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)

With the development of new treatments, there is an increasing need for early diagnosis of sporadic Alzheimer's disease. Therefore, biological markers allowing positive diagnosis early in the course of the disease are highly desirable. Cerebrospinal fluid levels of protein tau were shown to be significantly increased in patients with Alzheimer's disease. Although sensitivity is high, poor specificity limits the diagnostic value of this marker. The same is true for the 42 amino acid isoform of beta-amyloid protein that is significantly decreased in cerebrospinal fluid of Alzheimer's disease patients. However, combining both markers could improve specificity at least allowing differentiation between Alzheimer's disease, normal ageing and depressive pseudodementia. Other biological markers such as cerebrospinal fluid levels of neurotransmitters, cytokines or superoxide dismutase were shown to have even less diagnostic value. The apolipoprotein epsilon 4 allele is a risk factor for Alzheimer's disease but not a diagnostic marker as many individuals who inherit epsilon 4 do not develop the disease. Till now, a single diagnostic marker allowing discrimination between Alzheimer's disease and other dementias does not exist. Combined cerebrospinal fluid levels of beta-amyloid protein and tau protein might be used as a marker that helps discriminating Alzheimer's disease from normal ageing and depression.
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PMID:Biological and genetic markers of sporadic Alzheimer's disease. 1133

The epsilon4 allele of apolipoprotein (apo E) is one of the risk factors for late-onset Alzheimer's disease (AD). We evaluated the association between apo E genotypes and depression in patients with AD. A psychiatrist interviewed all patients and their caregivers for depression using a Chinese version of the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, and for the severity of depression using the Hamilton Depression Rating Scale (HDRS). Twenty-five of the 149 patients with AD were diagnosed with depressive disorders. The numbers of patients in each apo E genotype were 10 in epsilon2/3, 2 in epsilon2/4, 74 in epsilon3/3, 46 in epsilon3/4, and 17 in epsilon4/4. We did not find an association between depression and the presence or absence of the epsilon4 or epsilon2 allele. The HDRS scores were not different in patients with AD with the epsilon4 or epsilon2 allele or in those patients without them. Our study did not find an association between depression and the apo E epsilon4 or epsilon2 allele in AD.
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PMID:Lack of association between the apolipoprotein E genotype and depression in Alzheimer's disease. 1193 39

We examined individual-difference variables in relation to the rate of change in global cognitive performance, measured by the MMSE, from 3 years prior to diagnosis of Alzheimer's disease (AD) to the time of diagnosis. The population-based sample consisted of 230 incident AD persons who were followed over a 3-year interval. The average annual decline in MMSE was 1.81 points. Being older and acquiring additional diseases during the 3 years preceding diagnosis predicted a faster rate of decline in global cognitive functioning. However, other individual difference variables such as sex, education, depression, vitamin levels (vitamin B12 and folic acid), apolipoprotein status, and social network did not precipitate the rate of decline in the preclinical phase of AD.
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PMID:Predictors of cognitive change from preclinical to clinical Alzheimer's disease. 1525 92

There is increasing recognition that coronary artery bypass grafting (CABG) may be a risk factor for subtle cognitive decline although the presence and pattern of such decline has varied across studies. Cognitive deficits may present as short-term memory loss, executive dysfunction and psychomotor slowing. Although they are usually are not severe enough to meet criteria for mild cognitive impairment or vascular dementia, they lower quality of life and add to hospitalization and out-of-hospital costs. Proposed mechanisms include surgical-related trauma, genetic susceptibility (eg, apolipoprotein E4 allele), microembolization, other vascular or ischemic changes, and temperature during surgery. Depression and anxiety levels predict subjective perception of these deficits more than objective cognitive performance. Both nonpharmacologic (eg, emboli reduction, temperature, or glucose management) and pharmacologic (eg, dexanabinol, glypromate, nootropics) strategies to prevent post-CABG cognitive deficits are under investigation. Given the large numbers of subjects who may already have CABG associated cognitive deficits, clinical trials of agents being tested for Alzheimer's disease (eg, donepezil, rivastigmine, memantine, neramexane, ginkgo) may also be informative. The results of multicenter long-term outcome studies (with matched control groups) as well as ongoing treatment trials will more conclusively address some of these issues. These data emphasize the need for clinicians to monitor cognitive function before and after coronary bypass surgery, and to educate patients.
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PMID:Cognitive deficits following coronary artery bypass grafting: prevalence, prognosis, and therapeutic strategies. 1544 86

