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  • April 1, 2015
  • 05:37 AM

Gulf War agents and delayed onset of symptoms in mice

by Paul Whiteley in Questioning Answers

I was recently intrigued by the findings reported by Zuchra Zakirova and colleagues [1] (open-access) on what happened to mice following 'acute' exposure to pyridostigmine bromide (PB) and the pesticide permethrin (PER) in the context of these compounds being "key contributors to the etiology of GWI [Gulf War Illness] post deployment to the Persian GW [Gulf War]."I've covered the topic of Gulf War Syndrome (GWS) before on this blog (see here) and how, following one of the most toxic wars in history, quite a few service personnel (and local civilians) developed an array of symptoms which still confuse science and medicine today. There is no doubt that the conflict in 1990-1991 presented the military with a pretty hostile environment; not least because of the setting in the Persian Gulf. This was further compounded by burning oil fields, a variety of potential chemical exposures (including some rather nasty nerve agents) and issues like depleted urinanium tipped munitions to contend with. All-in-all, not a great place to be."We hypothesized that co-administration of PB and PER in our mouse model of GW agent exposure would recapitulate the late-onset symptom multiplicity and heterogeneity of symptoms observed in GW veterans, such as memory deficits and neurological deficits." That was the rationale behind the study bearing in mind that this was a study of mice for obvious ethical reasons.Said mice - "Forty-eight male C57BL6/J mice" - were given either the PB/PER mix (via intraperitoneal injection) or 100% DMSO (as a control). As you may appreciate, direct injection of PB/PER is probably not the same kind of exposure that veterans would have come across in active theatre. PB as NAPS (nerve agent pre-treatment tablet set) was given in an oral dosage form. PER would probably have been delivered as a cream (or aerosol). One perhaps needs to keep this potentially important difference in mind when interpreting the Zakirova findings.Dividing the mice groups up into a short-term cohort and a long-term cohort (18 days post exposure vs. 5 months post exposure respectively), various 'neurobehavioural' testing was undertaken on the cohorts. The mice participants were eventually euthanized so that any "neuropathological changes associated with GW agent exposure" could also be investigated.There were some interesting results (and non-results) to be had from the amassed data. Short-term exposure to the PB/PER mix resulted in, well, not very much difference when compared to control animals: "No cognitive deficits were observed at the short-term time point, and only minor neuropathological changes were detected."But longer-term, there were some potentially important differences noted between exposed and non-exposed animals. So for example: "Impairment for long-term memory formation was observed at day 106 days-post acute exposure to PB + PER." This was based on the results of a test of spatial memory. Further: "PB + PER exposure altered astrocytic activation in the hili of hippocampi and cerebral cortices of mice." Not being particularly au fait with all-things neuropathological, I can't readily put too much descriptive flesh on these experimental bones. I gather that "astroglial activation" might be something important when it comes to the destruction of neurons following injury or infection (but don't quote me on that). Potentially importantly too were the authors' findings that: "ACh [acetylcholine] levels were increased in the CNS [central nervous system] of exposed mice" and further "that exposure to GW agents may be attributed to the impaired cholinergic function observed in GWI and may in part contribute to deficits observed in long-term memory formation." I say this noting that permethrin is classified as a pyrethroid not an organophosphate (OP) which has a more classical relationship with acetylcholinesterase but PB has perhaps a more direct effect on acetylcholine.Reiterating that the Zakirova study reports results based on mice and 'acute' exposure of said mice to potentially important agents, these are interesting results mirroring other studies from the authors [2]. I note that there may be more to see from this research group in future with the anticipation that "subsequent studies will provide us with a more lifetime picture regarding the long-lasting consequences of GW agent exposure." If this is indeed something that can be garnered from such a mouse model and given the significant suffering endured by many veterans, a little more scientific knowledge to illuminate the way would be very welcome.Music: Tumbling Dice - The Rolling Stones.----------[1] Zakirova Z. et al. Gulf War Agent Exposure Causes Impairment of Long-Term Memory Formation and Neuropathological Changes in a Mouse Model of Gulf War Illness. PLoS One. 2015 Mar 18;10(3):e0119579.[2] Ojo JO. et al. Exposure to an organophosphate pesticide, individually or in combination with other Gulf War agents, impairs synaptic integrity and neuronal differentiation, and is accompanied by subtle microvascular injury in a mouse model of Gulf War agent exposure. Neuropathology. 2014 Apr;34(2):109-27.----------Zakirova, Z., Tweed, M., Crynen, G., Reed, J., Abdullah, L., Nissanka, N., Mullan, M., Mullan, M., Mathura, V., Crawford, F., & Ait-Ghezala, G. (2015). Gulf War Agent Exposure Causes Impairment of Long-Term Memory Formation and Neuropathological Changes in a Mouse Model of Gulf War Illness PLOS ONE, 10 (3) DOI: 10.1371/journal.pone.0119579... Read more »

