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  • August 28, 2014
  • 12:52 PM
  • 177 views

The Things Living on your Toothbrush…

by Gabriel in Lunatic Laboratories

Did you remember to brush? I hope you did, but you may be throwing away your toothbrush soon. Get ready for your daily amount of gross, because have I got a scientific discovery that will make you rethink your dental hygiene. Researchers have found that “solid-head” power toothbrushes have up to 3,000 times less bacteria when compared to “hollow-head” toothbrushes.[…]... Read more »

Morris DW, Goldschmidt M, Keene H, & Cron SG. (2014) Microbial contamination of power toothbrushes: a comparison of solid-head versus hollow-head designs. Journal of dental hygiene : JDH / American Dental Hygienists' Association, 88(4), 237-42. PMID: 25134956  

  • August 28, 2014
  • 04:29 AM
  • 125 views

Minocycline for schizophrenia?

by Paul Whiteley in Questioning Answers

"Minocycline may improve the psychopathology of schizophrenia, especially the negative symptoms, and seems to be well tolerated".A Bachelors Drawer (apparently) @ Wikipedia That was the finding from the systematic review and meta-analysis undertaken by Oya and colleagues [1] looking at the collected literature on the use of "minocycline augmentation therapy in patients with schizophrenia receiving antipsychotic agents". Augmentation therapy by the way, refers to the addition of minocycline to existing pharmacotherapy for schizophrenia.I wasn't all that surprised to read the Oya paper given that for some time now, there have been scientific rumblings about how antibiotics might do quite a bit more than just 'killing bacteria' [2]. "Scientists shocked" was how one media report has previously talked about this area of research; which conjures up all-manner of visions of stunned science-types walking around with lab coats on and mouths and eyes wide open in amazement.The reports that minocycline might act on the negative symptoms of schizophrenia (see here) is also quite an important detail, because these are often the symptoms which affect daily living skills, potentially manifesting as "losing interest and motivation in life and activities, including relationships and sex... [and a] lack of concentration, not wanting to leave the house and changes in sleeping patterns". These are also the symptoms which tend to respond less well to traditional management strategies like medication.The final question(s) are how and why does minocycline affect cases of schizophrenia? The paper from Zhang and Zhao [3] (open-access) provides quite a good overview of the various hypotheses put forward. Unsurprisingly, some effect on inflammation figures quite strongly in the suggestions put forward. I could go on and on and on about the various research in this area (see here for example) but won't on this occasion. Instead, I'll direct you to a previous post I wrote on minocycline and Fragile X syndrome (see here) which mentions some effect from minocycline on matrix metalloproteinase-9 (MMP-9). I'd like to think that this is a potentially important point because of the tie-in with something like homocysteine (see here), the big H, which has also been mentioned with schizophrenia in mind (see here). Just speculatin' of course.Music to close. Frank Sinatra and something about a lot of coffee in Brazil?----------[1] Oya K. et al. Efficacy and tolerability of minocycline augmentation therapy in schizophrenia: a systematic review and meta-analysis of randomized controlled trials. Hum Psychopharmacol. 2014 Aug 4.[2] Levkovitz Y. et al. A double-blind, randomized study of minocycline for the treatment of negative and cognitive symptoms in early-phase schizophrenia. J Clin Psychiatry. 2010 Feb;71(2):138-49.[3] Zhang L. & Zhao J. Profile of minocycline and its potential in the treatment of schizophrenia. Neuropsychiatr Dis Treat. 2014 Jun 17;10:1103-11.----------Oya K, Kishi T, & Iwata N (2014). Efficacy and tolerability of minocycline augmentation therapy in schizophrenia: a systematic review and meta-analysis of randomized controlled trials. Human psychopharmacology PMID: 25087702... Read more »