Several lines of evidence suggest that loss of estrogen after menopause may play a role in the cognitive declines associated with Alzheimer's disease (AD). Women with Down syndrome (DS) experience early onset of both menopause and AD. This timing provides a model to examine the influence of endogenous estrogen deficiency on risk of AD. We hypothesized that low serum levels of bioavailable estradiol (E2) would be associated with increased risk of AD. One hundred and nineteen postmenopausal women with DS, 42-59 years of age, were ascertained through the New York State developmental disability service system and followed at 18-month intervals. Information from cognitive assessments, caregiver interviews, medical record review and neurological examination was used to establish the diagnosis of dementia. Women with DS who developed AD had lower levels of bioavailable E2, lower levels of total estradiol, higher levels of sex-hormone binding globulin, and lower levels of dehydroepiandrosterone sulfate at baseline than women who remained dementia free over the course of follow-up. Women who had low levels of bioavailable E2 at baseline were four times as likely to develop AD (HR=4.1, 95% CI: 1.2-13.9) and developed AD, on average, 3 years earlier, than those with high levels of bioavailable E2, after adjustment for age, level of mental retardation, ethnicity, body mass index, history of hypothyroidism or depression and the presence of the apolipoprotein varepsilon4 allele. Our findings support the hypothesis that reductions in estrogen following menopause can contribute to the cascade of pathological processes leading to AD.
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PMID:Bioavailable estradiol and age at onset of Alzheimer's disease in postmenopausal women with Down syndrome. 1692 67

The present study examined the influence of genetic polymorphisms in the apolipoprotein (APOE) and the butyrylcholinesterase (BCHE) gene on GC secretion, cognition and personality in 66 healthy older adults. These particular variables were chosen given that they have been shown to be associated with human stress (i.e.stress markers). Measures included basal serum GC levels and cognitive scores on declarative memory obtained annually over 3 years. Also, self-esteem, neuroticism and depression were evaluated. Results showed that participants with the APOE E4-BCHE K variant (E4-K group) present increased basal levels of GCs and poorer cognitive performance when compared to non-carriers of these variants. In addition, the E4-K group reported lower self-esteem and higher levels of depression. These findings may indicate a genotype effect on markers of stress and cognitive integrity years before symptoms of dementia are apparent.
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PMID:Influence of genetic polymorphisms in the apolipoprotein (APOE) and the butyrylcholinesterase (BCHE) gene on stress markers in older adults: a 3-year study. 1799 34

Half the patients with mild cognitive impairment (MCI) will develop dementia over a four-year period. The scientific literature was searched and analysed for predictors of rapid decline (MCI-plus) in patients with MCI. The most important predictors of fast cognitive deterioration were found to be: old age, previous rapid decline, severity and multiplicity of cognitive deficits, somatic co-morbidity, vascular and Alzheimer-type changes in the brain, Alzheimer-type cerebrospinal fluid findings and apolipoprotein E4 polymorphism. Many patients with MCI suffer from anxiety, depression or apathy and subtle, but subjectively significant, difficulties in the activities of daily living. It is concluded that MCI-plus offers a window for medical and psychological prophylaxis and rehabilitation.
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PMID:[Mild cognitive impairment with predictors of rapid decline]. 1839 97

