"Among adult patients with epilepsy of unknown etiology, a significant minority had detectable serum Abs [autoantibodies] suggesting an autoimmune etiology."So said the findings reported by Divyanshu Dubey and colleagues  continuing a research theme previously discussed on this blog (see here) on how epilepsy / seizure-type disorder(s) for some might have more to do with immune function than many people might think.OK, a brief bit of background: epilepsy is a blanket term covering a wide variety of different presentations that affect the brain and specifically, 'the electrics' of the brain. Seizures are the most common symptom. Treatment typically comes in the form of anti-epileptic medicines (although other options are being considered for some). It's been known for a while that outside of the 'brain' focus of epilepsy, other biological systems might also play a role in the development/maintenance of the condition(s); specifically the immune system and quite often in cases where traditional anti-epileptic medicines don't seem to be able to control seizures effectively. The details are still a little sketchy but studies like the one from Dubey et al are trying to put some scientific flesh on to the bones of what facets of the immune system are potentially involved, specifically under 'autoimmune' conditions where the body fails to recognise 'self' as self and mounts an immune response against the body's own tissue(s).Dubey and colleagues looked at a group of participants "presenting to neurology services with new-onset epilepsy or established epilepsy of unknown etiology" and tested donated serum samples "for Abs reported to be associated with autoimmune epilepsy (NMDAR-Ab, VGKCc-Ab, leucine-rich glioma-inactivated protein 1 [LGI1] Ab, GAD65-Ab, γ-aminobutyric acid type B receptor [GABAB] Ab, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic receptor [AMPAR] Ab, antineuronal nuclear antibody type 1 [ANNA-1 or anti-Hu] Ab, Purkinje cell cytoplasmic antibody type 2 [PCA-2] Ab, amphiphysin Ab, collapsin-response mediator protein 5 [CRMP-5] Ab, and thyroperoxidase [TPO] Ab)." Quite a lot of those autoantibodies probably sound like gibberish to the lay reader but some of them have been discussed in other contexts on this blog (see here and see here for examples).Results: some (15) of the 127 participants initially enrolled in the study were "subsequently excluded after identification of an alternative diagnosis." This in itself is interesting, as diagnoses such as "hypoxic or anoxic injury following cardiac arrest" and "ischemic stroke" are mentioned, illustrating how several different roads can lead to epilepsy and/or the presentation of seizures.Then: "Serum Abs suggesting a potential autoimmune etiology were detected in 39 (34.8%) cases." Over a third of the cohort showed serological evidence of autoantibodies and some presented with more than one type of autoantibody as being present. Breaking down those serologically positive participants, we are told that: "19 patients (48.7%) had new-onset epilepsy and 20 patients (51.3%) had established epilepsy." The authors did also subsequently limit their findings to those cases excluding TPO-Ab and low-titer GAD65-Ab (autoantibodies where a specific role to epilepsy is unclear or not specific) but even then reported that: "23 patients (20.5%) with unexplained epilepsy had positive serologic findings strongly suggestive of an autoimmune cause of epilepsy." There is also a final part to the Dubey paper which also merits mention: "Among the 23 patients who were seropositive, 15 (65.2%) received some sort of immunotherapy. Better seizure outcome was associated with use of immunomodulatory therapy... especially with use of intravenous methylprednisolone... or plasmapheresis."Alongside other (independent) studies in this area, the peer-reviewed evidence does seem to growing to suggest that within the wide (and heterogeneous) 'spectrum' that is epilepsy, at least some of that epilepsy might have an important immune component to it. To quote again from Dubey: "The data presented here suggest that autoimmune encephalitis may explain at least 20% of adult-onset epilepsies of unknown etiology." Aside from the importance of screening for said autoantibodies when certain cases of epilepsy appear at clinic, there are a few other potentially important points that could be raised about such data. Autism is area that I would be interested to see some further investigations carried out on with the Dubey findings in mind. Epilepsy is an important comorbidity 'over-represented' when it comes to autism (see here) and given the suggestions down the years that immune function (specifically autoimmunity) might be a facet of 'some' autism (see here for example) it's not beyond the realms of possibility that comorbid epilepsy might be a further facet of any autoimmune processes. Birds of an autoimmune feather tend to stick together and all that (see here). Add in the findings specifically talking about 'anti-NMDA-receptor encephalitis "mimicking an autistic regression"' (see here) and how methlyprednisolone might not be an uncommon medicine for some types of (autoimmune-related autistic presentation) and the hypotheses to be tested are laid out in front of you. By saying that, I don't want to take anything away from the more typical forms of epilepsy that can present (either alone or alongside autism) but rather point to the expanding knowledge base suggesting that immune functions may extend much further than just protecting the host from infection et al...To close, slightly related to some of the content included in this post, the trailer for the film Brain on Fire (from the book of the same name) is out and looking like required viewing.---------- Dubey D. et al. Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA Neurol. 2017 Feb 6.----------Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S (2017). Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology PMID: 28166327... Read more »