  • August 27, 2014
  • 07:35 PM
  • 135 views

(False?) Positive Psychology Meets Genomics

by Neuroskeptic in Neuroskeptic_Discover

Academic bunfight ahoy! A new paper from Nick Brown – famed debunker of the “Positivity Ratio” – and his colleagues, takes aim at another piece of research on feel-good emotions. The target is a 2013 paper published in PNAS from positive psychology leader Barbara Fredrickson and colleagues: A functional genomic perspective on human well-being. The […]The post (False?) Positive Psychology Meets Genomics appeared first on Neuroskeptic.... Read more »

Brown, N., MacDonald, D., Samanta, M., Friedman, H., & Coyne, J. (2014) A critical reanalysis of the relationship between genomics and well-being. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1407057111  

  • August 27, 2014
  • 05:39 PM
  • 122 views

Climate change research roundup: hiding heat in the Atlantic and the Arctic carbon cycle

by Jonathan Trinastic in Goodnight Earth

A quick roundup of new climate change research in Science: the Atlantic Ocean may be hiding the missing heat to explain the global warming hiatus, and photochemical processes in the Arctic are releasing more CO2 than previously thought.... Read more »

  • August 27, 2014
  • 03:23 PM
  • 134 views

The Learning Brain Unravelled

by Gabriel in Lunatic Laboratories

As an engineer you would think math would come easy to me, it didn’t. Funny thing though, science in general and biology in particular came very easy to me. The big question is why? Why would math, something I need to know how to do for my work and my degree, be so hard to learn? Thankfully science has stepped in to answer the question, at least partially, about why somethings can come so easy to a person and other things (like me and math) take so much longer to pick up.[…]... Read more »

Patrick T. Sadtler,, Kristin M. Quick,, Matthew D. Golub,, Steven M. Chase,, Stephen I. Ryu,, Elizabeth C. Tyler-Kabara,, Byron M. Yu,, & Aaron P. Batista. (2014) Neural constraints on learning. Nature. info:/10.1038/nature13665

  • August 27, 2014
  • 09:45 AM
  • 123 views

Is it really possible for someone to turn into THE HULK? Don’t make me angry.

by Bill Sullivan in The 'Scope

Could epigenetics provide a bit of a biological explanation behind THE HULK?... Read more »

  • August 27, 2014
  • 09:38 AM
  • 82 views

Video Tip of the Week: Phenoscape, captures phenotype data across taxa

by Mary in OpenHelix

Development of the skeleton is a good example of a process that is highly regulated, requires a lot of precision, is conserved and important relationships across species, and is fairly easy to detect when it’s gone awry. I mean–it’s hard to know at a glance if all the neurons in an organism got to the […]... Read more »

Mabee By Paula, Balhoff James P, Dahdul Wasila M, Lapp Hilmar, Midford Peter E, Vision Todd J, & Westerfield Monte. (2012) 500,000 fish phenotypes: The new informatics landscape for evolutionary and developmental biology of the vertebrate skeleton. Zeitschrift fur angewandte Ichthyologie . PMID: 22736877  

Balhoff James P., Cartik R. Kothari, Hilmar Lapp, John G. Lundberg, Paula Mabee, Peter E. Midford, Monte Westerfield, & Todd J. Vision. (2010) Phenex: Ontological Annotation of Phenotypic Diversity. PLoS ONE, 5(5). DOI: http://dx.doi.org/10.1371/journal.pone.0010500  

  • August 27, 2014
  • 09:18 AM
  • 154 views

Co-Chaperone Keeps Close Watch on Mice Sperm Production

by Christina Szalinski in ASCB Post

Chaperones aren't just for high-school homecoming dances. Cells have chaperones as well, chaperone proteins that ensure newly made proteins are properly folded. If protein folding goes awry, diseases associated with misfolded proteins such as Alzheimer's and Parkinson's can arise. But if one set of chaperones can throw a wet blanket on a school dance, imagine a second set of co-chaperones just to keep the chaperones in check. That's the growing picture in cellular chaperoning as folding guardians of the cell turn out to have guardians of their own. Another example of co-chaperone proteins with an unexpected phenotype was just discovered by Jörg Höhfeld, professor at the Institute of Cell Biology at the University of Bern, and his colleagues who report a critical role for the co-chaperone, HSPBP1, in spermatogenesis in a mouse model. ... Read more »