  • March 31, 2015
  • 04:23 PM

Ovulation changes women’s desire for variety in products

by Dr. Jekyll in Lunatic Laboratories

We know that hormones affect who we are, even when we aren’t aware of it. In the past scientists have found that people who are hungry tend to buy more things, no surprise for those of us who have shopped hungry. However, new research shows that women seek a greater variety of products and services, specifically when they are ovulating.... Read more »

  • March 31, 2015
  • 05:27 AM

How time pressure improves decision making in emergency situations

by BPS Research Digest in BPS Research Digest

A new simulation of a complex, realistic disaster event suggests that time pressure facilitates better decision-making among emergency responders. The two-day training exercise, overseen by Liverpool’s Centre for Critical and Major Incident Psychology, looked at the impact of a hypothetical aeroplane crash over a city. Nearly two hundred professionals were split into different rooms based on the agency they belonged to (14 agencies in all, including police, transport, health and science advisors), and each received realistic data according to their function.As casualty data trickled into the Ambulance Room, did this give a clue to the cause of the crash? Could terrorism be ruled out? Would the hospital suffer outages, given damage to a power station? These were some of the considerations the teams had to contend with.The researchers focused on six critical issues identified by a panel of experts as being key, and as emblematic of the wider challenge of the exercise as a whole: effective cross-agency collaboration.Results showed that when issues needed responses from more than two agencies, successful action was actually more likely when there was a sense of time pressure. When this was missing, communication efforts were squandered as workers gathered more and more information from within their agency, as opposed to coordinating decisions and actions with other agencies.Why did time pressure improve emergency responders’ decision making and communication? It has to do with the way that human beings avoid tough choices when we can – anticipated regret is a powerful deterrent. But imperfect decisions can actually be better than none: once initiated they can be monitored, evaluated and altered, whereas inaction begets inaction. In addition, a deferred decision may continue to eat up mental resources, making other decisions more difficult.Evidence from this new field of “naturalistic decision making” suggests that time pressure leads experts into accurate intuitive “pattern-matching”. The "natural state" of expert decision-making involves leaps between decision stages rather than examination of every possibility, and time pressure encourages these leaps (or pattern matches).One of the crisis issues – the handover of disaster management from emergency services to the local authority – had no clear deadlines attached. But in this case, the strategy unit had set the handover as a clear overarching goal, which led to more effective communication on this issue, including less in-agency discussion (less back-covering and abstract debate, perhaps), and more time engaging with other agencies. Even though the handover was required in the later recovery phase, the group were already planning and building contingencies during the initial response phase.The message for organisations, then, is that human beings are tempted to delay when it’s most vital to act, thanks to anticipated regret. This is "The Psychology of Doing Nothing".  Clearly articulated strategic goals are one way to stave this off. When it comes to time boundaries, the authors consider these "difficult to influence." But artificial deadlines, or making unstated ones more explicit, may be useful ways to keep the urgency in the emergency services._________________________________ Alison, L., Power, N., van den Heuvel, C., Humann, M., Palasinksi, M., & Crego, J. (2015). Decision inertia: Deciding between least worst outcomes in emergency responses to disasters Journal of Occupational and Organizational Psychology DOI: 10.1111/joop.12108 Post written by Alex Fradera (@alexfradera) for the BPS Research Digest.

