ABSTRACT
Numerous cross-sectional studies confirm the long-theorized association between mothers' depression and lower parenting self-efficacy (PSE) beliefs. However, cross-sectional studies leave unanswered the direction of this association: Does depression predict PSE? Does PSE predict depression? Are both true? Does the strength of the association between depression and PSE, regardless of the direction, generalize across participant characteristics and study design features? How stable is PSE over time? And how effective are interventions at enhancing PSE? To answer these questions, we conducted a meta-analytic review of longitudinal studies. With 35 eligible studies (22,698 participants), we found support for both models: there was a significant pooled effect of both depression on PSE and of PSE on depression, with nearly identical effect sizes (d = - 0.21 and - 0.22, respectively). The association was stronger in samples with mothers' younger average age and studies that measured PSE among mothers relative to during pregnancy. We found a medium degree of stability in the index of PSE, d = 0.60. Finally, the estimated pooled effect size between being in an intervention group versus control group and PSE was 0.505. Overall, we found support for (1) bidirectional associations between depression and PSE in mothers, (2) the stability of PSE over time, and (3) the strength of the relationship between PSE and depression with intervention. These results suggest the importance of continuing to develop, test, and disseminate interventions to enhance PSE. We interpret these findings in the context of both depression and low PSE having serious consequences for child outcomes and maladaptive parenting.
Subject(s)
Mothers , Parenting , Child , Cross-Sectional Studies , Depression , Female , Humans , Pregnancy , Self EfficacyABSTRACT
Familial forms of amyotrophic lateral sclerosis (ALS) can be caused by mutations in copper, zinc-superoxide dismutase (SOD1). Mice expressing SOD1 mutants demonstrate a robust neuroinflammatory reaction characterized, in part, by up-regulation of tumor necrosis factor alpha (TNFalpha) and its primary receptor TNF-RI. In an effort to identify small molecule inhibitors of neuroinflammation useful in treatment of ALS, a microglial culture system was established to identify TNFalpha antagonists. Walker EOC-20 microglia cells were stimulated with recombinant TNFalpha, with or without inhibitors, and the cell response was indexed by NO2- output. Three hundred and fifty-five rationally selected compounds were included in this bioassay. The arachidonic acid 5-lipoxygenase (5LOX) and tyrosine kinase inhibitor nordihydroguaiaretic acid (NDGA), a natural dicatechol, was one of the most potent non-cytotoxic antagonists tested (IC50 8 +/- 3 microm). Investigation of the G93A-SOD1 mouse model for ALS revealed increased message and protein levels of 5LOX at 120 days of age. Oral NDGA (2500 p.p.m.) significantly extended lifespan and slowed motor dysfunction in this mouse, when administration was begun relatively late in life (90 days). NDGA extended median total lifespan of G93A-SOD1 mice by 10%, and life expectancy following start of treatment was extended by 32%. Disease-associated gliosis and cleaved microtubule-associated tau protein, an indicator of axon damage, were likewise reduced by NDGA. Thus, TNFalpha antagonists and especially 5LOX inhibitors might offer new opportunities for treatment of ALS.