The elderly population is currently increasing. In this population there is a high incidence of cognitive decline and dementia, which has a negative influence on personal life and family functioning, as well as economic and healthcare repercussions. The present article aims to indicate possible predictors of cognitive decline with a view to predicting this situation and intervening before the cognitive impairment is unavoidable. Some predictors of cognitive impairment could be the following: age, sex, education, a family history of dementia, objective and subjective difficulties with memory, several medical problems (hypertension and diabetes), sensory-motor difficulties, hypometabolism in some cerebral areas, reduced hippocampal size, carrying one or two apolipoprotein e4 alleles, a low score in cognitive tasks (especially immediate and delayed recall), deficits in associative learning and naming, low cognitive plasticity, depression, a low literacy level, poor general cognitive functioning, low participation in social activities, low physical activity, lack of social support, the use of medication and, finally, sleep-related problems. All of these factors could be important in predicting cognitive decline in very old age.
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PMID:[Predictors of cognitive decline in the elderly]. 1959 85

Studies suggest a link between bone loss and Alzheimer's disease. To examine bone mineral density (BMD) in early Alzheimer's disease (AD) and its relationship to brain structure and cognition, we evaluated 71 patients with early stage AD (Clinical Dementia Rating (CDR) 0.5 and 1) and 69 non-demented elderly control participants (CDR 0). Measures included whole body BMD by dual energy x-ray absorptiometry (DXA) and normalized whole brain volumes computed from structural MRI scans. Cognition was assessed with a standard neuropsychological test battery. Mean BMD was lower in the early AD group (1.11 +/- 0.13) compared to the non-demented control group (1.16 +/- 0.12, p = 0.02), independent of age, gender, habitual physical activity, smoking, depression, estrogen replacement, and apolipoprotein E4 carrier status. In the early AD group, BMD was related to whole brain volume (b = 0.18, p = 0.03). BMD was also associated with cognitive performance, primarily in tests of memory (logical memory [b = 0.15, p = 0.04], delayed logical memory [b = 0.16, p = 0.02], and the selective reminding task - free recall [b = 0.18, p = 0.009]). BMD is reduced in the earliest clinical stages of AD and associated with brain atrophy and memory decline, suggesting that central mechanisms may contribute to bone loss in early AD.
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PMID:Bone density and brain atrophy in early Alzheimer's disease. 1966 21

Depression associated with low plasma amyloid-beta peptide 42 (Abeta42) leading to a high ratio of Abeta40/Abeta42, a biomarker of Alzheimer disease (AD), may represent a unique depression subtype. The relationship between low plasma Abeta42 in depression and the major risk factor of AD, apolipoprotein E4 (ApoE4), is unknown. With the goal of clarifying this relationship, we analyzed 1060 homebound elders with ApoE characterization and depression status in a cross-sectional study. Plasma Abeta40 and Abeta42 were measured, and cognition were evaluated. In the absence of the ApoE4 allele, depressed subjects had lower plasma Abeta42 [median (Q1, Q3): 17.1 (11.6, 27.8) vs. 20.2 (12.9, 32.9) pg/mL, P=0.006], a higher Abeta40/Abeta42 ratio [median (Q1, Q3): 7.1 (4.6, 11.3) vs. 6.9 (3.4, 9.7), P=0.03], and lower cognitive function (mean+/-SD of Mini-Mental State Examination: 24.5+/-3.1 vs. 25.5+/-3.3, P<0.0001) than those without depression. In contrast, these relationships were not observed in the presence of ApoE4. Instead, regardless the depression status ApoE4 carriers had lower plasma Abeta42 and a higher Abeta40/Abeta42 ratio than non-ApoE4 carriers. Using multivariate logistic regression, it was found that depression was not associated with ApoE4 allele, but with the interaction between plasma Abeta42 and ApoE4 (odds ratio=3.94, 95% confidence interval=1.50, 10.33, P=0.005), denoting low plasma Abeta42 in the absence of ApoE4. Both ApoE4 carriers and non-ApoE4 carriers with depression had lower Abeta42 and a higher Abeta40/Abeta42 ratio in plasma compared with non-ApoE4 carriers without depression in the homebound elderly. As a combination of low plasma Abeta42 and high plasma Abeta40 has been shown to increase the risk of AD in 2 large cohort studies, amyloid-associated depression shown in this study may suggest a risk factor of AD in the absence of ApoE4.
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PMID:Depression and plasma amyloid beta peptides in the elderly with and without the apolipoprotein E4 allele. 1981 66


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