Dubey D, Alqallaf A, Hays R, Freeman M, Chen K, Ding K, Agostini M, & Vernino S. (2017) Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology. JAMA neurology. PMID: 28166327
Running economy barefoot, in minimalist shoes and traditional running shoes... Read more »
Cochrum RG, Connors RT, Coons JM, Fuller DK, Morgan DW, & Caputo JL. (2017) Comparison of Running Economy Values While Wearing No Shoes, Minimal Shoes, and Normal Running Shoes. Journal of strength and conditioning research, 31(3), 595-601. PMID: 28222048
Kristin Walovich holds the newly described species of ghost shark
Photo Credit: Kristin Walovich
Researchers recently announced the discovery of a new species of ghost shark, Hydrolagus erithacus. Ghost sharks - which aren’t actually sharks but instead their closest living relatives - are an extraordinarily rare sighting. Actually, it was just a few months ago, when a ghost shark was filmed... Read more »
Walovich KA, Ebert DA, & Kemper JM. (2017) Hydrolagus erithacus sp. nov. (Chimaeriformes: Chimaeridae), a new species of chimaerid from the southeastern Atlantic and southwestern Indian oceans. Zootaxa, 4226(4). PMID: 28187604
The main objective of SciELO Preprints is to speeding up the availability of research results and will contribute to an organized flow of potentially acceptable preprints by SciELO journals, in line with the advances and growing importance of preprints publication internationally. The cooperative construction of the SciELO Preprints modus operandi will encompass the promotion and debate of the preprints concept, the definition of governance and operations structures and the operational implementation. It is expected to be fully operational by mid-2018. … Read More →... Read more »
Berg, J., Bhalla, N., Bourne, P., Chalfie, M., Drubin, D., Fraser, J., Greider, C., Hendricks, M., Jones, C., Kiley, R.... (2016) Preprints for the life sciences. Science, 352(6288), 899-901. DOI: 10.1126/science.aaf9133
Callaway E. (2017) Heavyweight funders back central site for life-sciences preprints. Nature, 542(7641), 283-284. PMID: 28202994
"History of BD [bipolar disorder] is associated with significantly higher risk of dementia in older adults."So said the systematic review and meta-analysis published by Breno Diniz and colleagues  taking in the accumulated peer-reviewed literature on this topic. Including data for some 3000 individuals diagnosed with bipolar disorder and nearly 200,000 controls (without bipolar disorder), authors calculated something of a significantly higher risk of dementia in those with a documented history of bipolar disorder. They note that there is more research to do in this area, specifically on mechanisms and "to evaluate interventions that may reduce the risk of dementia in this population."Outside of the literature included in the Diniz study, similar findings have been reported in the science literature. The paper by Almeida and colleagues  noted that: "Bipolar disorder in later life is associated with increased risk of dementia" based on their analysis of ~38,000 older men (65-85 years old) and their "13-year risk of dementia." Perhaps more worryingly were their findings that: "Bipolar disorder was also associated with increased mortality" in relation to "death by suicide, accidents, pneumonia or influenza, and diseases of the liver and digestive system." Other data looking more generally at clinical depression paints a similar picture  suggesting something of a connection between various types of depression and risk of various types of dementia: "depressive symptomatology is associated with pathological mechanisms associated with neurodegeneration."I've tackled the topic of dementia a couple of times on this blog; most recently in relation to how incidental vitamin D deficiency *could be* something important when it comes to at least some cases of dementia (see here). Minus any sweeping generalisations and accepting that there may be many different roads leading to dementia and/or bipolar disorder, I am intrigued at the possibility that the sunshine vitamin might be something to consider as a 'connector' between elements of the depression and dementia spectrums as per other findings (see here for example). At the very least, it invites lots more targeted investigation, including whether vitamin D might indeed be a nootropic of choice for some (see here)...---------- Diniz BS. et al. History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American Journal of Geriatric Psychiatry. 2017. Jan 4. Almeida OP. et al. Risk of dementia and death in community-dwelling older men with bipolar disorder. Br J Psychiatry. 2016 Aug;209(2):121-6. Cherbuin N. et al. Dementia risk estimates associated with measures of depression: a systematic review and meta-analysis. BMJ Open. 2015 Dec 21;5(12):e008853.----------Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd (2017). History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry PMID: 28161155... Read more »
Diniz BS, Teixeira AL, Cao F, Gildengers A, Soares JC, Butters MA, & Reynolds CF 3rd. (2017) History of Bipolar Disorder and the Risk of Dementia: A Systematic Review and Meta-Analysis. The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry. PMID: 28161155
Are scientists smart when they promote their work on social media? Isn’t this a waste of time, time which could better be spent in the lab running experiments? No. An analysis of all available articles published by PLoS journals suggests otherwise. My own twitter activity might best be thought of as learning about science (in […]... Read more »
Peoples BK, Midway SR, Sackett D, Lynch A, & Cooney PB. (2016) Twitter Predicts Citation Rates of Ecological Research. PloS one, 11(11). PMID: 27835703
Renear AH, & Palmer CL. (2009) Strategic reading, ontologies, and the future of scientific publishing. Science (New York, N.Y.), 325(5942), 828-32. PMID: 19679805
Scientists have sequenced the DNA of two extinct birds: the moa and the elephantbird. Comparison with their living relatives led to some surprising findings.... Read more »