  • August 27, 2014
  • 08:25 AM
  • 174 views

Let’s Chew The Fat

by Mark Lasbury in As Many Exceptions As Rules

If vegetables are low fat, how can we make cooking oils from them? The key is that vegetable oils aren’t really vegetable oils- they’re fruit oils. In some plant fruits, the fats are sued to entice animals to eat them and disperse seeds. In other, the fats are used to provide energy for the embryonic plants. New research is showing that some plant oils have unique uses. A 2014 study shows that avocado oil is as good or better at stabilizing biochemical markers in patients with metabolic syndromes. A 2013 study suggests that palm kernel oil ester nanoemulsions will be useful in carrying antibiotics across the blood brain barrier to treat bacterial meningitis.... Read more »

Carvajal-Zarrabal O, Nolasco-Hipolito C, Aguilar-Uscanga MG, Melo Santiesteban G, Hayward-Jones PM, & Barradas-Dermitz DM. (2014) Effect of dietary intake of avocado oil and olive oil on biochemical markers of liver function in sucrose-fed rats. BioMed research international, 595479. PMID: 24860825  

  • August 27, 2014
  • 03:56 AM
  • 138 views

Prenatal SSRI exposure and autistic traits

by Paul Whiteley in Questioning Answers

A quote to start today's post: "Our results suggest an association between prenatal SSRI exposure and autistic traits in children". That was a primary finding reported by Hanan El Marroun and colleagues [1] who looked at whether maternal depressive symptoms or a class of quite commonly used pharmaceutics - the selective serotonin reuptake inhibitors (SSRIs) - used to manage depressive symptoms, during pregnancy might impact on offspring development."Everything the light touches is our kingdom" Before progressing through some of the details around this area, I'm going to also direct your attention to a couple of important accompanying commentaries on the Marroun findings from Jones & McDonald [2] and Petersen and colleagues [3] (open-access). Both caution about reading too much too soon into the reported association between SSRIs and offspring outcomes, and the very real outcomes that can come about if psychiatric issues such as depression are not properly managed. Something I think most people might have heard about recently.A few details about the Marroun paper might be useful:Following some previous discussions correlating maternal SSRI use during pregnancy and offspring outcome with autism in mind (see here) including the quite recent papers by Harrington and colleagues [4] and Rai and colleagues [5], the authors looked to "prospectively determine whether intra-uterine SSRI exposure is associated with childhood autistic symptoms in a population-based study". "A total of 376 children prenatally exposed to maternal depressive symptoms (no SSRI exposure), 69 children prenatally exposed to SSRIs and 5531 unexposed children were included" for study. The commentary from Petersen et al notes how small a group were actually exposed to SSRIs and how "these numbers rapidly dwindled when it came to the measurement of the outcome".The Child Behavior Checklist and Social Responsiveness Scale (SRS) were used to assess "pervasive developmental and affective problems" and "autistic traits" respectively. Results: aside from an association between prenatal selective serotonin reuptake inhibitor (SSRI) exposure and autistic traits in children, researchers also reported that: "Prenatal exposure to maternal depressive symptoms without SSRIs was related to both pervasive developmental (odds ratio (OR) = 1.44, 95% CI 1.07-1.93) and affective problems (OR = 1.44, 95% CI 1.15-1.81)". The suggested link between maternal depressive symptoms and autistic traits was to some degree weaker than the SSRI exposure correlation.The authors conclude that: "Long-term drug safety trials are needed before evidence-based recommendations are possible" as once again I'll direct you to the Jones and Petersen commentaries.In the same way that the emerging data on prenatal valproate exposure *might* link into offspring outcome including the presence of autism (see here), so the Marroun paper potentially adds another medicine to the list. I would perhaps temper that last sentence by adding that the valproate story is perhaps a little further along in terms of rodent models of prenatal valproate exposure mimicking some features of autism (see here) and the data providing something like mechanisms to be looked at with further investigations in mind [6]. Still, the CDC Treating for Two initiative might be