1. Johnson NL, Simpson PM. {{Lack of father involvement in research on children with autism spectrum disorder: maternal parenting stress and family functioning}}. {Issues Ment Health Nurs};2013 (Apr);34(4):220-228.
Autism Spectrum Disorder (ASD) has an estimated prevalence of greater than 1% of people in the US. Caring for children with ASD is stressful and challenging for parents. The purpose of the study is to understand the ramifications of the findings of a spouse/father’s lack of participation for a study focused on stress and family functioning that attempted to recruit both parents of a child with ASD. The Kruskal-Wallis test compared medians of three groups of mothers of children with ASD in order to assess differences in parenting stress and family functioning discrepancy depending on their marital status and spouse survey participation. There were differences across the groups of mothers of children with ASD for the discrepancy in expectations for help, from the participants’ spouse or relatives, with family tasks, meeting the demands of other work responsibilities, child care, challenging behaviors, and school absences. Mothers of children with ASD are at risk for isolation and stress from negotiating family functions with the fathers of the children. Health care providers can assess for stress and family functioning and may anticipate different needs based on marital status and by father’s involvement in decision-making.
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2. Lucock M, Leeming R. {{Autism, seasonality and the environmental perturbation of epigenome related vitamin levels}}. {Med Hypotheses};2013 (Apr 5)
An argument is put forward for environmental modulators of photolabile or photosynthetic vitamins mediating autism risk via a complex downstream interaction of genetic/epigenetic phenomena that provide an explanation for seasonality in this and other developmentally originated disorders.
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3. Mercadante MT, Leckman JF. {{More than two dozen « autisms »}}. {Rev Bras Psiquiatr};2013 (Mar);35(1):3-4.
4. Nicolaidis C, Raymaker D. {{Healthcare Experiences of Autistic Adults}}. {J Gen Intern Med};2013 (Apr 9)
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5. Pardo CA, Buckley A, Thurm A, Lee LC, Azhagiri A, Neville DM, Swedo SE. {{A pilot open-label trial of minocycline in patients with autism and regressive features}}. {J Neurodev Disord};2013 (Apr 8);5(1):9.
BACKGROUND: Minocycline is a tetracycline derivative that readily crosses the blood brain barrier and appears to have beneficial effects on neuroinflammation, microglial activation and neuroprotection in a variety of neurological disorders. Both microglial activation and neuroinflammation have been reported to be associated with autism. The study was designed to evaluate the effects of minocycline treatment on markers of neuroinflammation and autism symptomatology in children with autism and a history of developmental regression. METHODS: Eleven children were enrolled in an open-label trial of six months of minocycline (1.4 mg/kg). Ten children completed the trial. Behavioral measures were collected and cerebrospinal fluid (CSF), serum and plasma were obtained before and at the end of minocycline treatment and were analyzed for markers of neuroinflammation. RESULTS: Clinical improvements were negligible. The laboratory assays demonstrated significant changes in the expression profile of the truncated form of brain derived neurotrophic factor (BDNF) (P = 0.042) and hepatic growth factor (HGF) (P = 0.028) in CSF. In serum, the ratio of the truncated BDNF form and alpha-2 macroglobulin (alpha-2 M), was also significantly lower (P = 0.028) while the mature BDNF/alpha-2 M ratio revealed no difference following treatment. Only the chemokine CXCL8 (IL-8) was significantly different (P = 0.047) in serum while no significant changes were observed in CSF or serum in chemokines such as CCL2 (MCP-1) or cytokines such as TNF-alpha, CD40L, IL-6, IFN-gamma and IL-1beta when pre- and post-treatment levels of these proteins were compared. No significant pre- and post-treatment changes were seen in the profiles of plasma metalloproteinases, putative targets of the effects of minocycline. CONCLUSIONS: Changes in the pre- and post-treatment profiles of BDNF in CSF and blood, HGF in CSF and CXCL8 (IL-8) in serum, suggest that minocycline may have effects in the CNS by modulating the production of neurotrophic growth factors. However, in this small group of children, no clinical improvements were observed during or after the six months of minocycline administration. .Trail registration: NCT00409747.
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6. Romero-Martinez A, Polderman T, Gonzalez-Bono E, Moya-Albiol L. {{Masculinization in Parents of Offspring With Autism Spectrum Disorders Could Be Involved in Comorbid ADHD Symptoms}}. {J Atten Disord};2013 (Apr 8)
Objective: People with autism spectrum disorders (ASD) often have comorbid ADHD symptoms. ASD and ADHD are both associated with high intrauterine testosterone (T) levels. This study aims to investigate whether masculinization predicts inattention symptoms in parents, and in their ASD-affected offspring. Method: The sample consisted of 32 parents with ASD-affected children (13 male, 19 female) and 32 offspring individuals (28 male, 4 female). Masculinization of parents was measured by 2D:4D finger ratio, and current T levels. Inattention in both parents and in their offspring was measured with behavior questionnaires. Results: The results indicated that masculinized 2D:4D explains inattentive ADHD symptoms in ASD parents and in their offspring. These predictions are mediated by T and inattention symptoms of ASD parents, respectively. Conclusion: These findings suggest the existence of a masculinized endophenotype in ASD parents, which may be characterized by high attentional sensitivity to T effects. (J. of Att. Dis. 2013; XX(X) 1-XX).
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7. Sidorov MS, Auerbach BD, Bear MF. {{Fragile X mental retardation protein and synaptic plasticity}}. {Mol Brain};2013 (Apr 8);6(1):15.
Loss of the translational repressor FMRP causes Fragile X syndrome. In healthy neurons, FMRP modulates the local translation of numerous synaptic proteins. Synthesis of these proteins is required for the maintenance and regulation of long-lasting changes in synaptic strength. In this role as a translational inhibitor, FMRP exerts profound effects on synaptic plasticity.