Yonezawa T, Segawa T, Mori H, Campos PF, Hongoh Y, Endo H, Akiyoshi A, Kohno N, Nishida S, Wu J.... (2017) Phylogenomics and Morphology of Extinct Paleognaths Reveal the Origin and Evolution of the Ratites. Current biology : CB, 27(1), 68-77. PMID: 27989673
By Jefferson LeThe blue whale (Balaenoptera musculus) is the largest mammal on the planet. Image byNMFS Northeast Fisheries Science Center (NOAA) available at Wikimedia Commons.Helloooooo! My name is Bailey and I am a 25 meter long blue whale, the largest living mammal on Earth! My friend Finley, a 21 meter long fin whale comes in second for largest in size. We had an interesting adventure recently where we were followed by humans. While Finley and I were foraging for food, I overheard the humans talking about investigating our diving behavior when we hunt and not hunt. With that, I will tell you what these foreigners did to investigate our behavior and also what happens when we dive. A chart of whales of different sizes. Image by Smithsonian Institute.To record our dives, the humans travelled to Mexican waters to attach recorders onto our mid-backs using a crossbow. Now, it didn’t hurt much due to my thick blubber. These devices recorded depth of how far we dived, time of dives, and our location. These recorders eventually came off between 5 to 13 hours later. Finley and I were not the only test subjects. Other members of our species were also tagged. After all the data on the devices were collected, the humans finally left our waters and did statistical analyses on our diving behavior. The fin whale (Balaenoptera physalus) rarely exposes its fluke when it prepares to diveto the abyss. Image by Aqqa Rosing-Asvid at Wikimedia Commons.Now, before we talk about what the humans found, I want to share with you the whale secret to a great dive. In case that you ever find yourself in the ocean or your local pool, you can try it! The nose for Finley and I are called blowholes, which are found on top of our heads. This tract is separated from our digestive tract so we do not have to worry about having food go down our blowhole. When I am about to dive, instead of gulping in lots of oxygen, I exhale out as much as I can. This causes my lungs to collapse and flexible walls in my chest allow even more compression. Also, tiny structures in my lungs called alveoli collapse which halts any gas exchange. All of the decrease in lung space decreases buoyancy so I can descend down to the depths. As I descend, my heart rate lessens to reduce energy used during the dive. The oxygen that I had obtained before the dive is stored in my blood and muscle tissue. Since the deep depths are really cold, blood flow is temporarily halted at the thinner areas of my body, like flippers, and some organs to keep the main body going. When I ascend back up, I gradually increase space in my lungs and my alveoli regain full function to allow gas exchange. If you were to ascend too quickly, you could get shallow water blackout or even worse, the “bends” (where nitrogen bubbles in your blood) and I heard it is painful. After ascending is complete, I can release my blowhole open and take in fresh oxygen again. I was secretly told what the results to the humans’ experiments were. They found out that fin and blue whales dove deeper when hunting on shallow dives when not hunting. It makes sense! Why spend so much energy diving when not hunting? Also, they noted that our lunge feeding frequency was different. Lunge feeding is where we propel ourselves towards our prey with our mouth open and grab as much food as we can into our mouth. Blue whales lunged about 2.5 times more than fin whales! That’s a point for the blue! However, the record dive depth came from a fin whale. Hmm… I wonder if Finley broke that record. Did you find my secret and what the humans found interesting? I surely did. I never thought about how I dive and how I behave as it is practically in my blood! Well, the next time you are at a deep pool, try those secrets I spilled to you. It might be fun! Then again, you might be thinking, how does a whale communicate with a human and understand scientific data? That is a secret you may never know… Literature Cited:Croll DA, Acevedo-Gutiérrez A, Tershy BR, & Urbán-Ramírez J (2001). The diving behavior of blue and fin whales: is dive duration shorter than expected based on oxygen stores? Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 129 (4), 797-809 PMID: 11440866Hill, R. W., G. A., Wyse, M. Anderson. (2008). Animal Physiology. 2:641-660 ... Read more »
Croll DA, Acevedo-Gutiérrez A, Tershy BR, & Urbán-Ramírez J. (2001) The diving behavior of blue and fin whales: is dive duration shorter than expected based on oxygen stores?. Comparative biochemistry and physiology. Part A, Molecular , 129(4), 797-809. PMID: 11440866
"Given the modest magnitude of these findings in contrast to the clear public health benefits of the timely administration of vaccines in preventing mortality and morbidity in childhood infectious diseases, we encourage families to maintain vaccination schedules according to CDC guidelines."The quote opening this post comes from the paper published by Douglas Leslie and colleagues  (open-access) and offers not a conclusion from their study looking at the possibility that "the onset of some neuropsychiatric disorders may be temporally related to prior vaccinations in a subset of individuals" but a caution that cause-and-effect were not 'proven' in their study. Anyone with any knowledge about previous occasions where administration of vaccines have been correlated with specific psychiatric or behavioural outcomes (see here and see here for examples) will recognise how important such a caution is, bearing in mind that vaccines are medicines (albeit preventative) and are subject to similar monitoring for safety and the small possibility of adverse effects as other medicines.Based on the examination of "the MarketScan® Commercial Claims and Encounters database", a US drug and medical insurance claims database, researchers looked at various diagnoses of interest including OCD (obsessive compulsive disorder), AN (anorexia nervosa), anxiety disorder, tic