once again relevant.The added complication with the SSRI-autism correlation is the discussion about maternal depressive symptoms also potentially mediating any link with offspring autism or autistic traits. The paper by Sørensen and colleagues [7] (open-access here) kinda hinted that this and other important confounding factors might impact on any studies of association, including details like: "paternal antidepressant use during the time of pregnancy was not associated with an increased risk of autism spectrum disorders, except for a 30% increase when the fathers took SSRI". Even more recently Clements and colleagues [8] talked about how maternal "major depression" confounded any medication relationship with offspring presentation. They also talked about a link with ADHD which brings me back to yesterday's post on comorbidity (see here)...One would do well not to discount such confounding factors at this stage. Indeed, if one assumes that depression might have a physiological link to something like inflammation for example [9] we then start to arrive at the increasingly important research looking at maternal inflammation as being a risk factor for offspring autism (see here). And before you ask, yes, C-reactive protein (CRP) has been linked to depressive symptoms as per the meta-analysis by Valkanova and colleagues [10].The Marroun results are interesting and add something to an increasing bank of peer-reviewed literature [11] suggestive of a possible link between SSRI use during pregnancy and offspring outcomes. On the basis of the current existing literature and with my blogging caveat of no medical advice given or intended, I would be minded to conclude that there is quite a bit more experimental investigation to be done on this category of medicines. But I don't yet think there is enough clear evidence to conclusively put an elevated risk of offspring autism on the list of potential side-effects of these medicines.Music then. Scissor Sisters and Laura.----------[1] Marroun HE. et al. Prenatal exposure to selective serotonin reuptake inhibitors and social responsiveness symptoms of autism: population-based study of young children. The British Journal of Psychiatry. 2014; 205: 95-102.[2] Jones I. & McDonald L. Living with uncertainty: antidepressants and pregnancy. The British Journal of Psychiatry. 2014; 205: 103-104.[3] Petersen I. et al. Prenatal exposure to selective serotonin reuptake inhibitors and autistic symptoms in young children: another red herring? The British Journal of Psychiatry. 2014; 205: 105-106.[4] Harrington RA. et al. Prenatal SSRI Use and Offspring With Autism Spectrum Disorder or Developmental Delay. Pediatrics. 2014 Apr 14.[5] Rai D. et al. Parental depression, maternal antidepressant use during pregnancy, and risk of autism spectrum disorders: population base... Read more »

  • August 26, 2014
  • 02:50 PM
  • 107 views

August 26, 2014

by Erin Campbell in HighMag Blog

If you have little ones in your house, you might assume that the phrase “randomly fluctuating forces” is referring to your home. This phrase actually refers to the background force in a cell coming from active and motor-driven cell processes. Today’s image is from a study that developed a way to measure these forces. Actin- and microtubule-based motors move many types of material around a cell to drive critical cellular events. These motor-driven movements and other active processes in the cell contribute to a background of fluctuating forces in a cell. These stochastic forces collectively drive random motion of organelles and proteins within a cell, in turn affecting the dynamics and metabolic state of a cell. To measure these forces, Guo and colleagues developed force spectrum microscopy (FSM) to directly quantify the fluctuating forces in a cell’s cytoplasm, specifically by measuring the movements of individual injected particles. Guo and colleagues found that these forces are strong enough to move both large and small components, and that malignant cells have a higher level of fluctuating forces compared to benign cells. Image above shows a cell with injected particles (green), with the 2-minute trajectories (black) superimposed.Guo, M., Ehrlicher, A., Jensen, M., Renz, M., Moore, J., Goldman, R., Lippincott-Schwartz, J., Mackintosh, F., & Weitz, D. (2014). Probing the Stochastic, Motor-Driven Properties of the Cytoplasm Using Force Spectrum Microscopy Cell, 158 (4), 822-832 DOI: 10.1016/j.cell.2014.06.051Copyright ©2014 Elsevier Ltd. All rights reserved. ... Read more »

