A brief entry today and yet another blog post that starts with a quote (sorry)... "The offspring exposed to VPA [valproic acid] prenatally demonstrated a significant decrease in the number of play initiations/attacks and this was reversed with the KD [ketogenic diet]".Gloucester Old Spot @ Wikipedia That finding reported in the paper by Ahn and colleagues  continues my interest in all-things related to prenatal VPA exposure and the reported effects on some offspring (see here). The added bonus of including some discussion about how the use of a ketogenic diet might reverse some of the effects of VPA exposure (in rats at least) is also worthwhile mentioning.A couple of pointers perhaps...Rats, Sprague-Dawley mother rats, were given VPA or saline (as a control) during pregnancy and their pups (VPA-exposed vs. controls) were subjected to measures looking at "juvenile play behavior" and eventually "mitochondrial bioenergetic analysis" as a function of the use of a ketogenic or standard diet.Results: "Prenatal VPA exposure also disrupted the pattern of play responses". Not a great surprise there given everything else that has been linked to VPA exposure in-utero. But.. use of the ketogenic diet "was able to modify complex social behaviors and mitochondrial respiration". As noted previously, the reduction in play initiations made by the VPA exposed mice was to some degree rescued following use of the ketogenic diet.Yes, I know that this was a study of rats, and whilst useful, rats are rats not humans. But I am nevertheless intrigued by the suggestion that something like a ketogenic diet - more typically indicated for some types of treatment resistant epilepsy - might to some degree, affect the behaviour and physiology of animals exposed to a traditional anticonvulsant like valproate during the nine months that made them. Does anyone else find that a little ironic? Also throw in mention of the words 'autism spectrum disorder' alongside that animal VPA exposure model alongside the ketogenic diet (see here) and I'm sure there's some more research to be done in this area.Mode of action? I dunno. I will draw your attention to some interesting work on carnitine homoeostasis as a function of valproate administration  which might be relevant. Carnitine plays a role in mitochondrial function  and there is some suggestion that a ketogenic diet might help maintain carnitine levels in the presence of VPA . Whether this applies to brain structures or neurochemistry potentially already affected by prenatal exposure to VPA is a question not yet asked or answered. Bearing in mind the gastrointestinal (GI) effects also noted in VPA exposure models (see here) I might also be inclined to 'look to the bowels' in terms of any potential effects from the ketogenic diet in that organ too.Music to close and I was taken aback by the performance from Pumeza at the opening to the 2014 Commonwealth Games and her version of Freedom Come All Ye...---------- Ahn Y. et al. The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder. Dev Neurosci. 2014 Jul 8. Morand R. et al. Effect of short- and long-term treatment with valproate on carnitine homeostasis in humans. Ther Drug Monit. 2012 Aug;34(4):406-14. Zammit VA. et al. Carnitine, mitochondrial function and therapy. Adv Drug Deliv Rev. 2009 Nov 30;61(14):1353-62. Coppola G. et al. Plasma free carnitine in epilepsy children, adolescents and young adults treated with old and new antiepileptic drugs with or without ketogenic diet. Brain Dev. 2006 Jul;28(6):358-65.----------Ahn Y, Narous M, Tobias R, Rho JM, & Mychasiuk R (2014). The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder. Developmental neuroscience PMID: 25011527... Read more »
Ahn Y, Narous M, Tobias R, Rho JM, & Mychasiuk R. (2014) The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder. Developmental neuroscience. PMID: 25011527
Miguel Ramalho-Santos, PhDA new stem-cell discovery might one day lead to a more streamlined process for obtaining stem cells, which in turn could be used in the development of replacement tissue for failing body parts, according to UC San Francisco scientists who reported the findings in the current edition of Cell.The research builds on a strategy that involves reprogramming adult cells back to an embryonic state in which they again have the potential to become any type of cell.The efficiency of this process may soon increase thanks to the scientists' identification of biochemical pathways that can inhibit the necessary reprogramming of gene activity in adult human cells. Removing these barriers increased the efficiency of stem-cell production, the researchers found.Read More... Read more »
Qin, H., Diaz, A., Blouin, L., Lebbink, R., Patena, W., Tanbun, P., LeProust, E., McManus, M., Song, J., & Ramalho-Santos, M. (2014) Systematic Identification of Barriers to Human iPSC Generation. Cell, 158(2), 449-461. DOI: 10.1016/j.cell.2014.05.040
Attention deficit hyperactivity disorder (ADHD), characterized by inattention, hyperactivity, and impulsivity, is a common childhood disorder. ADHD can often persist into adolescence and adulthood. The prevalence of ADHD is thought to be between 6-7% among children and adolescents and ~5% among adults (Willcutt, 2012).