disorder, major depression, bipolar disorder and ADHD (attention-deficit hyperactivity disorder) in children/young adults aged 6-15 years old. This alongside several other classes of diagnosis including broken bones and 'open wounds'. Participants were matched one-to-one with controls without said neuropsychiatric diagnoses and exposure(s) to various vaccinations - "influenza, tetanus and diphtheria (TD), hepatitis A, hepatitis B, meningitis, and varicella" - were 'tracked'. Interestingly, this is not the lead authors' first foray into using the MarketScan database , where autism was the previous topic of analysis (specifically healthcare service use and costs).Results: bearing in mind that samples sizes varied according to those diagnoses under investigation, the authors report: "Receipt of any vaccine in the previous 6 months was highest for children with AN (21.4%), followed by OCD (15.9%) and tic disorder (15.8%), and was lowest for children with open wounds (10.3%)." This information needs to be treated carefully because - again - it tells us nothing about any cause-and-effect relationship, just correlation and trend; trends that could be there for all-manner of different reasons outside of the variables looked at. Further: "HRs [hazard ratio] associated with receipt of any vaccine were highest for children with AN... followed by OCD."The authors also looked at specific vaccinations in relation to those neuropsychiatric disorders included in their study. They report: "Influenza vaccinations during the prior 3, 6, and 12 months were... associated with incident diagnoses of AN, OCD, and an anxiety disorder." Conversely: "children with major depression were less likely to have received the influenza vaccine in the previous 3 months" and "children with bipolar disorder were also less likely to have received the influenza vaccine in the previous 3 or 6 months."OK, it is worth reiterating - yet again - that this was a study looking at possible associations and not necessarily cause-and-effect. Indeed, judging by that last paragraph and the table of HRs produced by the authors (see here) one might easily claim that flu vaccination might potentially shield someone from developing major depression as much as 'cause' AN, OCD and/or anxiety disorder. Such is the nature of such studies and the findings being reported. And indeed someone has actually looked at depressive symptoms (symptoms that is, not depression as a clinical diagnosis) before and after an influenza vaccination and found very little...I note that with specific regard to the influenza vaccine and the findings that "children with AN, OCD, or a tic disorder were more likely to have received the influenza vaccine in the preceding periods" the authors head into the research talking about narcolepsy and the "AS03-adjuvanted H1N1 vaccine" as a possible template for their findings. This despite not covering the diagnosis of narcolepsy in their study (they could have). I've touched upon this area of research before on this blog (see here) (something that continues to appear in media discussions) and whilst not disputing the findings, do for example, wonder why in the work of Szakács and colleagues  ADHD was picked up as a comorbidity present in their "post-H1N1 vaccination (PHV) narcolepsy group" but in the Leslie data the HRs showed little evidence of any relationship. Yes, H1N1 vaccination is not necessarily the same as influenza vaccination reported in the Leslie data (we don't actually know what specific influenza vaccines were administered), but surely if discussions turn to an 'autoimmune' element as a possible mechanistic feature potentially linking vaccination and [some] neuropsychiatric disorder(s), one would expect to see the same/similar pattern of conditions being represented and reported? For balance, I should also point out that other independent study has talked about eating disorders potentially having "immune-mediated mechanisms" connected, particularly those associated with autoimmunity  although I don't doubt such a connection is likely complicated and probably not universally applicable.It's not difficult to find issues with the Leslie paper and no doubt these will be emphasised in any further discussions about the data reported even when the authors stress throughout that "findings do not demonstrate a causal role of vaccination in the pathoetiology of any of these conditions." The strengths of the data - e.g. the use of that administrative database for confirming diagnoses and vaccine exposure - are worth mentioning again in light of other debates on data sources from other 'disappearing' manuscripts in this area. I might also add that by focusing in on various diagnoses but not autism (which again, they could have done) and not a certain vaccine, the authors seem well aware of the history in this area - "the association of the measles, mumps, and rubella vaccine with autism spectrum disorder has been convincingly disproven" - and probably either thought nothing more of it or chose to steer well clear of it (or perhaps a combination of both).Is there a 'where next' when it comes to the Leslie data? To quote again from the paper: "findings require replication in a larger population-based sample, possibly including assessments of various potentially important host factors, e.g., the individual’s ... Read more »
Leslie DL, Kobre RA, Richmand BJ, Aktan Guloksuz S, & Leckman JF. (2017) Temporal Association of Certain Neuropsychiatric Disorders Following Vaccination of Children and Adolescents: A Pilot Case-Control Study. Frontiers in psychiatry, 3. PMID: 28154539
When the psychiatrist Hermann Rorschach blotted ink onto paper to produce a series of abstract patterns, could he have known that nearly 100 years later, the Rorschach test would be a household name?
Although the use of the Rorschach to diagnose mental illness is mostly a thing of the past, research on the test continues. Last week, two new papers were published on the Rorschach blots, including a fractal analysis of the images themselves and a brain scanning study using fMRI.
