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  • September 11, 2014
  • 03:28 PM

September 11, 2014

by Erin Campbell in HighMag Blog

As your therapist likely tells you, understanding where you came from is key to accepting where you are now. Take that therapist’s task and multiply it by several million—you now understand the tough job ahead of developmental biologists trying to track cell lineages in complex organisms. Today’s colorful image is from a paper describing a new computational framework for reconstructing cell lineages. The successful tracking of cell position, division, and movement in a developing organism has been a goal for countless developmental biologists. Reconstructing cell lineages in organisms like fruit flies and mice, however, is difficult due to the complexity of cell organization and behavior, poor image quality of thick embryos, the enormous size of the data sets, and an uncompromising need for accuracy. A recent paper by Amat and colleagues describes the development and use of a new open-source framework that reconstructs cell lineages with high accuracy and speed. Their system uses four dimensional and terabyte-sized image data sets of nuclei-tracked embryos, imaged using three different types of fluorescence microscopy. The images above show the first reconstruction of early fruit fly nervous system development (S1 neuroblasts), with precursor cell tracks color-coded for time (purple to yellow).Amat, F., Lemon, W., Mossing, D., McDole, K., Wan, Y., Branson, K., Myers, E., & Keller, P. (2014). Fast, accurate reconstruction of cell lineages from large-scale fluorescence microscopy data Nature Methods, 11 (9), 951-958 DOI: 10.1038/nmeth.3036Adapted by permission from Macmillan Publishers Ltd, copyright ©2014 ... Read more »

Amat, F., Lemon, W., Mossing, D., McDole, K., Wan, Y., Branson, K., Myers, E., & Keller, P. (2014) Fast, accurate reconstruction of cell lineages from large-scale fluorescence microscopy data. Nature Methods, 11(9), 951-958. DOI: 10.1038/nmeth.3036  

  • September 11, 2014
  • 02:58 PM

SARS-CoV: formation of the RTC and mitophagy; role of p6 and orf9b

by thelonevirologist in Virology Tidbits

Whilst the nature of the RTC and the role of the CoV non-structural proteins as well the potential role of these proteins in the ER stress response have been discussed in detail before, the role of p6 has been not been discussed. p6 not only induces the formation of membranous vesicles but also recruits nsp-8 to nsp-5, the main viral RNA Polymerase, and induces a ER stress response.
Also the role of SARS-orf9b in the induction of mitophagy is discussed.... Read more »

Otera H, Ishihara N, & Mihara K. (2013) New insights into the function and regulation of mitochondrial fission. Biochimica et biophysica acta, 1833(5), 1256-68. PMID: 23434681  

Kumar P, Gunalan V, Liu B, Chow VT, Druce J, Birch C, Catton M, Fielding BC, Tan YJ, & Lal SK. (2007) The nonstructural protein 8 (nsp8) of the SARS coronavirus interacts with its ORF6 accessory protein. Virology, 366(2), 293-303. PMID: 17532020  

Cruz JL, Sola I, Becares M, Alberca B, Plana J, Enjuanes L, & Zuñiga S. (2011) Coronavirus gene 7 counteracts host defenses and modulates virus virulence. PLoS pathogens, 7(6). PMID: 21695242  

Subissi L, Posthuma CC, Collet A, Zevenhoven-Dobbe JC, Gorbalenya AE, Decroly E, Snijder EJ, Canard B, & Imbert I. (2014) One severe acute respiratory syndrome coronavirus protein complex integrates processive RNA polymerase and exonuclease activities. Proceedings of the National Academy of Sciences of the United States of America. PMID: 25197083  

Moshynskyy I, Viswanathan S, Vasilenko N, Lobanov V, Petric M, Babiuk LA, & Zakhartchouk AN. (2007) Intracellular localization of the SARS coronavirus protein 9b: evidence of active export from the nucleus. Virus research, 127(1), 116-21. PMID: 17448558  

  • September 11, 2014
  • 12:45 PM

The Origami Brain and a new marker for Schizophrenia

by Gabriel in Lunatic Laboratories

Anyone who has seen pictures or models of the human brain (like the one above) is aware that the outside layer, or cortex, of the brain is folded in an intricate pattern of “hills”, called gyri, and “valleys”, called sulci which give the brain it’s distinctive look. It turns out that the patterns of cortical folding are largely consistent across healthy humans, broadly speaking. However, disturbances in cortical folding patterns suggest deeper disturbances in brain structure and function.... Read more »

Nanda P, Tandon N, Mathew IT, Giakoumatos CI, Abhishekh HA, Clementz BA, Pearlson GD, Sweeney J, Tamminga CA, & Keshavan MS. (2014) Local gyrification index in probands with psychotic disorders and their first-degree relatives. Biological psychiatry, 76(6), 447-55. PMID: 24369266  