Increasingly, evidence from multiple studies has pointed to comorbidity between ADHD and eating disorders (EDs). For example, one study found that young females with ADHD were 5.6 times more likely to develop clinical (i.e., diagnosable according to DSM-5) or subthreshold (i.e., sub-clinical) bulimia nervosa (BN) (Biederman et al., 2007). Another study found that found that 21% of female inpatients at an ED unit had six or more ADHD symptoms (Yates et al., 2009).
However, most previous studies are limited by the fact that they assessed comorbidity between ADHD and EDs among patients. This limits our ability to generalize these findings to community samples, where many may experience symptoms of the disorders at subthreshold levels. Moreover, most studies focused on bingeing/purging behaviours and did not investigate differences between ADHD subtypes.
In the current study, Jennifer Bleck …
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Bleck, J., DeBate, R., & Olivardia, R. (2014) The Comorbidity of ADHD and Eating Disorders in a Nationally Representative Sample. The Journal of Behavioral Health Services . DOI: 10.1007/s11414-014-9422-y
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Londoño-Franco AL, Loaiza-Herrera J, Lora-Suárez FM, & Gómez-Marín JE. (2014) [Blastocystis sp . frequency and sources among children from 0 to 5 years of age attending public day care centers in Calarcá, Colombia]. Biomedica : revista del Instituto Nacional de Salud, 34(2), 218-27. PMID: 24967927
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Well this might seem weird, but today is world hepatitis day. I guess I should qualify weird with the fact that it’s only weird because no one really knows. What […]... Read more »
Lawitz, E., Sulkowski, M., Ghalib, R., Rodriguez-Torres, M., Younossi, Z., Corregidor, A., DeJesus, E., Pearlman, B., Rabinovitz, M., Gitlin, N.... (2014) Simeprevir plus sofosbuvir, with or without ribavirin, to treat chronic infection with hepatitis C virus genotype 1 in non-responders to pegylated interferon and ribavirin and treatment-naive patients: the COSMOS randomised study. The Lancet. DOI: 10.1016/S0140-6736(14)61036-9
C. Ronald KahnIn 2012, Japanese biologist Shinya Yamanaka won a Nobel Prize for discovering the so-called induced pluripotent stem cells" (iPSCs), cells derived from normal adult cells that have the ability to differentiate into almost any other kind of cells. Now, researchers at Joslin Diabetes Center say they have created the first iPSCs line that offers a human model for insulin resistance, a key driver of type 2 diabetes. "This is one of the very first studies of human iPSC models for type 2 diabetes, and it points out the power of this technology to look at the nature of diabetes, which is complex and may be different in different individuals." said C. Ronald Kahn, MD, Joslin's Chief Academic Officer and the Mary K. Iacocca Professor of Medicine at Harvard Medical School.Until now, scientists examining the causes and effects of insulin resistance have struggled with a general lack of human cell lines from tissues such as muscle, fat and liver that respond significantly to insulin, Kahn says. Studying insulin resistance as it progresses through pre-clinical stages of type 2 diabetes has been particularly challenging.Read More... Read more »
Iovino S, Burkart AM, Kriauciunas K, Warren L, Hughes KJ, Molla M, Lee YK, Patti ME, & Kahn CR. (2014) Genetic Insulin Resistance is a Potent Regulator of Gene Expression and Proliferation in Human iPS Cells. Diabetes. PMID: 25059784
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Acknowledging that some topics have the ability to furrow brows when it comes to autism research, mercury and autism is becoming something of a frequent talking point on this blog as a function of a whole slew of articles appearing in the peer-reviewed domain. If I were to [very tentatively] summarise the collected literature so far, it would be to say something like:Mosaic of mercury @ Wikipedia (i) there is quite a bit more research to be done on some sources of mercury being 'linked' to cases of autism i.e. air pollution, fish consumption (see here),and(ii) the body burden of mercury for some on the autism spectrum is elevated (see here) compared to other groups and potentially linked to "a decreased ability to excrete mercury due to a combination of lowered reduced glutathione, emergence of oxidative stress, and excessive use of oral antibiotics" according to the review by Francesca Gorini and colleagues  (open-access).I know some people may not like