The ... Read more »
Taylor RP, Martin TP, Montgomery RD, Smith JH, Micolich AP, Boydston C, Scannell BC, Fairbanks MS, & Spehar B. (2017) Seeing shapes in seemingly random spatial patterns: Fractal analysis of Rorschach inkblots. PloS one, 12(2). PMID: 28196082
Giromini L, Viglione DJ Jr, Zennaro A, & Cauda F. (2017) Neural activity during production of rorschach responses: An fMRI study. Psychiatry research, 25-31. PMID: 28208069
"Catatonic symptoms are more prevalent in young people with autism than previously thought" said the article recently published by Breen and Hare . Continuing a research theme of at least one of the authors , the idea that catatonic symptoms - primarily manifesting as stupor, unresponsiveness to light, noise or touch, mutism, etc - might be over-represented when it comes to autism is not a new one by any means.Breen & Hare set about looking for "the presence and nature of such attenuated behaviours in children and adolescents with autism" based on something called the Attenuated Behaviour Questionnaire. This was delivered to parents/caregivers online alongside looking at information from other measures based on the presence of repetitive behaviour and depression."Attenuated behaviour indicative of catatonia was relatively common in young people with autism with up to 20.2% having an existing diagnosis of catatonia and evidence of a relationship between attenuated behaviours and measures of depression and repetitive and restricted behaviours." Such findings as I said, are by no means novel but once again highlight how a diagnosis of autism or autism spectrum disorder (ASD) is seemingly protective of nothing when it comes to comorbidity. To quote another author on this topic: "an unabashed drumroll for increased recognition and treatment of catatonia in autism spectrum disorders (ASD)"  is needed.Catatonia appearing alongside [some] autism leads into a number of areas in relation to the 'closeness' of any relationship (some people have talked about 'autistic catatonia') and the management strategies that may be subsequently indicated. On the issue of management, guidance is available  albeit including a strategy - electroconvulsive therapy (ECT) - that is probably not going to win any awards in terms of popularity given its historical basis. Accepting that still today ECT as an 'intervention' option when it comes to autism still courts heated discussion (see here), there is the requirement for much greater study of catatonic symptoms in relation to autism and whether there may be several presentations ripe for more novel intervention  (in light of a growing area of research interest). Said intervention might also take into account the plurality of autism too (see here)...To close, yet another song for my brood and a very proud father who saw some real talent in the karate competition yesterday (those first place trophies are proof that team kata and team kumite are definitely the way forward)...---------- Breen J. & Hare DJ. The nature and prevalence of catatonic symptoms in young people with autism. J Intellect Disabil Res. 2017 Feb 1. Hare DJ. & Malone C. Catatonia and Autistic Spectrum Disorders. Autism. 2004; 8: 183-195. Dhossche DM. Decalogue of Catatonia in Autism Spectrum Disorders. Frontiers in Psychiatry. 2014;5:157. Mazzone L. et al. Catatonia in patients with autism: prevalence and management. CNS Drugs. 2014 Mar;28(3):205-15. Kiani R. et al. Anti-NMDA-receptor encephalitis presenting with catatonia and neuroleptic malignant syndrome in patients with intellectual disability and autism. BJPsych Bull. 2015 Feb;39(1):32-5.----------Breen J, & Hare DJ (2017). The nature and prevalence of catatonic symptoms in young people with autism. Journal of intellectual disability research : JIDR PMID: 28150394... Read more »
Breen J, & Hare DJ. (2017) The nature and prevalence of catatonic symptoms in young people with autism. Journal of intellectual disability research : JIDR. PMID: 28150394
Deep sea creatures come with all kinds of strange features that help them to survive their cold, dark habitat.. Some have eyes the size of a basketball, others come with appendages that blink and glow, deep-sea dwellers have developed some strange features and the "cockeyed" squid Histioteuthis heteropsis has one normal eye and one giant, bulging, yellow eye.
One ... Read more »
Thomas KN, Robison BH, & Johnsen S. (2017) Two eyes for two purposes: in situ evidence for asymmetric vision in the cockeyed squids Histioteuthis heteropsis and Stigmatoteuthis dofleini. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 372(1717). PMID: 28193814
Figure from Gauthier et al. (2005).
Alzheimer's Disease (AD) and other dementias are progressive neurodegenerative conditions that unfold over time. Subtle symptoms such as forgetfulness and word finding problems may progress to mild cognitive impairment (MCI), and then escalate to full-blown dementia. Recent efforts to classify prodromal states have included automated analysis of spontaneous... Read more »
Berisha V, Wang S, LaCross A, & Liss J. (2015) Tracking discourse complexity preceding Alzheimer's disease diagnosis: a case study comparing the press conferences of Presidents Ronald Reagan and George Herbert Walker Bush. Journal of Alzheimer's Disease, 45(3), 959-63. PMID: 25633673
Fraser, K., Meltzer, J., & Rudzicz, F. (2015) Linguistic Features Identify Alzheimer’s Disease in Narrative Speech. Journal of Alzheimer's Disease, 49(2), 407-422. DOI: 10.3233/JAD-150520
Thomas, C., Keselj, V., Cercone, N., Rockwood, K., . (2005) Automatic detection and rating of dementia of Alzheimer type through lexical analysis of spontaneous speech. IEEE International Conference, 1569-1574. info:/10.1109/ICMA.2005.1626789