Guo, M., Ehrlicher, A., Jensen, M., Renz, M., Moore, J., Goldman, R., Lippincott-Schwartz, J., Mackintosh, F., & Weitz, D. (2014) Probing the Stochastic, Motor-Driven Properties of the Cytoplasm Using Force Spectrum Microscopy. Cell, 158(4), 822-832. DOI: 10.1016/j.cell.2014.06.051  

  • August 26, 2014
  • 12:09 PM
  • 91 views

For These Bats, the Best Falsetto Wins Over the Ladies

by Elizabeth Preston in Inkfish

A bat’s voice is its livelihood. Chirping and squeaking at just the right frequencies lets it echolocate food and stay alive. Sounding pretty isn’t the point—except when it is. For the first time, scientists think they’ve found a bat species in which females choose mates based on their voices. Even if a lower-frequency squeak might […]The post For These Bats, the Best Falsetto Wins Over the Ladies appeared first on Inkfish.... Read more »

  • August 26, 2014
  • 04:39 AM
  • 138 views

Brian Hooker's Hooked Hoax: Measles-Mumps-Rubella (MMR) Vaccination and Autism Spectrum Disorder

by Alexis Delanoir in How to Paint Your Panda

10 years after the initial study by DeStefano et al. (2004) was conducted, famous anti-vaccine alarmist Brian Hooker, along with Andrew Wakefield, are talking about a "whistleblower" in the CDC claiming that the original data was fraudulent, and was masking a 336% increased risk in ASD in African American boys receiving the MMR vaccine "on time." Did Hooker prove anything in his new study, however? Only that he doesn't understand epidemiology or statistics.... Read more »

  • August 26, 2014
  • 03:55 AM
  • 111 views

76% of youths with autism meet ADHD diagnostic criteria?