hearing that summary but that's my interpretation of the various reviews and meta-analyses conducted so far. I should add that I'm not though passing any specific comment on whether mercury 'causes' autism bearing in mind what we know about the developmental consequences of exposure.The paper by Vincent Yau and colleagues  looking at maternal serum and infant newborn bloodspot levels of mercury adds to that literature with their conclusion: "levels of total mercury in serum collected from mothers during mid-pregnancy and from newborn bloodspots were not significantly associated with risk of ASD [autism spectrum disorder]". I believe we had seen this data presented before at the 2011 IMFAR conference too (see here).A few details first:Based on data obtained from the EMA (Early Markers of Autism) study, a cohort "identified from the California Department of Developmental Services (DDS)" records, mid-pregnancy maternal serum samples and the wonderful resource that is the neonatal bloodspots related to some 84 children diagnosed with an ASD were analysed for total mercury content (inorganic and organic mercury). Blinded results were compared with 159 population controls (asymptomatic) and 49 children diagnosed with a learning (intellectual) disability or developmental delay.ICP mass spectrometry was the name of the analytical game, which as I've talked about before, is one of the methods of choice when it comes to the analysis of the metallome. Archived blood spot samples were subject to laser ablation as a function of their mounting. Results: "Maternal serum and infant blood mercury levels were significantly correlated among all study groups". In other words, maternal mercury burden seemed to be associated with neonatal offspring burden (albeit with a correlation coefficient ~0.4 which is OK but not exactly great).Further: "Results for mercury levels in newborn blood samples were similar" across the groups. Ergo, at birth, levels of total mercury from neonatal bloodspots "were not significantly associated with risk of ASD". That's not to say that there weren't some differences in average levels of blood mercury levels across the groups, just that such differences were not deemed to elevate the risk of ASD overall.Like quite a lot of the science in this area, there are several ways you could interpret these results. You could, for example say that the maternal burden of mercury during pregnancy was not associated with offspring risk of autism. You could also say that 'at or shortly after birth' (remember those words), blood mercury levels do not seem to correlate with the risk of autism. Therefore mercury is not a factor in relation to autism as per other results in this area . You could say those things, as you might for several other variables supposedly related to autism... vitamin D for example? (see here and then see here).But you might also consider the bank of research which has reported elevated levels of mercury in various biofluids and tissues particularly focused on slightly older infants and children with autism as illustrative of something potentially important: increasing exposure to mercury with age. Take for example the paper by Majewska and colleagues  and their findings reporting: "Autistic children significantly differed from healthy peers in the concentrations of mercury in hair: younger autistics had lower levels, while older - higher levels than their respective controls". The results from Hertz-Picciotto and colleagues  (open-access here) also implied that behaviour might play a role in blood mercury levels: "Interestingly, although few children had Hg amalgams, those who did and who also either chewed gum or had bruxism appeared to have experienced sufficient release of inorganic Hg to be measurable in blood". I say this noting that not every child with autism has mercury amalgams, as neither do they all partake in teeth grinding.The Yau results make an important contribution to the issue of mercury and autism in terms of maternal contribution and mercury load at birth. As part of some further investigations, and bearing in mind that participants in the EMA initiative might also be involved in other State initiatives (beincharge!), I would like to see further follow-up of participants and if and how their mercury load might have changed as they matured. Analysis of other parameters mentioned in that Gorini review paper - such as glutathione measures for example - might also offer some important accompanying data on whether excretion factors are part of the issue here and what might be done to help relieve any excess burden of the troublesome heavy metal that is mercury. Oh, and given that genetic factors might also play some role in mercury accumulation as per the findings by Llop and colleagues  (open-access), there may also be more research to do here too...---------- Gorini F. et al. The Role of Heavy Metal Pollution in Neurobehavioral Disorders: a Focus on Autism. Review Journal of Autism... Read more »