Psychology experiments are not generally fodder for this blog when it comes to autism. The main reason being that quite a few appearing in the peer-reviewed literature tend to look at quite abstract features perhaps somewhat removed from the daily lives of autistic people and their significant others. A few also seem to struggle with the idea that grand over-arching psychological theories (that seem to inevitably follow psychological findings in particular) are not required when it comes to autism in these days of heterogeneity and plurality.I am making an exception today however with the paper by Noah Sasson and colleagues  (open-access) and their findings suggesting advocating "for a broader perspective of social difficulties in ASD [autism spectrum disorder] that considers both the individual’s impairments and the biases of potential social partners." In other words, it takes two to [socially, interactively] tango. I might add that a doctoral thesis by one of the co-authors on the Sasson paper (Daniel Faso) is also available for further inspection too (see here).Based on the idea that issues with social interaction "quantity and quality" might not be something exclusively under the control of those diagnosed with autism, Sasson et al devised a series of experiments to test their hypothesis: "three studies conceived and conducted independently by three research groups assessing observers’ first impressions of—and intentions to socially engage with— children and adults with ASD based upon “thin slices” of their real-world social behavior." I'm not going to go into too much detail about the experiments because the paper is open-access and you can read about them for yourselves. 'Thin slices' in the context of the experiments carried out referred to media that were rated pertinent to "observers’ first impressions of individuals with ASD engaging in real-world social behavior."The results make for some important reading as across the different experiments undertaken the key messages were that: "first impressions of individuals with ASD are significantly less favorable than those of matched TD [typically developing] controls, and are associated with greater reluctance on the part of observers to pursue social engagement." Further: "social interaction difficulties in ASD are not solely an individual impairment but also a relational one, and consideration of both of these factors is necessary for a full understanding of social impairment in ASD." I relay all of that bearing in mind that these were experiments carried out under controlled conditions (I don't know about you, but I don't generally rate people at first contact using a "0-3" Likert scale or a "non-graduated slider" on 'how approachable' they were or the likelihood of a friendship developing).Although important, I don't think anyone should be too surprised by the results reported in the context of how first impressions count and how people are generally quick to judge from "personality and character traits" whether social engagement with a person or group of people is going to be a short or longer-term thing. I say this also bearing in mind that minus any psychobabble, people generally take into account things like context, familiarity and similarity when it comes to their social interaction decisions too [if for example, you happen to be a fan of Star Wars or a Shotokan karateka, I might be more inclined to chat with you than say if you talked about the goings-on on various reality TV shows]. Indeed, the authors note: "these studies present only group-wise comparisons and do not address individual differences among those with ASD, nor whether individual characteristics of the raters (e.g., gender, personality, etc.) affect the results reported here." I'd also forward the idea that they might also include important concepts such as self-monitoring for example when it comes to future studies in this area. Similarly, it would also be handy to see if 'comorbidity counts' when it comes to further investigations on this topic in light of expanding links between different labels and traits (see here).The question of what to do about the Sasson findings similarly provide some food for thought. The authors suggest that: "intervention and education approaches that target both those with ASD as well as their TD [typically developing] peers may offer a more comprehensive approach for improving social and functional outcomes in autism." In the context of other studies looking at social interaction and autism particularly in the school setting (see here) I can see how this might work in terms of raising awareness of how people are not always the same when it comes to the presentation of their social persona. Intervening with a wider group (i.e. peers) and taking the onus off 'just the person with autism' is a win-win situation and will no doubt have other positive knock-on effects in terms of self-esteem and helping to remove barriers around the 'disability' framing of autism. I might add that in these days of the potential virality of personality traits, it makes sense to include everyone.In a wider context - outside of school - and in the big, wide [adult] world however, I'm slightly less sure of how such intervention is going to be achieved. Yes, we would all love people to be more understanding and less 'judgemental' in their first (and subsequent) impressions, but when it comes to influencing aspects such as views on "awkwardness, attractiveness, [and] likability" I'm not so sure that this can be universally achieved. Indeed, facets such as attractiveness and likability are probably going to be influenced by lots of variables outside of those just linked to an autism diagnosis and its presentation (frank or not). By saying all that, I'm not suggesting that we shouldn't try to educate and perhaps even move people away from the whole 'first impressions last'  thing, but rather am looking at the realistic prospect of achieving such a societal goal, mindful that it takes two to tango...And on the topic of first impressions, at least get the handshake right (i.e. let go)...---------- Sasson NJ. et al. Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Sci Rep. 2017 Feb 1;7:40700. Gunaydin G. et al. Impressions Based on a Portrait Predict, 1-Month Later, Impressions Following a Live Interaction. Social Psychological and Personality Science. 2017. 8: 36-44.----------Sasson NJ, Faso DJ, Nugent J, Lovell S, Kennedy DP, & Grossman RB (2017). Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Scientific reports, 7 PMID: 28145411... Read more »
Sasson NJ, Faso DJ, Nugent J, Lovell S, Kennedy DP, & Grossman RB. (2017) Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments. Scientific reports, 40700. PMID: 28145411
A peculiar new paper proposes the idea of "connecting two spinal cords as a way of sharing information between two brains". The author is Portuguese psychiatrist Amílcar Silva-dos-Santos and the paper appears in Frontiers in Psychology.
Frontiers are a publisher with a troubled history of publishing dubious science. But this paper is unusual, even by Frontiers' standards, because it contains virtually no science at all.