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Alison, L., Power, N., van den Heuvel, C., Humann, M., Palasinksi, M., & Crego, J. (2015) Decision inertia: Deciding between least worst outcomes in emergency responses to disasters. Journal of Occupational and Organizational Psychology. DOI: 10.1111/joop.12108  

  • March 31, 2015
  • 05:03 AM

How to improve memory five times in less than an hour?

by Usman Paracha in SayPeople

Main Point:

You can enhance your memory nearly five times with the help of 45-60 minutes of sleep.

Published in:

Neurobiology of Learning and Memory

Study Further:

Memory is the power of retaining, remembering, and recalling past experiences and knowledge. Normally, new information moves away from the mind quite rapidly as we are prone to forget things. Every one of us wants to have a good memory. Researchers are working on new techniques to improve memory that may range from exercise to practice.

In a study, researchers have found that a power nap of less than one hour can help in improving the performance of memory by about five times. Researchers have found that a short sleep of 45-60 minutes can help in retaining the knowledge more than in the awaken state.

In the study, researchers worked on two groups of people. Both of those groups were shown unconnected pairs of words, and after showing those words, one group was asked to sleep and the other group watched a DVD. Researchers explained that the people in the group, who watched DVD, performed significantly worse than the other group, who was asked to go to sleep. People in this nap (sleep) group were able to retrieve information from memory that is five-fold better than the other group.

Brain (Credit: cblue98/Flickr)
Brain (Credit: cblue98/Flickr)

Researchers have also studied hippocampus, the part of the brain where new information is transferred for long-term memory. Moreover, they have studied brain activity, referred to as “sleep spindles”, which is considered important in memory consolidation during sleep and can be seen as a short burst of rapid oscillations in the electroencephalogram (EEG). Researchers are of opinion that previously entered information is probably consolidated during this type of brain activity. They concluded, “Together, these results speak for a selective beneficial impact of naps on hippocampus-dependent memories.”

Researchers are of opinion that a short sleep (nap) in school or during office hours could help in significantly improving the learning process.

Studte, S., Bridger, E., & Mecklinger, A. (2015). Nap sleep preserves associative but not item memory performance Neurobiology of Learning and Memory, 120, 84-93 DOI: 10.1016/j.nlm.2015.02.012... Read more »

Studte, S., Bridger, E., & Mecklinger, A. (2015) Nap sleep preserves associative but not item memory performance. Neurobiology of Learning and Memory, 84-93. DOI: 10.1016/j.nlm.2015.02.012  

  • March 31, 2015
  • 04:35 AM

Is anhedonia a key component of depression comorbid to autism?