  • September 11, 2014
  • 09:55 AM

Treating autism in the first year of life

by Paul Whiteley in Questioning Answers

I had been waiting y'know. Waiting a while for the paper by Sally Rogers and colleagues [1] to finally appear quite a few days after the media headlines about 'reducing', 'reversing' and even 'eliminating' the signs and symptoms of autism in early infancy had appeared. Personally, I prefer the New Scientist headline: 'Early autism intervention speeds infant development' given the text of the paper. I should perhaps also add the words 'for some' to that sentence as you will hopefully see...I'm sure most people have already read about the study ins and outs: take an intervention called 'Infant Start' (IS), a relation of the Early Start Denver Model (ESDM), and apply it with a small (very small) group of "symptomatic" young infants (n=7, aged between 6-15 months old) showing signs and symptoms of autism. Plot baseline measures and progress of those children under IS using various psychometric tools including something like the Autism Observation Scale for Infants (AOSI) and old reliable: the ADOS (the Autism Diagnostic Observation Schedule) compared against four comparison groups. One of those control groups included those with similar early autism symptoms as judged by "elevated AOSI scores and clinician concerns" but who did not receive IS; a so-called "declined referral (DR) group" (n=4). Record results and report outcome based on said 12-week program and added extra sessions a few months down the line.The headline conclusion: "At 36 months, the treated group had much lower rates of both ASD [autism spectrum disorder] and DQs [developmental quotients] under 70 than a similarly symptomatic group who did not enroll in the treatment study". Further: "the pilot study outcomes are promising". I should add that when it came to the "final visit" and "based on standardized assessments and clinical judgement" 2 of the 7 children in the IS group did eventually receive a diagnosis of ASD/PDD-NOS (pervasive developmental disorder not otherwise specified). This compared with 3 of the 4 children in the DR group who met criteria for ASD/PDD-NOS (the other child "presented with intellectual disability"). Insofar as DQ - specifically "overall DQ at or below 70 at 36 months" - well, one child in the IS group fell into this category compared with 3 children in the DR group (note to authors, you've called this the 'DE' group... sorry to be pedantic). You can um-and-ah about the links between ASD and PDD-NOS for example, but suffice to say that any effect from IS was not universal across all participants included in the trial. If you'd like a few more details about the trial and results, I'll refer you to the press release from UC Davis (see here).Of course this is not the first time that this type of very early intervention has been discussed in the peer-reviewed domain. Take for example another paper by Rogers and colleagues [2] (open-access) talking about the use of ESDM with a cohort of 14-24 month old toddlers "at risk for autism spectrum disorders". The results on that occasions were slightly less dramatic than the more recent ones with the caveat that "both younger child age at the start of intervention and a greater number of intervention hours were positively related to the degree of improvement in children's behavior for most variables". I talked about this in a previous post (see here). Indeed it appears that age at start of intervention might be an important variable after all.So, where next with this research? Well, aside from some discussions reiterating how useful it would be to have something to aid early diagnosis (see here) bearing in mind that it has not been conclusively proven that all autism is present from birth (see here), discussions have turned to why such early intervention might have had the effect that it had. Brain plasticity has been mentioned, and how critical periods in early development might be particularly amenable to such intensive intervention. Of course, without the all-important "testing the treatment’s efficacy" under more controlled conditions and with larger groups, one cannot discount some role for chance in the recent findings. Not buying that as an answer? How about differing developmental trajectories then?----------[1] Rogers SJ. et al. Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants. Journal of Autism and Developmental Disorders. 2014. 12 September.[2] Rogers SJ. et al. Effects of a brief Early Start Denver model (ESDM)-based parent intervention on toddlers at risk for autism spectrum disorders: a randomized controlled trial. J Am Acad Child Adolesc Psychiatry. 2012 Oct;51(10):1052-65.----------S. J. Rogers, L. Vismara, A. L. Wagner, C. McCormick, G. Young, & S. Ozonoff (2014). Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants Journal of Autism and Developmental Disorders : 10.1007/s10803-014-2202-y... Read more »

S. J. Rogers, L. Vismara, A. L. Wagner, C. McCormick, G. Young, & S. Ozonoff. (2014) Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants. Journal of Autism and Developmental Disorders. info:/10.1007/s10803-014-2202-y

  • September 11, 2014
  • 09:52 AM

Stop Worrying, Good-Looking Dudes: Your Sperm Is Fine

by Elizabeth Preston in Inkfish

You may have seen headlines over the past week proclaiming that handsome men have lower-quality sperm. If this made you panic because you happen to be a great-looking guy, you can stop. (If you’re an un-handsome man who’s been gloating—sorry.) This scientific study did say a few interesting things about Spaniards, Colombians, and cheekbones. But […]The post Stop Worrying, Good-Looking Dudes: Your Sperm Is Fine appeared first on Inkfish.... Read more »

Soler C, Kekäläinen J, Núñez M, Sancho M, Alvarez JG, Núñez J, Yaber I, & Gutiérrez R. (2014) Male facial attractiveness and masculinity may provide sex- and culture-independent cues to semen quality. Journal of evolutionary biology, 27(9), 1930-8. PMID: 25056484  

