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 distress level of parents who had infants with Down syndrome (study parents) was compared to that of control parents of infants without disability (infants were all less than 2 years of age). Data were collected in two independent surveys. We matched subjects case-by-case on socioeconomic status. Analysis of pooled data indicated significantly greater depression for the study parents. However, effect sizes were small, and the prevalence of clinical depression was 5.56% (n = 108) among matched study parents and 4.26% (n = 188) among unmatched study parents. Parenting an infant with Down syndrome may cause less distress than previously thought.
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PMID:Psychological distress of parents of infants with Down syndrome. 932 91

In a previous report, Alzheimer's disease risk factors, including alcohol abuse, depression, Down's syndrome, cerebral glucose metabolism defect, head trauma, old age, Parkinson's disease, sleep disturbance, and underactivity, were shown to have an association with reduced cerebral blood flow. In this report an attempt is made to strengthen a hypothesis that reduced cerebral blood flow may be a required cofactor in the cause of Alzheimer's disease with examples of additional putative risks, including aluminum, ApoE 4 alleles, estrogen deficiency, family history of dementia, low education-attainment, olfactory deficit, and underactivity coupled with gender, considered to have a relationship or potential relationship with reduced cerebral blood flow. Factors, believed to ameliorate Alzheimer's disease, associated with improved or stabilized cerebral blood flow are tabulated. A tentative cerebral blood flow nomogram is shown as a potential model to possibly help predict Alzheimer's disease susceptibility.
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PMID:Alzheimer's disease risk factors as related to cerebral blood flow: additional evidence. 948 78

Many efforts have been made to trace the causes of Alzheimer's disease (AD). There are, however, many points of controversy among reports from the same country as well as among reports from different countries. The current study is a case-control study to determine the risk factors in the development of AD in Greece. Sixty-five patients with AD and 69 age-matched controls were examined. All patients with AD fulfilled the DSM-IV criteria for AD and NINCDS-ADRDA criteria for probable AD. Demographic characteristics such as gender, current marital status, who he/she is living with, education, main place of residence in childhood, adulthood, and late life, occupational hazards, patient's medical history (history of diabetes mellitus and hypertension), life habits like alcohol consumption and smoking, and a history of head trauma, heart attack, stroke, parkinsonism, or depression were collected from the subject or from an informant. A family history of selected diseases (hypertension, diabetes mellitus, dementia, Parkinson's disease, Down's syndrome, stroke) was also elicited. Ages of father and mother at birth were also recorded. Chi-square test, Kruskal-Wallis analysis of variance, cluster analysis, and logistic regression analysis were used for statistical analysis. The results (chi-square test) showed a statistically significant difference between patients with dementia of the Alzheimer type and controls as far as marital status (p = .04), the subject's history of major depressive episode (p = .02), and family history of dementia (p = .002) were concerned. Logistic regression analysis results produced a complex model of family aggregation of dementia, with patients with a history of depression and family history of dementia having an up to seven times higher risk of developing AD. These findings, especially a family history of dementia, are consistent with most of the literature.
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PMID:Risk factors for clinically diagnosed Alzheimer's disease: a case-control study of a Greek population. 951 31

Calcium is an important second messenger that affects metabolic and physiological activities of developing and mature neurons. It has been reported that electrical activity is abnormal in cultured hippocampal and DRG neurons from the trisomy 16 (Ts16) mouse, a model for Down syndrome (trisomy 21-Ts21 in human). Whole-cell voltage-clamp, radiolabeled ligand binding techniques and mRNA measurements were used to study the effect of Ts16 on voltage-dependent calcium currents in cultured fetal hippocampal neurons from the Ts16 mouse. In neither Ts16 nor control diploid neurons were low-voltage-activated calcium currents detected. However, a high-voltage-activated (HVA) calcium current was identified and shown to be dihydropyridine sensitive. The density of this HVA calcium current was 80% greater in Ts16 neurons than in control. This difference correlated with a 70% increase in binding of radiolabeled dihydropyridine, PN200-110, a marker of L-type calcium channels. However, mRNA levels encoding the alpha1C and alpha1D subunits were unchanged in the Ts16 neurons. In contrast, mRNA level of the myo-inositol transporter, the gene for which is located on mouse chromosome 16, was elevated in Ts16 neurons due to a gene-dosage effect. Therefore, it is likely that posttranscriptional regulation of dihydropyridine-sensitive voltage-dependent calcium channels is abnormal in Ts16. As dihydropyridine sensitive HVA Ca channels are implicated in heterosynaptic long-term depression and long-term potentiation, the differences reported here, if also present in the Down syndrome brain, may contribute to mental retardation in that disorder.
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PMID:Increased expression of voltage-activated calcium channels in cultured hippocampal neurons from mouse trisomy 16, a model for Down syndrome. 960 27