by Paul Whiteley in Questioning Answers

Anhedonia: the inability to experience pleasure from activities usually found enjoyable.Although by no means an expert on anhedonia (or much else), I believe that it is a concept quite important when it comes to making a diagnosis of depression although the precise hows and whys of connecting anhedonia to other symptoms are still the source of some discussion [1].The paper from Vicki Bitsika & Christopher Sharpley [2] brings the concepts of anhedonia and depression into view with autism in mind. Based on the analysis of self-reported symptoms on the "Depression subscale of the Child and Adolescent Symptoms Inventory (CASI-D)" for 70 males diagnosed with an autism spectrum disorder (ASD) and 50 asymptomatic controls matched for age, authors reported that: "The MDD [major depressive disorder] profiles for the ASD participants were dominated by anhedonia."Accepting that the label of autism seemingly very rarely exists in a diagnostic vacuum (see here) and that there is still some debate about whether comorbidity is just that or something rather more integral to parts of the growing pluralisation of autism (see here), the Bitsika/Sharpley paper is a potentially important one. Getting into the nitty-gritty details of how issues such as depression manifest on top of a diagnosis of autism is important as per the discussions by Vannucchi et al [3] (see here) on the "atypical presentation" of bipolar disorder with Asperger syndrome in mind. Knowing for example, that anhedonia might be more characteristic of MDD in cases of autism or even more centrally to autism [4], may offer not only a more detailed perspective on screening for and managing such issues as and when they occur, but also a little bit more detail about the mechanisms through which such symptoms may come about.Music: Mercury Rev - Goddess on a Highway.----------[1] Gaillard R. et al. Anhedonia in depression. Encephale. 2013 Sep;39(4):296-305.[2] Bitsika V. & Sharpley CF. Differences in the Prevalence, Severity and Symptom Profiles of Depression in Boys and Adolescents with an Autism Spectrum Disorder versus Normally Developing Controls. International Journal of Disability, Development and Education. 2015; 62: 158-167.[3] Vannucchi G. et al. Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. J Affect Disord. 2014 Jul 8;168C:151-160.[4] Chevallier C. et al. Brief report: Selective social anhedonia in high functioning autism. J Autism Dev Disord. 2012 Jul;42(7):1504-9.----------Bitsika, V., & Sharpley, C. (2015). Differences in the Prevalence, Severity and Symptom Profiles of Depression in Boys and Adolescents with an Autism Spectrum Disorder versus Normally Developing Controls International Journal of Disability, Development and Education, 62 (2), 158-167 DOI: 10.1080/1034912X.2014.998179... Read more »

  • March 30, 2015
  • 11:32 AM

Gut Feelings

by Miss Behavior in The Scorpion and the Frog

This boy may be influencing who he will marry when he grows up. Photo by Orrling at Wikimedia Commons.Animals (including humans) are swarming with microorganisms both on and in our bodies. Humans harbor so many different microorganisms that we have over 150 times more microbial genes than mammalian genes, and it is reasonable to suspect that this scenario is similar for most animals. But before you run to soak in a tub of hand sanitizer, you should realize that many of these microorganisms are actually beneficial to the health of both your body and your mind. Although this field is still very much in its infancy, we have found that the microbes that live in digestive tracts in particular significantly influence their host animal’s behaviors. This connection between our digestive communities and our behaviors has been termed the microbiota–gut–brain axis. Much of the early research on the microbiota-gut-brain axis was done using specialized mice that have never been exposed to any bacteria. You may think this sounds like a healthy lifestyle, but these so-called germ-free mice have all kinds of health and behavioral problems. They often have digestive difficulties and high levels of anxiety, symptoms common of people with irritable bowel syndrome (IBS). They also typically have deficits in social behavior and increased repetitive behaviors. Similar to autism-spectrum disorders and obsessive compulsive disorder (OCD), these behavioral problems are more likely to occur in males than in females. When faced with a challenge, many struggle with solving the problem and show a higher tendency to give up, symptoms common in patients with depression. Interestingly, simply feeding germ-free mice some species of Bifidobacteria and Lactobacilli bacteria (similar to bacterial strains found in different brands of yogurt) can reduce symptoms of anxiety, depression, cognitive difficulties, autism, and OCD. This has led to a boom in biomedical research on the benefits of probiotics (that contain microbes that live in our guts) and prebiotics (that contain things that the microbes in our guts eat).Yogurt bacteria. Photo by Josef Reischig at Wikimedia Commons.These gut microbes don’t just help animals maintain their physical and mental health, they are also involved in complex social behaviors. For example, fruit flies prefer mates that grew up eating the same diet that they grew up eating. However, if they are treated with antibiotics, which kill the gut bacteria, they lose their mate choice preferences. If they are then treated again with microbes from their initial diet (with one Lactobacillus bacteria in particular), they gain their mate choice preferences back. This all makes me wonder, how important is yogurt to choosing the people we date and marry? How do microbes in our guts affect our brains anyway? Although the answer to this is still mostly unknown, we know that the gut has the potential to influence the brain through multiple means, including hormone production, immune function, and even directly through specific nerves. The specific mechanisms are still being very actively researched, but it is clear that microscopic critters living in our guts likely influence our brains and behaviors in many different physiological ways. Microbiota-gut-brain axis research is revolutionizing the way we think about health, medical treatments, behavior and even existential questions like who am I? But one thing is for sure: I’m gonna go have another yogurt. Want to know more? Check these out: Cryan, J., & Dinan, T. (2015). More than a Gut Feeling: the Microbiota Regulates Neurodevelopment and Behavior Neuropsychopharmacology, 40 (1), 241-242 DOI: 10.1038/npp.2014.224 Ezenwa, V., Gerardo, N., Inouye, D., Medina, M., & Xavier, J. (2012). Animal Behavior and the Microbiome Science, 338 (6104), 198-199 DOI: 10.1126/science.1227412 ... Read more »