  • September 11, 2014
  • 09:37 AM

What’s The Answer? (gene essentiality)

by Mary in OpenHelix

Biostars is a site for asking, answering and discussing bioinformatics questions and issues. We are members of the community and find it very useful. Often questions and answers arise at Biostars that are germane to our readers (end users of genomics resources). Every Thursday we will be highlighting one of those items or discussions here […]... Read more »

  • September 11, 2014
  • 04:42 AM

Omega-3 fatty acids rescues Fragile X phenotypes in Fmr1-Ko mice

by Paul Whiteley in Questioning Answers

"These results demonstrate that n-3 PUFAs dietary supplementation, although not a panacea, has a considerable therapeutic value for FXS [Fragile X syndrome] and potentially for ASD [autism spectrum disorder], suggesting a major mediating role of neuroinflammatory mechanisms".A view @ Wikipedia That was the conclusion reached by Susanna Pietropaolo and colleagues [1] who "evaluated the impact of n-3 PUFA dietary supplementation in a mouse model of fragile X syndrome (FXS), i.e., a major developmental disease and the most frequent monogenic cause of ASD". Looking at the Fmr1-KO mouse model of FXS, a mouse specifically bred to mimic the silencing of the FMR1 gene noted in FXS (see here) with onwards adverse effects for the production of FMRP, researchers looked at what happened when diets were "enriched or not with n-3 PUFAs from weaning until adulthood when they were tested for multiple FXS-like behaviors". The results seemed to indicate that "n-3 PUFA supplementation rescued most of the behavioral abnormalities displayed by Fmr1-KO mice, including alterations in emotionality, social interaction and non-spatial memory, although not their deficits in social recognition and spatial memory". Neuroinflammatory imbalances noted in the knock-out mice were also positively affected by omega-3 supplementation.I don't need to remind you that the Pietropaolo study was a study of mice and one needs to be quite careful about extrapolating animal results when it comes to humans. That being said, given the quite extensive work that has been done on FXS and the detailing of it's molecular background, one might assume that the current results are treated with a little less scepticism than in relation to other more idiopathic 'types' of autism. Still, proper trials with people are indicated as per other research.Omega-3 fatty acids have been discussed before on this blog with autism in mind (see here). The collected literature on their usefulness as supplements for autism is rather mixed at present [2] despite some emerging evidence on their involvement in various biological processes in cases of autism (see here). That being said, I'm not getting too down on omega-3 fatty acids in light of some associations being made with specific skills over and above any condition-specific relationship and some new light being shed on their use in other conditions [3]. I'm yet to find anything like an experimental trial of fatty acids in real people with FXS but did chance(!) upon the study by Lachance and colleagues [4] (open-access) talking about the use of fenretinide (N-(4-hydroxyphenyl) retinamide (4HPR)) in the test-tube and effects "associated with the normalization of arachidonic acid/docosahexaenoic acid ratio in macrophages". The effect talked about translates as a down-regulation in the "production of arachidonic acid (AA), a pro-inflammatory omega-6 polyunsaturated fatty acid, and to increase levels of omega-3 polyunsaturated docosahexaenoic acid (DHA), which has an anti-inflammatory effect". Mmm... possibly some new targets to replace quite a few disappointments when it comes to FXS therapeutics (see here).Music to close. Fontella Bass and Rescue Me.----------[1] Pietropaolo S. et al. Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology. 2014 Jul 9;49C:119-129.[2] James S. et al. Omega-3 fatty acids supplementation for autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2011 Nov 9;(11):CD007992.[3] Hawkey E. & Nigg JT. Omega-3 fatty acid and ADHD: Blood level analysis and meta-analytic extension of supplementation trials. Clin Psychol Rev. 2014 Jun 2;34(6):496-505.[4] Lachance C. et al. Fenretinide corrects the imbalance between omega-6 to omega-3 polyunsaturated fatty acids and inhibits macrophage inflammatory mediators via the ERK pathway. PLoS One. 2013 Sep 12;8(9):e74875.----------Pietropaolo S, Goubran MG, Joffre C, Aubert A, Lemaire-Mayo V, Crusio WE, & Layé S (2014). Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology, 49C, 119-129 PMID: 25080404... Read more »

Pietropaolo S, Goubran MG, Joffre C, Aubert A, Lemaire-Mayo V, Crusio WE, & Layé S. (2014) Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology, 119-129. PMID: 25080404  

  • September 10, 2014
  • 02:26 PM

Multiple Sclerosis and Myelin loss

by Gabriel in Lunatic Laboratories

Multiple sclerosis (MS) is an unpredictable, often disabling disease of the central nervous system that disrupts the flow of information within the brain, and between the brain and body. The exact cause is unknown, however people with multiple sclerosis lose myelin in the gray matter of their brains and the loss is closely correlated with the severity of the disease, according to a new magnetic resonance imaging (MRI) study.... Read more »