Parental stress was examined in socioeconomically matched samples of mothers and fathers of children with Down syndrome and typically developing children. Parents of children with Down syndrome perceived more caregiving difficulties, child-related stress (distractibility, demandingness, unacceptability), and parent-related stress (incompetence, depression, health problems, role-restriction) than did parents of typically developing children. For the combined groups of parents, mothers' stress was associated with children's caregiving difficulties; fathers' stress, with children's group status (Down syndrome, typically developing). Mothers who reported more responsibility for childcare perceived more difficulties with health, role restriction, and spousal support. Fathers who reported more responsibility for childcare perceived fewer difficulties with attachment and parental competence. Partner stress was associated both with mothers' and with fathers' stress.
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PMID:Mothers and fathers of children with Down syndrome: parental stress and involvement in childcare. 1054 13

This study assesses the longitudinal effects of an original early intervention programme on the adaptation of parents of children with a disability (Down syndrome and cleft lip/palate, i.e. DS and CLP). Variations in the effects of the programme according to the time of measurement, the type of disability and parent's gender are also examined. Globally, the results show a better adaptation among parents who participated in the intervention programme compared to those who did not participated in the programme. These parents had lower levels of parental stress, they had more positive perceptions and attitudes concerning their child's disability and their parental situation, they were more confident in their own resources and the help they could receive from others, they had lower levels of emotional distress, anxiety and depression and they perceived more emotional support from their spouse. In general, these gains were maintained throughout the year when the children were between six and 18 months of age, they were relatively similar for parents of children with DS and parents of children with CLP, as well as for mothers and fathers.
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PMID:Longitudinal effects of an early family intervention programme on the adaptation of parents of children with a disability. 1057 17

Long-term potentiation (LTP) and depression (LTD) were investigated in hippocampus of a genetic model of Down syndrome, the segmental trisomy (Ts65Dn) mouse. Field excitatory postsynaptic potentials were recorded from hippocampal slices and LTP and LTD evoked sequentially. LTP decreased whereas LTD increased significantly in Ts65Dn compared with control hippocampus.
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PMID:Increased synaptic depression in the Ts65Dn mouse, a model for mental retardation in Down syndrome. 1060 87

Studies of immune function during depression in persons without intellectual disability (ID) have revealed elevated levels of alpha2 macroglobulin (alpha2M) and an acute phase protein (APP) response. Clinical observation suggests that people with Down's syndrome (DS) may have associated genetic abnormalities in their immune systems. The APP response and alpha2M changes in depressed versus non-depressed adults with DS was the subject of the present study. The serum pan-proteinase inhibitor alpha2M, and the AP proteins c-reactive protein (CRP), alpha1 antitrypsin (alpha1AT), ceruloplasmin (Cp), beta2 Macroglobulin (beta2M), transthyretin (Trans), serum amyloid protein (SAP), and albumin (Alb) were measured in 38 adults with DS, 19 of whom were diagnosed with and 19 without depression using a sandwich enzyme-linked immunosorbent assay (ELISA). The DSM-IV criteria were used for diagnoses. Medical and neurological examinations excluded medical disorders associated with APP response. Only alpha2M and CRP were significantly different in the depressed versus non-depressed groups. The alpha2M was higher, a response similar to one observed in depressed people without ID, but the CRP was lower in the depressed group, especially in those subjects not on psychotropic medications, contrary to the expected APP response to depression. The results suggest that alpha2M elevation in depressed adults with DS is independent of the APP response. An alternative explanation for its elevation is proposed linking the core symptom of depression with the mammalian dormancy/hibernation process. Further studies are needed to confirm that alpha2M elevation is specific to depression and that it might provide a helpful marker for the diagnosis of depression in people with ID.
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PMID:Alpha2 macroglobulin elevation without an acute phase response in depressed adults with Down's syndrome: implications. 1111 19