by Paul Whiteley in Questioning Answers

Autism is not normally a stand-alone diagnosis. I've mentioned that point a few times on this blog, stressing how a clinical diagnosis of autism appears to increase the risk of various other behavioural, psychiatric and somatic diagnoses also [variably] being present over a lifetime. Part of that comorbidity has been talked about in discussions about ESSENCE (see here) and the excellent document produced by Treating Autism on medical comorbidities occurring alongside autism (see here) for example. Prof. Gillberg's recent scientific publication called 'Autism Plus Versus Autism Pure' [1] kinda adds to this notion and his very strongly worded sentiments: "It is high time that the comorbidities, sometimes even more important than the autism, came back on the diagnostic agenda".Cheeky... @ Wikipedia Outside of the more traditional comorbidities mentioned in the same breath as some autism, such as learning disability (intellectual disability) and epilepsy or seizure-type disorders, quite a lot of attention is being focused on the overlap between autism and attention-deficit hyperactivity disorder (ADHD). Indeed, the paper by Gagan Joshi and colleagues [2] very much thrusts ADHD into the autism diagnostic arena with their assertion of: "A high rate of comorbidity with ADHD was observed in psychiatrically referred youth with ASD [autism spectrum disorder], with a clinical presentation typical of the disorder".The Joshi paper sought to "compare the clinical presentation of ADHD between youth with autism spectrum disorder (ASD) and ADHD and a sample of youth with ADHD only". What they found is something remarkably similar to the typical presentation of ADHD (without autism) insofar as age of onset and "distribution of diagnostic subtypes, the qualitative and quantitative symptom profile, and symptom severity". I might add that their participant group was classified as "High-Functioning" (their words not mine) so one needs to be mindful that only one part of the autism spectrum was surveyed.What is perhaps slightly worrying from the Joshi results was the finding that: "a significant majority of ASD youth with ADHD failed to receive appropriate ADHD treatment". ADHD treatment, as I've mentioned in previous posts, normally implies pharmacotherapy but can also include other intervention options as per discussions on things like dietary changes potentially being useful for some (see here). Indeed, I've talked about the some of the results from things like the use of a gluten- and casein-free (GFCF) diet when applied to autism and how ADHD-type symptoms might be the more important targets for intervention (see here). The idea also that outside of just affecting ADHD symptom profiles, intervention might also have knock-on effects for other areas as per the review by Daley and colleagues [3] is similarly important.I don't want to linger further on this issue aside from reiterating that the presentation of autism is, more often than not, part of a complex tapestry of presentation which can cover various other diagnostic categories. ADHD or sub-threshold ADHD-type symptoms are being realised as fairly frequent companions to a diagnosis of autism. The changes to the diagnostic criteria for ADHD (see here) will no doubt further expand the link between autism and ADHD, placing yet more emphasis on how autism is not normally a stand-alone diagnosis.Music to close. Ray Charles and You Don't Know Me.----------[1] Gillberg C. & Fernell E. Autism Plus Versus Autism Pure. J Autism Dev Disord. 2014 Jun 24.[2] Joshi G. et al. Symptom Profile of ADHD in Youth With High-Functioning Autism Spectrum Disorder: A Comparative Study in Psychiatrically Referred Populations. J Atten Disord. 2014 Aug 1. pii: 1087054714543368.[3] Daley D. et al. Behavioral Interventions in Attention-Deficit/Hyperactivity Disorder: A Meta-Analysis of Randomized Controlled Trials Across Multiple Outcome Domains. J Am Acad Child Adolesc Psychiatry. 2014 Aug;53(8):835-847.e5.----------Joshi G, Faraone SV, Wozniak J, Tarko L, Fried R, Galdo M, Furtak SL, & Biederman J (2014). Symptom Profile of ADHD in Youth With High-Functioning Autism Spectrum Disorder: A Comparative Study in Psychiatrically Referred Populations. Journal of attention disorders PMID: 25085653... Read more »

  • August 25, 2014
  • 07:13 PM
  • 101 views

Zombie Ant Fungi knows it’s prey

by Gabriel in Lunatic Laboratories

So awhile back I was bored and to kill some time wisely I wrote this little bit on real life (sometime potential) zombies. It featured a special section on a particular group of fungi that created some really crazy zombie ants. Ants, which would do the bidding of the fungus, would eventually latch itself in a “death bite” and sprout the parasite from its head. Yeah I know, not a pleasant death. In any case new research is showing just how cool — and evidently smart — these fungi really are.[…]... Read more »

de Bekker C, Quevillon LE, Smith PB, Fleming KR, Ghosh D, Patterson AD, & Hughes DP. (2014) Species-specific ant brain manipulation by a specialized fungal parasite. BMC evolutionary biology, 14(1), 166. PMID: 25085339  

  • August 25, 2014
  • 02:56 PM
  • 97 views

Coronavirus proteases, p62/SQSTM1, and Deubiquitinases

by theloenvirologist in Virology Tidbits

Ubiquitin is a small protein of 9kDa inside present in all eukaryotic cells and involved in the degradation of proteins by covalently binding target proteins which requires different enzymes, the E1 activating enzyme, the E2 conjugation enzymes, and the E3 ubiquitin ligase. Deubiquitinating enzymes (DUBs) can reverse the ubiquitination of substrates thus preventing the degradation of proteins and can be classified into two main classes, cysteine proteases and metalloproteases. Here the role of the coronaviral proteases 3CLpro and 3Cpro is discussed in relation to p62/SQSTM1 induced autophagy. ... Read more »

van Kasteren PB, Bailey-Elkin BA, James TW, Ninaber DK, Beugeling C, Khajehpour M, Snijder EJ, Mark BL, & Kikkert M. (2013) Deubiquitinase function of arterivirus papain-like protease 2 suppresses the innate immune response in infected host cells. Proceedings of the National Academy of Sciences of the United States of America, 110(9). PMID: 23401522  