In a nutshell, Silva-Dos-Santos suggests that it would be interest... Read more »
Silva-Dos-Santos A. (2017) The Hypothesis of Connecting Two Spinal Cords as a Way of Sharing Information between Two Brains and Nervous Systems. Frontiers in psychology, 105. PMID: 28197119
by Rita Handrich in The Jury Room
It’s time again for another combination post featuring fascinating tidbits you may have missed were it not for our eagle eyes and constant efforts to keep you informed. And yes, we’ll start at the end since we know you are wondering if smart-phone blindness is really a thing. Would we steer you wrong? Smart-phone blindness […]... Read more »
Share, EF. (2017) Hillary Rodham versus Hillary Clinton: Consequences of surname choice in marriage. Gender Issues. info:/
We know that music training causes intelligence to increase, but why? In this post I 1) propose a new theory, and 2) falsify it immediately. Given that this particular combination of activities is unpublishable in any academic journal, I invite you to read the whole story here (in under 500 words). 1) Proposing the ISAML Incredible but […]... Read more »
Carey, D., Rosen, S., Krishnan, S., Pearce, M., Shepherd, A., Aydelott, J., & Dick, F. (2015) Generality and specificity in the effects of musical expertise on perception and cognition. Cognition, 81-105. DOI: 10.1016/j.cognition.2014.12.005
Jongman, S., Meyer, A., & Roelofs, A. (2015) The Role of Sustained Attention in the Production of Conjoined Noun Phrases: An Individual Differences Study. PLOS ONE, 10(9). DOI: 10.1371/journal.pone.0137557
Kaviani, H., Mirbaha, H., Pournaseh, M., & Sagan, O. (2013) Can music lessons increase the performance of preschool children in IQ tests?. Cognitive Processing, 15(1), 77-84. DOI: 10.1007/s10339-013-0574-0
Kunert R, & Jongman SR. (2017) Entrainment to an auditory signal: Is attention involved?. Journal of experimental psychology. General, 146(1), 77-88. PMID: 28054814
Olivers, C., & Nieuwenhuis, S. (2005) The Beneficial Effect of Concurrent Task-Irrelevant Mental Activity on Temporal Attention. Psychological Science, 16(4), 265-269. DOI: 10.1111/j.0956-7976.2005.01526.x
by Piter Kehoma Boll If you have your face buried in the mud at the bottom of a European lake, you may end up finding some of those tiny little roundworms known as Monhystera stagnalis. As usual, there is no common … Continue reading →... Read more »
Pehofer, H. (1989) Spatial Distribution of the Nematode Fauna and Production of Three Nematodes (Tobrilus gracilis, Monhystera stagnalis, Ethmolaimus pratensis) in the Profundal of Piburger See (Austria, 913 m a.s.l). Internationale Revue der gesamten Hydrobiologie und Hydrographie, 74(2), 135-168. DOI: 10.1002/iroh.19890740203
Traunspurger, W. (1996) Autecology of Monhystera paludicola De Man, 1880 – Seasonal, Bathymetric and Vertical Distribution of a Free-living Nematode in an Oligotrophic Lake. Internationale Revue der gesamten Hydrobiologie und Hydrographie, 81(2), 199-211. DOI: 10.1002/iroh.19960810205
"Overall, the study said one person would be spared infection for every 33 taking vitamin D supplements. That is more effective than flu vaccination, which needs to treat 40 to prevent one case, although flu is far more serious than the common cold."That was some of the media interpretation of the paper - "systematic review and meta-analysis of individual participant data" - published by Adrian Martineau and colleagues  looking at the collected data on vitamin D supplementation "on risk of acute respiratory tract infection." Including data on approximately 11,000 'randomised' participants reported in 25 studies, authors assessed whether the quite messy data on vitamin d supplementation potentially decreasing the risk of acute respiratory tract infection showed any semi-definitive trends.Results: "Vitamin D supplementation resulted in a statistically significant reduction in the proportion of participants experiencing at least one acute respiratory tract infection." Further: "Use of vitamin D did not influence risk of serious adverse events of any cause... or death due to any cause. Instances of potential adverse reactions to vitamin D were rare." And finally: "Subgroup analysis revealed that daily or weekly vitamin D supplementation without additional bolus doses protected against acute respiratory tract infection, whereas regimens containing large bolus doses did not."I note that in the BBC news report on the Martineau paper we are told: "Public Health England (PHE) says the infections data is not conclusive, although it does recommend supplements." This slightly counter-intuitive position follows more general advice from the powers-that-be that perhaps we should all be taking a little more vitamin D (see here) given what is emerging when it comes to the varied functions of the sunshine vitamin/hormone. But bear in mind that supplementation comes with potential risks too (see here) particularly when people forget to treat their vitamins and minerals as what they are: biologically active pharmaceutics. Neither is everyone completely sold on the idea that vitamin D 'could stop colds or flu' as an accompanying editorial to the Martineau paper makes clear : "The results are heterogeneous and not sufficiently applicable to the general population."What such research does advance however, is that vitamin D is a potentially important nutrient (more so for some groups) and one that we should be [cautiously] dedicating a lot more investigation to for all-manner of possible reasons (see here and see here) outside of just bone health and the English disease. And within that scheme of research, don't forget a few things: (a) there's more to vitamin D metabolism than just 'getting enough' and (b) even today, science is still finding out new things about the chemistry of vitamin D . In short, the scheme of science around vitamin D needs to be broad...---------- Martineau AR. et al. Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ 2017; 356: i6583. Bolland MJ. & Avenell A. Do vitamin D supplements help prevent respiratory tract infections? BMJ 2017; 356: j456. Pauwels S. et al. 1β,25-Dihydroxyvitamin D3: A new vitamin D metabolite in human serum. J Steroid Biochem Mol Biol. 2017 Feb 10. pii: S0960-0760(17)30040-7.----------Adrian R Martineau, David A Jolliffe, Richard L Hooper, Lauren Greenberg, John F Aloia, Peter Bergman, Gal Dubnov-Raz, Susanna Esposito, & et al (2017). Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data BMJ : 10.1136/bmj.i6583... Read more »