Yau VM, Green PG, Alaimo CP, Yoshida CK, Lutsky M, Windham GC, Delorenze G, Kharrazi M, Grether JK, & Croen LA. (2014) Prenatal and neonatal peripheral blood mercury levels and autism spectrum disorders. Environmental research, 294-303. PMID: 24981828
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Barnum CJ, Chen X, Chung J, Chang J, Williams M, Grigoryan N, Tesi RJ, & Tansey MG. (2014) Peripheral Administration of the Selective Inhibitor of Soluble Tumor Necrosis Factor (TNF) XPro1595 Attenuates Nigral Cell Loss and Glial Activation in 6-OHDA Hemiparkinsonian Rats. Journal of Parkinson's disease. PMID: 25061061
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Koubeissi, M., Bartolomei, F., Beltagy, A., & Picard, F. (2014) Electrical stimulation of a small brain area reversibly disrupts consciousness. Epilepsy , 32-35. DOI: 10.1016/j.yebeh.2014.05.027
Sleep disturbance following traumatic brain injury (TBI) is a common clinical challenge.Hypersomnia and insomnia can both been seen in the TBI population.The risk factors related to TBI-related sleep disturbance are not well known. Identification of risk factors can provide insight into clinical assessment and management.Lijun Hou and colleagues recently examined risk factors related to subjective sleep complaints in a series of 98 TBI subjects.The study sample include adults admitted to a one of two Chinese hospitals following a initial episode of TBI. For enrollment, subjects were required to have evidence of a brain imaging abnormality on CT after their TBI.Subjects were interviewed by phone one to four years following TBI and administered three questionnaires including:Pittsburgh Sleep Quality IndexEpworth Sleepiness ScaleHospital Anxiety and Depression Scale The key findings from this study included:Severity of TBI ratings for the sample were mild (70%), moderate (15%) and severe (15%)Prevalence of sleep disturbance was 38% in the sample overallSleep disturbance rates increased with increasing TBI severity with rates of 30% in the mild TBI group, 53% in the moderate TBI group and 57% in the severe TBI groupThe predominant risk factor for hypersomnia was severity of TBI. Those with severe TBI were most likely to have hypersomniaRisk factors for insomnia included post-TBI headache and dizziness complaints and post-TBI anxiety and depression symptomsThis study was unable to identify specific brain CT findings as risk factors for later sleep disturbance. Sleep disturbance rates were similar for subjects with frontal lobe injury and those with injury to other brain regions. The authors conclude sleep disturbance is a common complication of TBI and often is not diagnosed and not treated.A weakness of this study is the relatively small sample size and the use of self-report measures rather than sleep laboratory confirmed sleep disturbance.Insomnia after TBI may be part of a broader presentation of an anxiety disorder or mood disorder. Clinicians should screen TBI patients for presence of psychiatric disorders when a insomnia is present.Hypersomnia following severe TBI may contribute to significant morbidity. Pharmacological interventions for hypersomnia such as modafanil are available and may be part of a multidisciplinary treatment program.Readers with more interest in this research can access the free full-text manuscript by clicking on the PMID link in the reference below.Photo of a tricolor heron is from the author's files.Follow the author on Twitter at WRY999.Hou L, Han X, Sheng P, Tong W, Li Z, Xu D, Yu M, Huang L, Zhao Z, Lu Y, & Dong Y (2013). Risk factors associated with sleep disturbance following traumatic brain injury: clinical findings and questionnaire based study. PloS one, 8 (10) PMID: 24098425... Read more »