Ratia K, Saikatendu KS, Santarsiero BD, Barretto N, Baker SC, Stevens RC, & Mesecar AD. (2006) Severe acute respiratory syndrome coronavirus papain-like protease: structure of a viral deubiquitinating enzyme. Proceedings of the National Academy of Sciences of the United States of America, 103(15), 5717-22. PMID: 16581910  

Clementz MA, Chen Z, Banach BS, Wang Y, Sun L, Ratia K, Baez-Santos YM, Wang J, Takayama J, Ghosh AK.... (2010) Deubiquitinating and interferon antagonism activities of coronavirus papain-like proteases. Journal of virology, 84(9), 4619-29. PMID: 20181693  

  • August 25, 2014
  • 11:11 AM
  • 106 views

E-cigs Aren't Safe

by Viputheshwar Sitaraman in Draw Science

Vaping through e-cigs brings out the harms in components of nicotine that are considered nanoparticles that can clog the smaller airways in our lungs.... Read more »

Grana, R., Benowitz, N., & Glantz, S. (2014) E-Cigarettes: A Scientific Review. Circulation, 129(19), 1972-1986. DOI: 10.1161/​CIRCULATIONAHA.114.007667  

  • August 25, 2014
  • 08:28 AM
  • 146 views

Chinese Food And The One Hour Dilemma

by Mark E. Lasbury in The 'Scope

Everyone thinks they have the answer to why you get hungry soon after eating a plate of Chinese food, but it may be more complex than a simple answer. Some people blame MSG, others say it is the higher glycemic index of rice and noodles, while others claim it is the low fat, low protein aspects of Chinese food. New studies shows that MSG, high glycemic index foods and vegetable protein diets do not alter satiety and hunger hormone levels as compared to other meal types. It may be that the satiety index is more telling. Americans accustomed to potatoes feel hungrier after rice or noodles because potatoes have the highest satiety index of any food tested. ... Read more »

  • August 25, 2014
  • 07:00 AM
  • 89 views

The Curious Case of a Protein and a Pilus

by Moselio Schaechter in Small Things Considered

by Monika Buczek | If you’re like me, every morning you reluctantly roll out of bed and automatically reach for your toothbrush. One of the earliest learned practices of personal hygiene, brushing surely serves more than just preventing daybreak halitosis- but have you ever pondered about the plaque you try to dislodge from your…... Read more »

Reardon-Robinson ME, Wu C, Mishra A, Chang C, Bier N, Das A, & Ton-That H. (2014) Pilus hijacking by a bacterial coaggregation factor critical for oral biofilm development. Proceedings of the National Academy of Sciences of the United States of America, 111(10), 3835-40. PMID: 24567409  

