26 research outputs found

    Women's mental health in Mozambique: is maternity a protective factor?

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    Abstract Backgroud Globally, women have been shown to have high rates of common mental disorders (CMDs). In low and middle-income countries (LMICs), women face significant challenges related to maternity. However, no study has compared mental health problems among pregnant/post-partum women, childless women of childbearing age, and women with children in a low-income country. We sought to compare the frequency of CMD and suicide risk in a sample of women presenting or accompanying patients in primary care in two Mozambican semi-urban settings. Methods We administered the MINI International Neuropsychiatric Interview to 853 women, of whom 220 (25.8%) were pregnant/post-partum, 177 (20.8%) were non-pregnant and childless, and 456 (53.5%) were non-pregnant and with children more than 1-year-old. Logistic regression models compared the likelihood of a psychiatric disorder across groups, adjusting for sociodemographic and chronic-illness covariates. Results We found a high frequency of CMD and suicide risk among all women in this low-income context sample. In adjusted models, no differences in rates of depression, anxiety, or panic disorder were observed among groups. However, suicide risk was higher in women without children than pregnant/post-partum women. Conclusion The frequency of CMD among women of childbearing age in our study was higher than documented rates in high-income countries and other LMIC. Additionally, we found that motherhood was not protective and that pregnancy and the postpartum period were not stages of increased risk for most disorders. This highlights the need to expand mental health services not only for perinatal women but all women of childbearing age in this and possibly similar settings

    The Child Mental Health Treatment Gap in an Urban Low-Income Setting: Multisectoral Service Use and Correlates

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    OBJECTIVE: To efficiently target capacity-building efforts for child mental health services in low- and middle-income countries (LMICs), it is critical to define how care is structured across sectors and individual-level factors. METHODS: In a community-based sample of 1,408 children and adolescents (ages 6-15 years) from Itaboraí, Brazil, the authors assessed need and service use across four care systems (mental health specialty, health, welfare, and informal). Individual-level factors included child gender and age, maternal perception of child mental health need, paternal absence, maternal education, and maternal anxiety and depression. RESULTS: The mental health treatment gap was 88%, with only 12% of children with psychiatric problems using mental health services. Children with mental health problems were more likely than those without these problems to use health and other sectors of care and to use services in more than one sector of care. Overall, 46% of the children with any clinical mental health problems and 31% of those with only internalizing problems were identified by their mothers as having a mental health need. Among those with clinical mental health problems, factors associated with mental health service use were being a boy and paternal absence but not mental health problem type or maternal awareness. CONCLUSIONS: Closing the child mental health treatment gap in urban settings in LMICs where resources are scarce will likely require system-level changes, such as engagement of diverse service sectors of care. Interventions need to target increased maternal awareness about mental health problems and encourage provision of mental health services to girls

    The LGI1–ADAM22 protein complex directs synapse maturation through regulation of PSD-95 function

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    Synapse development is coordinated by a number of transmembrane and secreted proteins that come together to form synaptic organizing complexes. Whereas a variety of synaptogenic proteins have been characterized, much less is understood about the molecular networks that support the maintenance and functional maturation of nascent synapses. Here, we demonstrate that leucine-rich, glioma-inactivated protein 1 (LGI1), a secreted protein previously shown to modulate synaptic AMPA receptors, is a paracrine signal released from pre- and postsynaptic neurons that acts specifically through a disintegrin and metalloproteinase protein 22 (ADAM22) to set postsynaptic strength. We go on to describe a novel role for ADAM22 in maintaining excitatory synapses through PSD-95/Dlg1/zo-1 (PDZ) domain interactions. Finally, we show that in the absence of LGI1, the mature synapse scaffolding protein PSD-95, but not the immature synapse scaffolding protein SAP102, is unable to modulate synaptic transmission. These results indicate that LGI1 and ADAM22 form an essential synaptic organizing complex that coordinates the maturation of excitatory synapses by regulating the functional incorporation of PSD-95

    Knockdown of SynDIG1 results in a reduction in both AMPAR and NMDAR EPSCs.

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    <p>(A+B) AMPAR- and NMDAR-mediated EPSCs recorded simultaneously from a neuron expressing shRNA to knockdown SynDIG1 and a neighboring control neuron. Scatter plots show amplitudes of EPSCs for single pairs (open circles) and mean ± SEM (filled circles). Scale bars represent 20 ms and 10 pA. Bar graphs plotting average AMPAR and NMDAR EPSCs reveal a 40% decrease in transmission after knockdown (AMPA n = 25, <i>p</i> = 0.01; NMDA n = 20, <i>p</i> = 0.01). Error bars denote SEM.</p

    SynDIG1 overexpression increases both AMPAR and NMDAR EPSCs.

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    <p>(A+B) AMPAR- and NMDAR-mediated EPSCs recorded simultaneously from a neuron overexpressing SynDIG1 and a neighboring control neuron. Scatter plots show amplitudes of EPSCs for single pairs (open circles) and means ± SEM (filled circles). Inset are example traces for wildtype (black) and transfected (green) neurons. Scale bars represent 20 ms and 20 pA. Bar graphs (right) show average AMPAR and NMDAR EPSCs normalized to control (AMPA n = 33, <i>p = </i>0.0001; NMDA n = 25, <i>p</i> = 0.0009). Error bars denote SEM.</p

    SynDIG1 expression does not alter probability of release.

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    <p>(A) Sample traces (above) and bar graph showing paired-pulse ratio mean ± SEM of control and SynDIG overexpressing cells. No change in paired pulse ratio was detected (n = 9, <i>p</i> = 0.69). (B) Sample traces (above) and bar graph showing paired-pulse ratio mean ± SEM of control and SynDIG shRNA-transfected cells. No change in paired pulse ratio was detected (n = 10, <i>p</i> = 0.71). Scale bars represent 15 ms and 10 pA.</p
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