Vasily L. Yarnykh, James D. Bowen, Alexey Samsonov, Pavle Repovic, Angeli Mayadev, Peiqing Qian, Beena Gangadharan, Bart P. Keogh, Kenneth R. Maravilla, & Lily K. Jung Henson. (2014) Fast Whole-Brain Three-dimensional Macromolecular Proton Fraction Mapping in Multiple Sclerosis. Radiological Society of North America . info:/10.1148/radiol.14140528

  • September 10, 2014
  • 11:49 AM

Apple Does 3D Cell Culture

by Nicholas Miliaras in ASCB Post

Andrew Pelling has a new application for the apple, but it is not the latest i-gizmo from Cupertino, CA. Pelling and colleagues at the University of Ottawa have come up with a possible solution to the limitations of traditional, two-dimensional (2D) cell culture, which does not reproduce the microenvironment and tissue architecture that surrounds cells in a living organism—the apple, the one-a-day fruit that keeps the doctor away and is an essential ingredient to the All-American pie. Pelling believes that apples have something to offer beyond health benefits; apples could revolutionize the fields of cell culture and tissue engineering by providing a low-cost and sustainable alternative to synthetic three-dimensional (3D) culture systems.... Read more »

Modulevsky DJ, Lefebvre C, Haase K, Al-Rekabi Z, & Pelling AE. (2014) Apple derived cellulose scaffolds for 3D mammalian cell culture. PloS one, 9(5). PMID: 24842603  

  • September 10, 2014
  • 09:40 AM

Midi-chlorians gave Jedi knights their power. Is there something like this on Earth?

by Bill Sullivan in The 'Scope

A strange and provocative paper by Alexander Panchin and colleagues proposes an unorthodox new idea called the “biomeme hypothesis”, which posits that the impulse behind some religious rituals could be driven by mind-altering parasites.... Read more »

  • September 10, 2014
  • 09:36 AM

Video Tip of the Week: #Docker, shipping containers for software and data

by Mary in OpenHelix

Breaking into the zeitgeist recently, Docker popped into my sphere from several disparate sources. Seems to me that this is a potential problem-solver for some of the reproducibility and sharing dramas that we have been wrestling with in genomics. Sharing of data sets and versions of analysis software is being tackled in a number of […]... Read more »

  • September 10, 2014
  • 08:00 AM

Return of Results from Next-gen Sequencing

by Daniel Koboldt in Massgenomics

The rapid adoption of next-gen exome and genome sequencing for clinical use (i.e. with patient DNA) raises some difficult questions about the return of results to patients and their families. In contrast to traditional genetic testing, which usually checks for variants in specific genes, high-throughput sequencing has the potential to reveal a number of secondary […]... Read more »

  • September 10, 2014
  • 08:00 AM

Bacteria Can Really Get Around

by Mark Lasbury in As Many Exceptions As Rules

Bacteria have evolved a type of motion that is a lot like a snot-powered rocket, so getting from point A to point B must be pretty important. Bacteria have evolved no fewer, and probably a lot more, than eight different ways to move around. New research is defining the physics and molecular biology of these modes of transportation, including a pseudo-cytoskeleton, helical conveyor belts, and something called “reverse and flick.”... Read more »

Kinosita Y, Nakane D, Sugawa M, Masaike T, Mizutani K, Miyata M, & Nishizaka T. (2014) Unitary step of gliding machinery in Mycoplasma mobile. Proceedings of the National Academy of Sciences of the United States of America, 111(23), 8601-6. PMID: 24912194  

Jin F, Conrad JC, Gibiansky ML, & Wong GC. (2011) Bacteria use type-IV pili to slingshot on surfaces. Proceedings of the National Academy of Sciences of the United States of America, 108(31), 12617-22. PMID: 21768344  

Stocker R. (2011) Reverse and flick: Hybrid locomotion in bacteria. Proceedings of the National Academy of Sciences of the United States of America, 108(7), 2635-6. PMID: 21289282  

  • September 10, 2014
  • 07:42 AM

Indian Purple Frog (Pignosed Frog)

