison subjects without the apoE E4. The hippocampal volumes were manually assessed. We applied a diffeomorphic template generation procedure for creating the hippocampal templates based on a subset of the population. The LDDMM mappings were used to generate the hippocampal shape of each subject and characterize the surface deformation of each hippocampus relative to the template. Such deformation was modeled as random field characterized by the Laplace-Beltrami basis functions in the template coordinates. Linear regression was used to examine group differences in the hippocampal volume and shape. We found that there were significant hippocampal shape alternations in both depressed groups while the groups of depressed patients and the group of healthy subjects did not differ in the hippocampal volume. The depressed patients with one apoE E4 show more pronounced shape inward-compression in the anterior CA1 than the depressed patients without the apoE E4 when compared with the healthy controls without the apoE E4. Thus, hippocampal shape abnormalities in late-onset depressed patients with one apoE E4 may indicate future conversion of this group to AD at higher risk than depressed patients without the apoE E4.
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PMID:APOE related hippocampal shape alteration in geriatric depression. 1901 Apr 25

Chemotherapy-related cognitive impairment (CRCI) was first described in the 1970s, but significant recognition of CRCI did not emerge with consistency until the late 1990s. Estimates of frequency now range from 17%-75%, and evidence suggests that CRCI, or "chemobrain" as it is referred to in the lay literature, is of significant concern to patients. A variety of potentially associated factors have been identified, including age, education level, intelligence, and social support; anxiety, depression, and fatigue; disease site, stage, and comorbidities; treatment regimen, timing, duration, and concomitant therapies; and hormonal levels, cytokine levels, damage to neural progenitor cells, and the presence of the apolipoprotein E 4 allele. Controversy exists as to the most suitable neurocognitive tests to evaluate this sequeal of treatment. Neuroimaging techniques are beginning to reveal affected areas of the brain. A neuropsychologist is essential for the assessment, diagnosis, and recommendation of appropriate management strategies for this patient population. Oncology nurses should be aware of available resources, such as relevant Web sites, support groups, neuropsychologists, and cognitive retraining programs, and provide support for patients concerned about or experiencing CRCI.
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PMID:Chemotherapy-related cognitive impairment. 1964 97

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline including loss of memory, orientation and reasoning. However, a relevant aspect of AD is the presence of a variety of behavioural and psychological symptoms in dementia (BPSD), beyond the well-known progressive cognitive impairment. Approximately 50% to 80% of patients diagnosed with AD present behavioural or psychiatric disturbances such as psychosis, depression, agitation, disinhibition, aggression, hyperactivity, and socially intrusive behaviours. These symptoms may be burdensome for physicians and caregivers and lead to earlier institutionalization and increased social and economic costs. In this view, recent literature has considered the likely genetic component of BPSD in AD, defining different clusters. Several studies have investigated whether the main recognised genetic risk factor for late-onset AD, namely the apolipoprotein E (APOE) gene, is associated with BPSD, with conflicting results. The involvement of dopamine- or serotonin-related pathways and associated genetic variabilities has been demonstrated as being interesting candidates for the neuropsychiatry manifestations of dementia. Moreover, genetic variations of neurotrophins, such as brain-derived neurotrophic factor (BDNF), have been related to depression susceptibility in AD. In the present review, we summarise the current literature on genetic risk factors to BPSD susceptibility in AD and discuss future possible treatment strategies.
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PMID:Genetic susceptibility to behavioural and psychological symptoms in Alzheimer disease. 1971 53

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