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"These results confirm the elevation of urinary p-cresol in a sizable set of small autistic children and spur interest into biomarker roles for p-cresol and p-cresylsulfate in autism".The peasant dance @ Wikipedia That was the primary conclusion from the paper by Gabriele and colleagues  looking at "three components of urinary p-cresol, namely p-cresylsulfate, p-cresylglucuronate and free p-cresol" in samples from 33 participants diagnosed with an autism spectrum disorder (ASD) compared with matched asymptomatic controls. The confirmation bit of that quote refers to the fact that members of this authorship group have previously reported on elevated urinary p-cresol in cases of autism  which was talked about in the very first proper research-based post on this blog (see here).Before proceeding, perhaps it might be worth my while going through a few descriptive details. p-cresol (para-cresol) otherwise known as 4-methylphenol is a compound of some note in terms of the various ways and means one arrives at this organic aromatic compound. The solvent toluene is eventually metabolised into p-cresol, as is the amino acid tyrosine in the presence of strains of the anaerobic bacterium Clostridium difficile  for example. That being said, there are quite a few other ways in which one might come into contact with this compound.According to the paper by Vanholder and colleagues  there is quite a bit of evidence to suggest that whilst p-cresol and its metabolites are compounds found in some quantity in just about everyone, under certain circumstances, elevations in amount may not be particularly desirable  particularly when it comes to renal functions. Indeed, quite a bit of the focus has been on the conjugated derivative p-cresylsulfate (formed through O-sulfonation) when it comes to toxicity . I'll come back to this issue shortly.A few points on the Gabriele paper might be useful:Based on a small participant group comprising 33 participants of various ages on the autism spectrum and 33 sex- and age-matched asymptomatic controls, levels of free p-cresol and it's two metabolites were measured via HPLC with fluorescence detection.All metabolites were "significantly elevated" in ASD cases compared to controls."This increase was limited to ASD children ≤8 [less than or equal to 8] years". Also: "Urinary levels of p-cresol and p-cresylsulfate were associated with stereotypic, compulsive/repetitive behaviors (p < 0.05), although not with overall autism severity".I probably don't need to say it, but when it comes to talk about biomarkers and autism, I do tend to be a little restrained about the promise of any results. Think back to my recent post on organic acids as biomarkers for autism (see here) and just about all the caveats talked about then in terms of heterogeneity and comorbidity come into play here too. That also this and other results from this group are based on HPLC with either UV (ultraviolet) or fluorescence detection could also be considered problematic as a function of the many and varied components found in urine and how without mass spectrometry or NMR, assigning labels to compounds is slightly problematic. Think casomorphins as another example...Elevated levels of urinary p-cresol are also not a feature of every metabolomic study looking at autism. In their review of all-things p-cresol and autism, Persico & Napolioni  talked about how the results from Yap and colleagues  reported "blunted and not increased levels of p-cresylsulfate in autistic patients". The Yap study did utilise (1)H NMR spectroscopy and so did not suffer the same analytical shortcomings as the more recent trials. That all being said, I don't want to come down too hard on the latest results from Gabriele and colleagues. They got what they got and now put their results out for further inspection and hopefully, independent verification.I am also wondering whether the paper by Clayton and colleagues  might also be relevant in this case. Dr Clayton, who some might remember from other work talked about on this blog (see here), discussed how "in individuals with high bacterially mediated p-cresol generation, competitive O-sulfonation of p-cresol reduces the effective systemic capacity to sulfonate acetaminophen [paracetamol]". Sulphation capacity when it comes to autism is already something of a research interest (see here) which when added to a growing body of work looking at paracetamol use during pregnancy and possible links to offspring development (see here) might indicate some other interesting investigations to be done. I wonder if perhaps even the sulphation depleting metabolism of something like p-cresol might actually be the more important part of such investigations to autism research?Music to close, and are you a troublemaker?---------- Gabriele S. et al. Urinary p-cresol is elevated in young French children with autism spectrum disorder: a replication study. Biomarkers. 