  • August 25, 2014
  • 04:40 AM
  • 121 views

mTOR-regulated autophagy and autism mouse models

by Paul Whiteley in Questioning Answers

I was intrigued to read the paper by Guomei Tang and colleagues [1] (open-access) and their assertion that: "mTOR [mammalian target of rapamycin]-regulated autophagy is required for developmental spine pruning, and activation of neuronal autophagy corrects synaptic pathology and social behavior deficits in ASD [autism spectrum disorder] models with hyperactivated mTOR"."Re-verify our range to target... one ping only".If that opening paragraph sounds like scientific gibberish, I'll refer you to one of the many media write-ups of the study (see here) describing how, among other things, researchers looked at brain tissue from the deceased with autism compared with those asymptomatic for autism and counted 'spines' (dendritic spines) - protrusions from a neuron. They reported "increased dendritic spine density with reduced developmental spine pruning in layer V pyramidal neurons in postmortem ASD temporal lobe". This is interpreted as "an oversupply of synapses" in certain parts of the brain and lead to headlines such as: "Scientists discover people with autism have too many brain 'connections'". All of this ties into the debates about brain connectivity in autism [2].The next part of the Tang findings revolve around one of the possible 'whys' for their surplus of synapses findings talking about possible issues with the process of autophagy [3] - a sort of cellular housekeeping. The idea being that there are processes at work which clear out cells which we don't need or that are damaged including synaptic pruning. Here, the authors focused on something called mTOR (which has been previously discussed on this blog) specifically with it's link to autophagy [4]. Based on a mouse model of tuberous sclerosis (see here), a condition associated with autistic-like behaviour [5], researchers reported issues with mTOR activity which seemed to overlap with the findings of synaptic oversupply noted in brain samples from those with autism. Further "the medication rapamycin both restores normal synaptic pruning and reduces autism-like behaviors in a mouse model of autism" according to another commentary on the Tang study.The NHS Choices website has already given the Tang study the once-over (see here) and noted: "this research is in its very early stages. It mainly helps our understanding of the brain changes that may be involved in this condition. It is too soon to say whether it could lead to any treatment for autism spectrum disorders, and even if it does it is likely to be a long way off". I'd echo those sentiments as well as adding a few of my own.First, although no expert on the analysis of neural tissue, I note some more knowledgeable commentators have talked about how careful one has to be when drawing too many conclusions based on postmortem studies (see here). This also means taking into account the effect of any comorbidity that appeared alongside the diagnosis of autism and what role that might play in any results obtained. Second, is the reliance on a mouse model of autism (emphasis on 'mouse model') which, although overlapping with some autistic behaviours and with possibly related findings [6], is not necessarily representative of quite a lot of autism. Tuberous sclerosis for example, does seem to show some kind of relationship with autism [7] but as with other proposed less idiopathic types of autism (see here) one has to be a little bit careful in over-extrapolating any connection. Same goes for when one talks about increased spine density being found in all autism [8]. Finally, rapamycin is not exactly what one might call a desirable medication as a consequence of it's primary use and possible side-effects. I'm not saying that it doesn't have it's uses, just that when applied to real people with autism (not mouse models), the peer-reviewed literature is currently very, very sparse when it comes to efficacy and importantly safety. That being said, there may be other ways to inhibit mTOR [9] bearing in mind my caveat about not giving medical or clinical advice on this blog...Music then. Rather Be...----------[1] Tang G. et al. Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits. Neuron. 2014. August 21.[2] Uddin LQ. et al. Reconceptualizing functional brain connectivity in autism from a developmental perspective. Front Hum Neurosci. 2013 Aug 7;7:458.[3] Glick D. et al. Autophagy: cellular and molecular mechanisms. J Pathol. 2010 May;221(1):3-12.[4] Jung CH. et al. mTOR regulation of autophagy. FEBS Lett. 2010 Apr 2;584(7):1287-95.[5] Reith RM. et al. Loss of Tsc2 in Purkinje cells is associated with autistic-like behavior in a mouse model of tuberous sclerosis complex. Neurobiol Dis. 2013 Mar;51:93-103.[6] Isshiki M. et al. Enhanced synapse remodelling as a common phenotype in mouse models of autism. Nat Commun. 2014 Aug 21;5:4742.[7] Smalley SL. Autism and tuberous sclerosis. J Autism Dev Disord. 1998 Oct;28(5):407-14.[8] Wei H. et al. The therapeutic effect of memantine through the stimulation of synapse formation and dendritic spine maturation in autism and fragile X syndrome. PLoS One. 2012;7(5):e36981.[9] Theoharides TC. et al. Focal brain inflammation and autism. J Neuroinflammation. 2013 Apr 9;10:46.----------... Read more »

Tang, G., Gudsnuk, K., Kuo, S., Cotrina, M., Rosoklija, G., Sosunov, A., Sonders, M., Kanter, E., Castagna, C., Yamamoto, A.... (2014) Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits. Neuron. DOI: 10.1016/j.neuron.2014.07.040  

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