by beredim in Strange Animals

Indian Purple FrogCredit: Karthickbala at ta.wikipedia (CC-BY-SA-3.0)via Wikimedia CommonsKingdom: AnimaliaPhylum: ChordataClass: AmphibiaOrder: AnuraFamily: SooglossidaeGenus: NasikabatrachusSpecies: Nasikabatrachus sahyadrensisConservation Status: EndageredCommon name(s):  Indian purple frog, Pignosed frog, Indian purple frogMeet the Indian puple frog, an endangered and odd-looking species of frog from the mountains of India’s Western Ghats.The species was formally described only in 2003, although there was a lot of anecdotal evidence surrounding its existence. Other than its weird spherical looks, the pignosed frog also has a very unique and unusual burrowing lifestyle which is covered down below.Distribution & HabitatInitially believed to be restricted to the south of the Palghat Gap in the Western Ghats, additional research has revealed that the species distribution extends further north of the gap. Today, the pig-nosed frog is known to be distributed in the Western Ghats, ranging from the Camel's Hump Hill Range in the north, all the way to the northernmost portions of the Agasthyamalai Hill Range in the south.Purple frog distribution map(click to enlarge)DescriptionAdults have a plump, round body with a pointed, pig-like snout. The head is conical and very small compared to the rest of the body. The eyes are small and rounded, with a horizontal pupil. The skin is smooth and has a dark purple coloration that fades into grey along the stomach.Adults are about 7 cm (~2.7 in.) long, with males being about one third the size of females. The fore and hindlimbs are short but strong, allowing it to dig as far as 3.7 m (12 ft) below ground. The limbs end in partially webbed feet with rounded toes. Εach hind foot possesses a large, white wart-like growth, probably used for digging purposes.The purple frog has a skeletal structure that is characteristic of most burrowing frogs, with a strongly ossified skull and well-calcified bones.Dorsolateral (left) and frontal (right) views of a calling male that was removed from under the soil at the entrance of the tunnel from which it had been calling. The male was induced to call above ground after brief exposure to a female.Credit: Ashish Thomas [2](CC-BY-3.0)Behavior & ReproductionPignosed frogs spend most of the year underground, coming out in the surface only for about two weeks each year, to reproduce. This is why the species had gone unnoticed for so long by biologists, until 2003 when it was officially described.Mating occurs during the pre-monsoon rains, primarily in May. Males use strange calls to attract females, from burrows beside headwater streams. Once approached by females, they mount them in the amplexus position. While in amplexus in the pectoral position, the male tightly holds the vertebral column of the female. The pair then enters a crevice in a rock pool amid a flowing stream and the female lays the eggs in a clutch comprised of more than 3000 eggs. The hatchlings are tadpoles and metamorphose after about 100 days.Male frog calling from above groundDietContrary to most other burrowing frogs that emerge and feed above the ground, the purple frog forages exclusively underground, feeding primarily on termites using the tongue and a special buccal groove. It occasionally also feeds on ants and small worms. It is presumed to use its smell to forage due to the lack of light and its poor vision.N. sahyadrensis has a narrow mouth with a small gape that prevents it from catching and consuming larger prey items.Conservation StatusThis strange animal is listed by the IUCN as an endangered species, because its known distribution area covers less than 5,000 km2, with all individuals occurring in fewer than five locations. The IUCN also notes the continuing decline in the extent and quality of its habitat in the Cardamom Hills.Their main threat is forest loss due to expanding cultivation (of coffee, cardamom, ginger and other crops). The purple frog has not been reported in any protected areas, making the protection of its known habitat an urgent priority.Other Interesting Facts about the purple frog- N. sahyadrensis tadpoles were first described in 1918, without specimens of adults. The species was tentatively assigned to the family Cystignathidae.- The pignosed frog used to be considered the only extant member of an ancient amphibian family called Nasikabatrachidae. However, in 2006 the family was incorporated into the Sooglossidae- Only 135 specimens have so far been observed or collected. Only three of them were females.You may also likeTurtle Frog: A bizarre frog with a turtle-shaped body.References & Further Reading-  Biju SD, & Bossuyt F (2003). New frog family from India reveals an ancient biogeographical link with the Seychelles. Nature, 425 (6959), 711-4 PMID: 14562102- Thomas A, Suyesh R, Biju SD, & Bee MA (2014). Vocal behavior of the elusive purple frog of India (Nasikabatrachus sahyadrensis), a fossorial species endemic to the Western Ghats. PloS one, 9 (2) PMID: 24516517- C. Radhakrishnan, K. C. Gopi and Muhamed Jafer Palot (2007) Extension of range of distribution of Nasikabatrachus sahyadrensis Biju & Bossuyt (Amphibia: Anura: Nasikabatrachidae) along Western Ghats, with some insights into its bionomics. Current Science, 92(2):213-216-&nb... Read more »