2014 Jul 10:1-8. Altieri L. et al. Urinary p-cresol is elevated in small children with severe autism spectrum disorder. Biomarkers. 2011 May;16(3):252-60. Dawson LF. et al. The analysis of para-cresol production and tolerance in Clostridium difficile 027 and 012 strains. BMC Microbiology 2011, 11:86  Vanholder R. et al. p-cresol: a toxin revealing many neglected but relevant aspects of uraemic toxicity. Nephrol Dial Transplant. 1999 Dec;14(12):2813-5. Liabeuf S. et al. Free p-cresylsulphate is a predictor of mortality in patients at different stages of chronic kidney disease. Nephrol Dial Transplant. 2010 Apr;25(4):1183-91. Vanholder R. et al. The Uremic Toxicity of Indoxyl Sulfate and p-Cresyl Sulfate: A Systematic Review. J Am Soc Nephrol. 2014 May 8. [Epub ahead of print] Persico AM. & Napolioni V. Urinary p-cresol in autism spectrum disorder. Neurotoxicol Teratol. 2013 Mar-Apr;36:82-90. Yap IK. et al. Urinary metabolic phenotyping differentiates children with autism from their unaffected siblings and age-matched controls. J Proteome Res. 2010 Jun 4;9(6):2996-3004. Clayton TA. et al. Pharmacometabonomic identification of a significant host-microbiome metabolic interaction affecting human drug metabolism. Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14728-33.----------... Read more »
Gabriele S, Sacco R, Cerullo S, Neri C, Urbani A, Tripi G, Malvy J, Barthelemy C, Bonnet-Brihault F, & Persico AM. (2014) Urinary p-cresol is elevated in young French children with autism spectrum disorder: a replication study. Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals, 1-8. PMID: 25010144
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Lewandowski, G., & Steward, O. (2014) AAVshRNA-Mediated Suppression of PTEN in Adult Rats in Combination with Salmon Fibrin Administration Enables Regenerative Growth of Corticospinal Axons and Enhances Recovery of Voluntary Motor Function after Cervical Spinal Cord Injury. Journal of Neuroscience, 34(30), 9951-9962. DOI: 10.1523/JNEUROSCI.1996-14.2014
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Bernard JJ, Cowing-Zitron C, Nakatsuji T, Muehleisen B, Muto J, Borkowski AW, Martinez L, Greidinger EL, Yu BD, & Gallo RL. (2012) Ultraviolet radiation damages self noncoding RNA and is detected by TLR3. Nature medicine, 18(8), 1286-90. PMID: 22772463
The paper by Amanda Wood and colleagues  (open-access) makes a potentially very important contribution to the growing literature looking at how prenatal exposure to sodium valproate (VPA) may affect some children. Authors reported on: "regional structural cortical brain changes in humans exposed to VPA in utero" and specifically, increased cortical thickness in the left inferior frontal gyrus.Lightning and lava @ Oliver Spalt @ Wikipedia In case you need any background on the story behind pregnancy exposure to VPA, I would direct you to a few previous posts where the topic has been covered on this blog (see here and see here) with an autism slant. You might also read my small contribution to a more formal article on this topic here.Outside of any reported elevated risk of offspring autism or autistic traits associated with prenatal VPA exposure, I'm also minded to bring in some interesting work on intestinal inflammation being reported in a VPA mouse model (see here) to further highlight that important gut-brain axis which I seem to be a little obsessed with.The Wood paper is open-access and has some accompanying media coverage but a few pointers might be useful...Following other work by the authors on this topic  the idea behind this latest research was to apply the science of neuroimaging to a participant group comprising 16 children exposed to VPA in-utero compared with age- and sex-matched children not exposed to such pharmaceutics prenatally.MRI scans were taken and analysed and "whole brain group differences" assessed. Results: well, as discussed, there were some findings in terms of cortical thickness but also specifically with language skills in mind. To quote again: "Asymmetry of cortical thickness in the inferior frontal lobes was seen in controls but not cases". I understand that this finding might have some relevance to language processing  although set my non-expert stall out on such matters. As per that previous link  and other evidence , language functions in VPA exposed children tend to poorer compared to controls and to those exposed to other anti-convulsant medication during the nine months that made us. This last point on different medications potentially carrying different risk profiles  is something equally interesting.Allowing for the relatively