Down syndrome (DS, trisomy 21, Ts21) is the most common known cause of mental retardation. In vivo structural brain imaging in young DS adults, and post-mortem studies, indicate a normal brain size after correction for height, and the absence of neuropathology. Functional imaging with positron emission tomography (PET) shows normal brain glucose metabolism, but fewer significant correlations between metabolic rates in different brain regions than in controls, suggesting reduced functional connections between brain circuit elements. Cultured neurons from Ts21 fetuses and from fetuses of an animal model for DS, the trisomy 16 (Ts16) mouse, do not differ from controls with regard to passive electrical membrane properties, including resting potential and membrane resistance. On the other hand, the trisomic neurons demonstrate abnormal active electrical and biochemical properties (duration of action potential and its rates of depolarization and repolarization, altered kinetics of active Na(+), Ca(2+) and K(+) currents, altered membrane densities of Na(+) and Ca(2+) channels). Another animal model, the adult segmental trisomy 16 mouse (Ts65Dn), demonstrates reduced long-term potentiation and increased long-term depression (models for learning and memory related to synaptic plasticity) in the CA1 region of the hippocampus. Evidence suggests that the abnormalities in the trisomy mouse models are related to defective signal transduction pathways involving the phosphoinositide cycle, protein kinase A and protein kinase C. The phenotypes of DS and its mouse models do not involve abnormal gene products due to mutations or deletions, but result from altered expression of genes on human chromosome 21 or mouse chromosome 16, respectively. To the extent that the defects in signal transduction and in active electrical properties, including synaptic plasticity, that are found in the Ts16 and Ts65Dn mouse models, are found in the brain of DS subjects, we postulate that mental retardation in DS results from such abnormalities. Changes in timing and synaptic interaction between neurons during development can lead to less than optimal functioning of neural circuitry and signaling then and in later life.
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PMID:On the cause of mental retardation in Down syndrome: extrapolation from full and segmental trisomy 16 mouse models. 1133 79

While a complete understanding of the pathogenesis of Alzheimer's disease (AD) remains elusive, many conclusions can be drawn from the numerous epidemiological studies undertaken to date. Prevalence and incidence estimates show consistency, following a roughly exponential pattern with a doubling of both parameters roughly every five years after age 65. Roughly 7% of the population aged 65 and over has AD. The clinical course of the disease is reasonably well established and mortality rates rise with increasing levels of cognitive deficit. Four risk factors for AD are firmly established: increasing age, the presence of the apolipoproteinE-epsilon4 allele, familial aggregation of cases, and Down's syndrome. Numerous other associations have been shown in some studies, but not in others. For example, women generally appear at higher risk than men, as do people with lower levels of education; depression is probably prodromal; head injury is an established risk factor, and may interact with the apoE gene; several occupational exposures appear hazardous, and exposure to aluminum in the water supply confers excess risk. Hypertension and other vascular symptoms appear to predispose to AD, which is now seen as nosologically closer to vascular dementia than was previously believed. Several apparently protective factors have been identified, although preventive trials based on these have so far shown minimal effectiveness. The use of non-steroidal anti-inflammatory drugs to treat arthritis is associated with a reduced risk of AD, as is estrogen use by post-menopausal women. Physical activity appears beneficial, as does a diet with high levels of vitamins B6, B12 and folate. while red wine in moderate quantities appears protective. This review concludes with a discussion of the strengths and limitations of current epidemiological methods for studying Alzheimer's disease.
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PMID:Alzheimer's disease: insights from epidemiology. 1144 98


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