  • September 10, 2014
  • 05:01 AM

Donepezil and D-cycloserine rescue behaviours in VPA exposed animals

by Paul Whiteley in Questioning Answers

In a post not-so-long-ago I talked about an interesting piece of research by Ahn and colleagues [1] suggesting that a ketogenic diet might yet hold some promise to "modify complex social behaviors and mitochondrial respiration" affected in the "prenatal valproic acid (VPA) rodent model of ASD [autism spectrum disorder]". The idea being that exposure to valproic acid (valproate) during the nine months that made us might carry some heightened risk for adverse effects on offspring development (see here) and a dietary change might rescue some functions."Daisy, Daisy, give me your answer do"Well, the floodgates have well and truly opened when it comes to looking at various pharmacological agents that 'might' also rescue abilities thought to be affected by prenatal valproate exposure as today I discuss two papers.First up is the paper by Wellmann and colleagues [2] which reported that: "D-cycloserine normalized the VPA-induced increase in play fighting in males and also increased social motivation in females". Second is the paper by Kim and colleagues [3] (open-access here) who observed: "Subchronic treatment of donepezil improved sociability and prevented repetitive behavior and hyperactivity of VPA-treated mice offspring".Aside from reiterating that these were studies of rodents and not humans, I was slightly taken aback by the reported findings. Cycloserine is normally packaged as an antibiotic but, as with many medicines these days, the pharmacological effects of the compound seem to extend far beyond the intended (antimicrobial) action [4]. I've talked about D-cycloserine before on this blog (see here) and some rather interesting research linking administration to several conditions. With autism in mind, I'll bring to your attention the paper by Urbano and colleagues [5] as one example of how far and wide this pharmaceutic is venturing. As to mode of action, well, I'd be clutching at straws if I was to hazard any guess. I might suggest that something around glutamate metabolism might be something to look at [6] which coincides with one of the proposed actions of D-cycloserine [7].Donepezil (Aricept®) falls under the category of acting as a reversible acetylcholinesterase inhibitor (AChEI). More usually indicated for dementia and particularly Alzheimer's disease [8] Kim et al describe how "prenatal exposure of valproic acid (VPA) induced dysregulation of cholinergic neuronal development, most notably the up-regulation of acetylcholinesterase (AChE) in the prefrontal cortex of affected rat and mouse offspring". You can, therefore, perhaps see the logic in using donepezil as an AChEI particularly when one takes into account how other AChE inhibitors have been studied with autistic behaviours in mind [9]. Indeed, this is not the first time that donepezil has specifically been talked about in relation to autism, mouse models of autism, as per the findings from Karvat & Kimchi [10] and their discussions based on the BTBR 'dangermouse' where: "i.p. [intraperitoneal] injection of AChEI to BTBR mice significantly relieved autism-relevant phenotypes, including decreasing cognitive rigidity, improving social preference, and enhancing social interaction, in a dose-dependent manner". And there is the promise of more to come with this medicine.Reiterating that the Wellmann and Kim results (and the Ahn results) are based on studies of rodents not people, these are an interesting datasets crying out for further replication and study. Scientific glimmers are appearing which provide further data on what biological functions might be affected by prenatal valproate exposure and importantly, what might be done to [safely] rescue certain functions. But we're not there yet... and I haven't even mentioned epigenetics [11] ...An unusual song from Ween to close... Push th' Little Daisies. Having said that, Ween are/were an unusual band...----------[1] 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.[2] Wellmann KA. et al. D-Cycloserine Ameliorates Social Alterations That Result From Prenatal Exposure To Valproic Acid. Brain Res Bull. 2014 Aug 14. pii: S0361-9230(14)00120-8.[3] Kim JW. et al. Subchronic Treatment of Donepezil Rescues Impaired Social, Hyperactive, and Stereotypic Behavior in Valproic Acid-Induced Animal Model of Autism. PLoS One. 2014 Aug 18;9(8):e104927.[4] Rodrigues H. et al. Does D-cycloserine enhance exposure therapy for anxiety disorders in humans? A meta-analysis. PLoS One. 2014 Jul 3;9(7):e93519.[5] Urbano M. et al. A trial of D-cycloserine to treat stereotypies in older adolescents and young adults with autism spectrum disorder. Clin Neuropharmacol. 2014 May-Jun;37(3):69-72.[6] Bristot Silvestrin R. et al. Animal model of autism induced by prenatal exposure to valproate: altered glutamate metabolism in the hippocampus. Brain Res. 2013 Feb 7;1495:52-60.[7] Hashimoto K. Targeting of NMDA receptors in new treatments for schizophrenia. Expert Opin Ther Targets. 2014 Sep;18(9):1049-63.[8] McGleenon BM. et al. Acetylcholinesterase inhibitors in Alzheimer’s disease. British Journal of Clinical Pharmacology. 1999; 48: 471-480.[9] Ghaleiha A. et al. Galantamine efficacy and tolerability as an augmentative therapy in autistic children: A randomized, double-blind, placebo-controlled trial. J Psychopharmacol. 2013 Oct 15;28(7):677-685.[10] Karvat G & Kimchi T. Acetylcholine elevation relieves cognitive rigidity and social deficiency in a mouse model of autism. Neuropsychopharmacology. 2014 Mar;39(4):831-40.[11] Tordjman S. et al. Gene × Environment interactions in autism spectrum disorders: role of epigenetic mechanisms. Front Psychiatry. 2014 Aug 4;5:53.----------... Read more »

