030, p = .001), and in girls, to a lesser extent, the association was stronger following lower prenatal depressive symptoms (interaction term coeff = -.012, p = .221). CONCLUSIONS We replicated the finding from the WCHADS that prenatal depression modifies the association between postnatal depression and children's emotional problems in a sex-dependent fashion. In ALSPAC, the sex difference was explained mainly by a protective effect of low prenatal depression in boys, while in WCHADS, it arose from greater vulnerability of girls to postnatal depression following low prenatal depression. In the light of these findings, in evaluating and implementing early interventions, there is need to consider that risks associated with postnatal depression may vary depending on maternal mood during pregnancy and may differ between boys and girls. © 2020 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.Prevention of epilepsy is a great unmet need. Acute central nervous system (CNS) insults such as traumatic brain injury (TBI), cerebrovascular accidents (CVA), and CNS infections account for 15%-20% of all epilepsy. Following TBI and CVA, there is a latency of days to years before epilepsy develops. This allows treatment to prevent or modify postinjury epilepsy. https://www.selleckchem.com/products/evobrutinib.html No such treatment exists. In animal models of acquired epilepsy, a number of medications in clinical use for diverse indications have been shown to have antiepileptogenic or disease-modifying effects, including medications with excellent side effect profiles. These include atorvastatin, ceftriaxone, losartan, isoflurane, N-acetylcysteine, and the antiseizure medications levetiracetam, brivaracetam, topiramate, gabapentin, pregabalin, vigabatrin, and eslicarbazepine acetate. In addition, there are preclinical antiepileptogenic data for anakinra, rapamycin, fingolimod, and erythropoietin, although these medications have potential for more serious side eed clinically, for example, treatment initiation before or at the time of injury and dosing higher than tolerated human equivalent dosing. Here, we review animal and human antiepileptogenic evidence for these medications. We highlight the gaps in our knowledge for each molecule that need to be filled in order to consider clinical translation, and we suggest a platform of preclinical antiepileptogenesis evaluation of potentially repurposable molecules or their combinations going forward. Wiley Periodicals, Inc. © 2020 International League Against Epilepsy.In Alzheimer's disease (AD), the most common form of dementia, microtubules (MTs) play a pivotal role through their highly dynamic structure and instability. They mediate axonal transport that is crucial to synaptic viability. MTs assembly, dynamic instability and stabilization are modulated by tau proteins, whose detachment initiates MTs disintegration. Albeit extensive research, the role of GTPase activity in molecular mechanism of stability remains controversial. We hypothesized that GTPase activity is altered in AD leading to microtubule dynamic dysfunction and ultimately to neuronal death. In this paper, fresh tubulin was purified by chromatography from normal young adult, normal aged, and Alzheimer's brain tissues. Polymerization pattern, assembly kinetics and dynamics, critical concentration, GTPase activity, interaction with tau, intermolecular geometry, and conformational changes were explored via Förster Resonance Energy Transfer (FRET) and various spectroscopy methods. Results showed slower MT assembly process in samples from the brains of people with AD compared with normal young and aged brains. This observation was characterized by prolonged lag phase and increased critical and inactive concentration of tubulin. In addition, the GTPase activity in samples from AD brains was significantly higher than in both normal young and normal aged samples, concurrent with profound conformational changes and contracted intermolecular MT-tau distances as revealed by FRET. These alterations were partially restored in the presence of microtubule stabilizer, paclitaxel. We proposed that alterations of both tubulin function and GTPase activity may be involved in the molecular neuropathogenesis of AD, thus providing new avenues for therapeutic approaches. This article is protected by copyright. All rights reserved.BACKGROUND Young people in out-of-home care are substantially more likely to meet criteria for PTSD than their peers, while their early maltreatment exposure may also place them at greater risk of developing the newly proposed complex PTSD. Yet, there remains limited empirical evidence for the mechanisms that might drive either PTSD or complex features in this group, and ongoing debate about the suitability of existing cognitive behavioural models and their related NICE-recommended treatments. In a prospective study of young people in out-of-home care, we sought to identify demographic and cognitive processes that may contribute to the maintenance of both PTSD symptom and complex features. METHODS We assessed 120 10- to 18-year-olds in out-of-home care and their primary carer at two assessments an initial assessment and 12-month follow-up. Participants completed questionnaires on trauma history, PTSD symptoms and complex features, while young people only also self-reported on trauma-related (a) maladaptive appraisals, (b) memory quality and (c) coping. Social workers reported on maltreatment severity. RESULTS Young people's maltreatment severity was not a robust predictor of either PTSD symptoms or complex features. All three cognitive processes were moderately-to-strongly correlated with baseline and 12-month PTSD symptoms and complex features, with maladaptive appraisals the most robust unique driver of both, even when controlling for initial PTSD symptom severity. CONCLUSIONS Existing cognitive models of PTSD are applicable in this more complex sample of young people. The model was also found to be applicable to the additional features of complex PTSD, with the same processes driving both outcomes at both time points. Clinical implications are discussed. © 2020 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.