Adrian R Martineau, David A Jolliffe, Richard L Hooper, Lauren Greenberg, John F Aloia, Peter Bergman, Gal Dubnov-Raz, Susanna Esposito, & et al. (2017) Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data. BMJ. info:/10.1136/bmj.i6583
The paper by Charlotte Willfors and colleagues  (open-access) provides some food for thought today and the observation that various individual and cumulative medical events - "early medical events likely to be caused by environmental factors" - may be important to at least some autism.Researchers "scrutinized the early medical histories of a rare and informative sample of 13 MZ [monozygotic] twin pairs discordant for clinical ASD [autism spectrum disorder]" also including "13 MZ typically developing (TD) control pairs (n=52) matched for sex" as an 'exploratory step. Discordant for autism means that one twin had autism and the other did not.This research first step looked at medical events (likely to be caused by environmental factors!) included things like delivery and neonatal variables (e.g. foetal distress, hypoxia), minor and frequent infections (e.g. ear infections), allergy and epilepsy to name a few. Data was acquired from a few sources including medical records and medical history "assessed from a parent reported questionnaire." They examined exposure to the medical events "in relation to either quantitative or qualitative discordance for ASD." Qualitative discordance referred to when "only one twin within a pair meeting the diagnostic criteria of ASD." A 'confirmatory' study was also carried out whereby a larger, independent cohort of 100 twin pairs "quantitatively discordant for autistic traits" were also quizzed and findings cross-validated.Results: a few non-shared environmental (NSE) events seemed to be important based on their analysis. So: "Single early medical factors, likely to be caused by NSE, that discriminated between twins in qualitative ASD discordant pairs were dysregulation during the first year of life (comprising feeding and sleeping problems, excessive crying and worrying) and birth weight." Authors also reported that cumulatively, the appearance of early medical events were significantly different in MZ twins with autism compared with their non-ASD co-twin. It's worth mentioning that some of those 'dysregulation' events have been talked about in the earliest descriptions of autism (see here). Birth weight too has something of a long-standing connection to [some] autism (see here). When it came to analysis based on autistic traits (the confirmatory study) it seemed that "early dysregulation and the cumulative load of a variety of early adverse medical events" continued to be important variables (although birth weight linked to ASD traits lost its significance).These are important findings. The focus on MZ twins (who share a common structural genetic blueprint) means that the genetics side of things is to a large extent 'controlled for' and the results are more likely to reflect some environmental or, more accurately, non-genetic influence. There is a caveat to this though, as per the authors recognition: "with the exception of putative post-twinning de novo mutations." I might also add that MZ twins are also not necessarily epigenetically the same too so gene expression can (and does) differ. What causes these epigenetic differences is still the source of some debate but I might chime in with one idea (see here) out of many possibilities."Our data indicate that taking into account the cumulative load of early medical factors might strengthen or discourage a suspicion of ASD, at least in a minority of cases." This is an interesting thought provided by the authors based on their findings. It ties in well with the idea that although behavioural presentation is core to autism presentation and diagnosis, behaviour might not be the only important feature present in relation to autism. I do have to express a degree of caution however with such an approach based on the idea that various types of regression have been noted in the peer-reviewed literature to accompany some autism (see here) and with it, the concept of 'acquired autism' should really be properly recognised (see here for example) in these days of the plural 'autisms'. Indeed, there's a research study idea for anyone out there: looking at MZ twins discordant for autism with onset of said autism tied into a regression of skills?Scientific replication is the name of the [future] game in this area of study, drawing on larger cohorts and perhaps based in other geographical areas outside of Sweden. We also need to find out what mechanisms might be potentially associating something like 'early dysregulation' with the onset of autism, taking into account how factors such as early feeding practices/issues for example, might provide at least one avenue for future study (see here).To close, in light of some recent media headlines about the 'myth' that autism rates are on the up (and quite significantly so over past two decades), I offer some past posts suggesting that the word 'myth' should be reserved for other [non-peer-reviewed] matters (see here and see here and see here) and not this particular branch of epidemiological science. As to what may be 'causing' the upswing in numbers of diagnosed cases, well, it's likely to be very, very, very complicated (and without any need for sweeping generalisations please)...---------- Willfors C. et al. Medical history of discordant twins and environmental etiologies of autism. Transl Psychiatry. 2017 Jan 31;7(1):e1014.----------Willfors C, Carlsson T, Anderlid BM, Nordgren A, Kostrzewa E, Berggren S, Ronald A, Kuja-Halkola R, Tammimies K, & Bölte S (2017). Medical history of discordant twins and environmental etiologies of autism. Translational psychiatry, 7 (1) PMID: 28140403... Read more »
Willfors C, Carlsson T, Anderlid BM, Nordgren A, Kostrzewa E, Berggren S, Ronald A, Kuja-Halkola R, Tammimies K, & Bölte S. (2017) Medical history of discordant twins and environmental etiologies of autism. Translational psychiatry, 7(1). PMID: 28140403
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