  • September 9, 2014
  • 09:49 PM

Prejudice in the brain

by neurosci in Neuroscientifically Challenged

Despite the great strides that have been made toward a more egalitarian society in the United States over the past 50 years, events like what occurred in Ferguson last month are a bleak reminder of the racial tensions that still exist here. Of course, the United States is not alone in this respect; throughout the world we can see abundant examples of strain between different races, as well as between any groups with dissimilar characteristics. In fact, it seems that the quickness with which we form a negative opinion about those who are not members of the same group as us may be characteristic of human nature in general, as its effects have been pervasive throughout history, and it persists even when we attempt fastidiously to stamp it out.Indeed, it may be that our inclination towards prejudicial thinking has its roots in what was once an adaptive behavior. Some argue that our ancient hominid ancestors may have benefited from living in small groups, as this allowed for joint efforts in gathering and protecting resources. A logical offshoot of the development of group living would have been the emergence of skill in being able to tell members of your group apart from those who were not. It might have paid off to be wary of those who were not part of your group, as they would have been more likely to pose a threat. According to this evolutionary hypothesis, prejudice--which can be defined as an opinion of someone that is formed based on their group membership--may be the result of this strategy being so effective in the past. In essence, we may be saddled with the mindset of our evolutionary ancestors that makes us more skeptical at first of anyone whom we see as "different" than us.Prejudice and the amygdalaIf prejudice is a deep-seated human behavior, it would not be surprising to find networks in the brain that are selectively activated when someone has xenophobic thoughts. One area of the brain that has been investigated in this context is the amygdala.The amygdala is often associated with emotion, and is perhaps best known for its role in fear and the recognition of threats. If you were walking in the woods and saw a bear, your amygdalae would immediately become activated, helping to bring about a fear response that would encourage you to run away (or maybe cause you to freeze in place).Several neuroimaging studies have looked at what happens in the brains of people when they see images of others outside of their racial group (e.g. white people looking at images of black faces). Some findings from these studies include: the amygdala is activated upon seeing such images, amygdala activation is correlated with xenophobic attitudes of the viewer, and amygdala activity in white people is higher when viewing black faces with darker skin tone.Thus, the amygdala may serve as a threat-detection mechanism that is reflexive activated when we see an outsider. Perhaps because this has been adaptive in the past, it may act to put our brain on alert when someone outside of our racial group is near. In many societies today, however, where we are attempting to make racial divisions less distinct, this knee-jerk reaction may be counterproductive.Prejudice and the insulaAnother area of the brain that has been associated with prejudice in neuroimaging studies is the insula. The insula is also involved in processing emotional states, and has been linked to mediating feelings of social disapproval. For example, one study found that the insula and amygdala were activated in individuals while they viewed pictures of of people deemed to be social outcasts, such as homeless people or drug addicts. Because the insula is also activated when viewing pictures of people outside one's racial group, it has been hypothesized that the insula is involved in feelings of distaste that may arise when experiencing prejudicial thoughts.Prejudice and the striatumThe striatum, a subcortical area thought to play an important role in reward processing, also has been implicated in prejudice--albeit in a very different way than the amygdala and insula. Activity in the striatum correlates with rewarding experiences, and neuroimaging studies have found that the striatum is also activated when looking at pictures of individuals from one's own racial group. When white participants were tested for implicit preferences (i.e. preferences they may not state or even be aware of, but that they still seem to possess) for people of their own race, activity in the striatum was stronger in response to white faces in those who scored higher on the test for implicit preferences.Thus, there may be activity in the brain that reinforces our tendency toward prejudice in at least two ways: 1) we may be more likely to feel fear and aversion when seeing someone of another race, and 2) we may be more likely to experience positive emotions in response to seeing someone of our own race.So, if there are structures in our brains that promote prejudice, does it mean attempts to reduce our prejudices--both individually and societally--are a lost cause? Of course not. Just as there are brain structures that may make us more likely to recognize differences, there are also structures (e.g. areas of the frontal cortex) that allow us to exert control over these reflexive reactions.It's possible that the recognition of deep-seated mechanisms for prejudice could help us to understand racism a little better. It could, for example, provide insight into why people in high-stress situations may be more likely to see things as divided down racial lines. For, if their brains are already inclined to see people of another race as more threatening and they are in a stressful situation, they may be quicker to identify someone of a different race as the threat.However, the extent to which such innate responses to outsiders affects our behavior is still somewhat unclear, and the hypothesis that they are remnants of once-adaptive behavior is just that: a hypothesis. For practical purposes, it may not matter exactly what the basis of prejudicial thinking is, as we are certain it's a thought pattern that doesn't have much remaining value in today's world. However, being open to the idea that we have some inclinations toward prejudicial thinking may help us to be able to train people to more mindfully deal with high-stress interactions with people of another race. For, instead of pretending these prejudicial thoughts don't (or shouldn't) happen, it would allow us to focus more on ways to mitigate the damage that might occur when they do.Amodio DM (2014). The neuroscience of prejudice and stereotyping. Nature reviews. Neuroscience PMID: 25186236... Read more »