small participant groups studied and the lack of any other research parameter such as looking at accompanying brain chemistry which may be important , the Wood paper offers some intriguing insights into how pregnancy VPA use might affect infant brain development. The very important detail of analysis being based on real human children and not rat offspring also invites some further examination of previous results based on rodents . Rats are rats, children are children.I'm going to leave you with a quote from the authors about their study: "VPA remains an important medication for people with epilepsy. What this study really tells us is that further research is required so that all women with epilepsy can make informed decisions about their medication use during pregnancy". I couldn't agree more, and as per the Treating for Two initiative, I'm not the only one.Music then... HRH Gaga and Just Dance.---------- Wood AG. et al. Altered cortical thickness following prenatal sodium valproate exposure. Annals of Clinical and Translational Neurology. 2014. July 3. doi: 10.1002/acn3.74 Nadebaum C. et al. Language skills of school-aged children prenatally exposed to antiepileptic drugs. Neurology. 2011 Feb 22;76(8):719-26. Powell HWR. et al. Hemispheric asymmetries in language-related pathways: A combined functional MRI and tractography study. NeuroImage. 2006; 32: 388-399. Shallcross R. et al. In utero exposure to levetiracetam vs valproate: development and language at 3 years of age. Neurology. 2014 Jan 21;82(3):213-21. Vajda FJE. et al. The teratogenicity of the newer antiepileptic drugs – an update. Acta Neurol Scand. 2014. July 18 Almeida LE. et al. Increased BDNF expression in fetal brain in the valproic acid model of autism. Mol Cell Neurosci. 2014 Mar;59:57-62. Mychasiuk R. et al. Effects of rat prenatal exposure to valproic acid on behaviour and neuro-anatomy. Dev Neurosci. 2012;34(2-3):268-76.----------Wood, A., Chen, J., Barton, S., Nadebaum, C., Anderson, V., Catroppa, C., Reutens, D., O'Brien, T., & Vajda, F. (2014). Altered cortical thickness following prenatal sodium valproate exposure Annals of Clinical and Translational Neurology DOI: 10.1002/acn3.74... Read more »
Wood, A., Chen, J., Barton, S., Nadebaum, C., Anderson, V., Catroppa, C., Reutens, D., O'Brien, T., & Vajda, F. (2014) Altered cortical thickness following prenatal sodium valproate exposure. Annals of Clinical and Translational Neurology. DOI: 10.1002/acn3.74
New research suggests patients with both bipolar disorder and obsessive compulsive disorder should receive treatments for bipolar disorder alone. Bipolar and obsessive compulsive disorder therapies taken together can cause worsening of disease symptoms, making it difficult for physicians to treat both conditions. This is a concern as over 1 in 5 patients with bipolar disorder develop obsessive compulsive disorder during their lifetime.... Read more »
Pacchiarotti I, Bond DJ, Baldessarini RJ, & et al. (2013) The International Society for Bipolar Disorders (ISBD) task force report on antidepressant use in bipolar disorders. The American journal of psychiatry, 170(11), 1249-62. PMID: 24030475
Writing in the European Journal of Clinical Investigation, three Dutch researchers say that All preclinical trials should be registered in advance in an online registry Citing the fact that all clinical trials are (in theory) already registered, authors Jansen of Lorkeers et al say that the system should be extended to cover preclinical medical research, […]The post Preregistration for All Medical Animal Research appeared first on Neuroskeptic.... Read more »
Jansen of Lorkeers, S., Doevendans, P., & Chamuleau, S. (2014) All preclinical trials should be registered in advance in an online registry. European Journal of Clinical Investigation. DOI: 10.1111/eci.12299
[Another version of this article was first published on SciDev.Net. Click here for link.] A vaccine that can half the number of dengue cases will soon be available. A recent trial conducted in Southeast Asia shows that this dengue vaccine achieves a vaccine efficacy of 56.5%: the vaccine reduces an individual’s chance of getting […]... Read more »
Capeding, M., Tran, N., Hadinegoro, S., Ismail, H., Chotpitayasunondh, T., Chua, M., Luong, C., Rusmil, K., Wirawan, D., Nallusamy, R.... (2014) Clinical efficacy and safety of a novel tetravalent dengue vaccine in healthy children in Asia: a phase 3, randomised, observer-masked, placebo-controlled trial. The Lancet. DOI: 10.1016/S0140-6736(14)61060-6
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