1. Al-Qabandi M, Gorter JW, Rosenbaum P. {{Early Autism Detection: Are We Ready for Routine Screening?}}. {Pediatrics};2011 (Jun 13)
BACKGROUND: Autism is a serious neurodevelopmental disorder that has a reportedly rising prevalence rate. The American Academy of Pediatrics recommends that screening for autism be incorporated into routine practice. It is important to consider the pros and cons of conducting autism screening as part of routine practice and its implications on the community. We have explored this question in the context of screening from a scientific point of view. Method: A literature search was conducted to assess the effectiveness of community screening programs for autism. Results: Judged against critical questions about autism, screening programs failed to fulfill most criteria. Good screening tools and efficacious treatment are lacking, and there is no evidence yet that such a program would do more good than harm. Conclusions: On the basis of the available research, we believe that we do not have enough sound evidence to support the implementation of a routine population-based screening program for autism. Ongoing research in this field is certainly needed, including the development of excellent screening instruments and demonstrating with clinical trials that such programs work and do more good than harm.
2. Baker JK, Seltzer MM, Greenberg JS. {{Longitudinal effects of adaptability on behavior problems and maternal depression in families of adolescents with autism}}. {J Fam Psychol};2011 (Jun 13)
Research on families of individuals with autism has tended to focus on child-driven effects utilizing models of stress and coping. The current study used a family systems perspective to examine whether family level adaptability promoted beneficial outcomes for mothers and their adolescents with autism over time. Participants were 149 families of children diagnosed with autism who were between the ages of 10 and 22 years during the 3-year period examined. Mothers reported on family adaptability, the mother-child relationship, their own depressive symptoms, and the behavior problems of their children at Wave 1, and these factors were used to predict maternal depression and child behavior problems 3 years later. Family level adaptability predicted change in both maternal depression and child behavior problems over the study period, above and beyond the contribution of the dyadic mother-child relationship. These associations did not appear to depend upon the intellectual disability status of the individual with autism. Implications for autism, parent mental health, family systems theory, and intervention with this population are discussed. (PsycINFO Database Record (c) 2011 APA, all rights reserved).
3. Mironov S, Skorova E, Hartelt N, Mironova LA, Hasan MT, Kugler S. {{Erratum to: Remodelling of the respiratory network in a mouse model of Rett syndrome depends on brain-derived neurotrophic factor regulated slow calcium buffering by S. L. Mironov, E. Skorova, N. Hartelt, L. A. Mironova, M. T. Hasan, and S. Kugler. J Physiol June 1, 2009 587 (11) 2473-2485; doi:10.1113/jphysiol.2009.169805}}. {J Physiol};2011 (Jun 13)
The article by Mironov et al. (2009) contained an error in Fig. 7B. Figure 7 should have appeared as follows. It should be noted that the error does not alter results or discussion in the text.
4. Siller SS, Broadie K. {{Neural circuit architecture defects in a Drosophila model of Fragile X syndrome are alleviated by minocycline treatment and genetic removal of matrix metalloproteinase}}. {Dis Model Mech};2011 (Jun 13)
Fragile X syndrome (FXS), caused by loss of the fragile X mental retardation 1 (FMR1) product (FMRP), is the most common cause of inherited intellectual disability and autism spectrum disorders. FXS patients suffer multiple behavioral symptoms, including hyperactivity, disrupted circadian cycles, and learning and memory deficits. Recently, a study in the mouse FXS model showed that the tetracycline derivative minocycline effectively remediates the disease state via a proposed matrix metalloproteinase (MMP) inhibition mechanism. Here, we use the well-characterized Drosophila FXS model to assess the effects of minocycline treatment on multiple neural circuit morphological defects and to investigate the MMP hypothesis. We first treat Drosophila Fmr1 (dfmr1) null animals with minocycline to assay the effects on mutant synaptic architecture in three disparate locations: the neuromuscular junction (NMJ), clock neurons in the circadian activity circuit and Kenyon cells in the mushroom body learning and memory center. We find that minocycline effectively restores normal synaptic structure in all three circuits, promising therapeutic potential for FXS treatment. We next tested the MMP hypothesis by assaying the effects of overexpressing the sole Drosophila tissue inhibitor of MMP (TIMP) in dfmr1 null mutants. We find that TIMP overexpression effectively prevents defects in the NMJ synaptic architecture in dfmr1 mutants. Moreover, co-removal of dfmr1 similarly rescues TIMP overexpression phenotypes, including cellular tracheal defects and lethality. To further test the MMP hypothesis, we generated dfmr1;mmp1 double null mutants. Null mmp1 mutants are 100% lethal and display cellular tracheal defects, but co-removal of dfmr1 allows adult viability and prevents tracheal defects. Conversely, co-removal of mmp1 ameliorates the NMJ synaptic architecture defects in dfmr1 null mutants, despite the lack of detectable difference in MMP1 expression or gelatinase activity between the single dfmr1 mutants and controls. These results support minocycline as a promising potential FXS treatment and suggest that it might act via MMP inhibition. We conclude that FMRP and TIMP pathways interact in a reciprocal, bidirectional manner.