  • September 9, 2014
  • 02:35 PM

Autism and Testosterone

by Gabriel in Lunatic Laboratories

As a male we are at higher risk for heart disease, we are also at higher risk for stroke. It’s that pesky testosterone, sure it has its benefits, don’t get me wrong I think testosterone over all is great. Estrogen has it’s own downsides too, things like certain cancers for example. Well estrogen has some other benefits and as it turns out, the same sex hormone that helps protect females from stroke may also reduce their risk of autism.... Read more »

Amanda Crider,, Roshni Thakkar,, Anthony O Ahmed, & Anilkumar Pillai. (2014) Dysregulation of estrogen receptor beta (ERβ), aromatase (CYP19A1), and ER co-activators in the middle frontal gyrus of autism spectrum disorder subjects. Molecular Autism . info:/10.1186/2040-2392-5-46

  • September 9, 2014
  • 09:37 AM

Elderly Seabirds Dive Just as Well as Young Ones

by Elizabeth Preston in Inkfish

If your grandma got up from the sofa, did a couple toe-touches, and then ran a mile at her college track pace, she might be approaching the athletic skill of a thick-billed murre. These seabirds make incredibly deep, long dives to catch prey. As they age, their bodies slow and change like ours. But the […]The post Elderly Seabirds Dive Just as Well as Young Ones appeared first on Inkfish.... Read more »

  • September 9, 2014
  • 04:35 AM

The gondii and generalised anxiety disorder

by Paul Whiteley in Questioning Answers

Toxoplasma gondii (T. gondii) has been absent from discussions on this blog for a while now. I'm going to remedy that today with this post talking about the paper from Markovitz and colleagues [1] who concluded: "T. gondii infection may play a role in the development of GAD [generalized anxiety disorder]"."You have saved our lives. We are eternally grateful"Based on participants taking part in the Detroit Neighborhood Health Study exposure to T. gondii "defined by seropositivity and IgG antibody levels" was measured in approaching 500 people. Psychiatric diagnoses including depression, PTSD (posttraumatic stress disorder) and GAD were ascertained and data analysed to see if there was anything correlation-wise between T. gondii exposure and the various conditions.The results suggested that T. gondii exposure was "associated with a 2 times greater odds of GAD" when taking into account various potential confounding variables. Those with some of the highest antibody levels to T. gondii were over three times at greater risk of GAD, potentially suggesting a dose-response relationship. Ergo, "T. gondii infection is strongly and significantly associated with GAD" but with more research to do.Although no expert on GAD, I was a little puzzled by the Markovitz results. My previous musings on T. gondii and how it manages to alter rodent behaviour would seem to imply that this protozoan has an opposite effect on animal anxiety (i.e. reducing or modifying anxiety and predation-related fear [2]). Of course mice/rats are mice/rats and not humans but one might have expected something of an opposite effect [3].That being said, this is not the first time that anxiety (human anxiety) has been mentioned alongside T. gondii as per the paper by Groër and colleagues [4] (open-access). In that case authors concluded that: "Higher T gondii immunoglobulin G titers in infected women were related to anxiety and depression during pregnancy". Some clarification is perhaps needed in this area...To close, music I've probably linked to before but it's so good I'm gonna do it again: REM and It's the End of the World...----------[1] Markovitz A. et al. Toxoplasma gondii and anxiety disorders in a community-based sample. Brain Behav Immun. 2014 Aug 11. pii: S0889-1591(14)00418-8.[2] Kaushik M. et al. The role of parasites and pathogens in influencing generalised anxiety and predation-related fear in the mammalian central nervous system. Horm Behav. 2012 Aug;62(3):191-201.[3] Gonzalez LE. et al. Toxoplasma gondii infection lower anxiety as measured in the plus-maze and social interaction tests in rats A behavioral analysis. Behav Brain Res. 2007 Feb 12;177(1):70-9.[4] Groër MW. et al. Prenatal depression and anxiety in Toxoplasma gondii-positive women. Am J Obstet Gynecol. 2011 May;204(5):433.e1-7.----------Markovitz A, Simanek AM, Yolken R, Galea S, Koenen KC, Chen S, & Aiello AE (2014). Toxoplasma gondii and anxiety disorders in a community-based sample. Brain, behavior, and immunity PMID: 25124709... Read more »

Markovitz A, Simanek AM, Yolken R, Galea S, Koenen KC, Chen S, & Aiello AE. (2014) Toxoplasma gondii and anxiety disorders in a community-based sample. Brain, behavior, and immunity. PMID: 25124709  

  • September 8, 2014
  • 09:05 PM

The atmosphere and what we eat: significant increases in greenhouse gas emissions predicted for high-calorie diets recommended by USDA

by Jonathan Trinastic in Goodnight Earth

New research shows that shifting to recommended, high-calorie USDA diets could increase GHG emissions due to the dairy required to make up for reduced meat/poultry calories. What we eat impacts our long-term environment!... Read more »

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