Ezenwa, V., Gerardo, N., Inouye, D., Medina, M., & Xavier, J. (2012) Animal Behavior and the Microbiome. Science, 338(6104), 198-199. DOI: 10.1126/science.1227412  

  • March 30, 2015
  • 07:02 AM

Simple Jury Persuasion: “Hey, look over here for a second!” 

by Doug Keene in The Jury Room

This is sort of scary research. We all like to think our views on moral issues are pretty consistent and not easily shaken. That would be incorrect. They are not consistent and they are easily shaken. At least these are the conclusions reached by this research. We’ve written before about on which side of the […]

Related posts:
Simple Jury Persuasion: Telling jurors where to look
Simple Jury Persuasion: Activate the ‘intuitive prosecutor’
Simple Jury Persuasion: It’s really pretty black and white….

... Read more »

Pärnamets P, Johansson P, Hall L, Balkenius C, Spivey MJ, & Richardson DC. (2015) Biasing moral decisions by exploiting the dynamics of eye gaze. Proceedings of the National Academy of Sciences of the United States of America. PMID: 25775604  

  • March 30, 2015
  • 04:58 AM

Could you tell the difference between a person's memory and their imagination?

by BPS Research Digest in BPS Research Digest

If I gave you a written description of an object – let's say a boat – would you be able to judge whether the author had written about the boat from their memory of it, as opposed to having written about a boat they'd imagined?It's a question with real-world importance because, in court, we often rely on eyewitness memories and it's up to a jury to determine their source and veracity. But memory, like the imagination, is a creative process. Sometimes the two even become blurred – it's quite common for people to lose faith in an apparent memory, to wonder if they had in fact imagined it. Deliberate deception aside, how well can we judge the source of another person's recall?Arlo Clark-foos and his colleagues recruited 20 volunteers to either look at pictures of various objects  or to imagine those objects after being prompted by the words denoting them. Examples include boat, microwave, and chair. These volunteers were told they'd later have to recall as much about the imagined or viewed objects as possible. After a five minute distraction period during which they answered maths questions, the volunteers were asked to write about the objects, both those they'd looked at, and those they'd imagined. The transcripts were cleaned up to remove any overt clues as to the source of the descriptions – such as phrases like "I imagined ...". Then the transcripts were shown to thirty participants recruited from a  university, whose task was to read each one and decide if the description was based on the author's memory for the object, or on their having imagined the object. The participants were told that there had been no deliberate deception in the written accounts.To the researchers' surprise, the participants were able to make this distinction with modest accuracy. Specifically, descriptions of seen objects were correctly identified as such 63 per cent of the time, descriptions of imagined objects 57 per cent of the time. Although only modestly accurate, this is significantly more accurate than you'd expect had the participants simply been guessing.The researchers said this result was all the more remarkable because when they'd carefully analysed the accounts of seen and imagined objects looking for qualitative differences along 40 dimensions, they found very few – descriptions of seen objects contained more references to the season of the year (perhaps because the pictures gave relevant clues) and more author doubts about memory accuracy; by contrast, in the descriptions of imagined objects, there tended to be more references to sounds and locations (perhaps because this information was missing from the pictures).In further experiments, the researchers established that people could be trained to be even more accurate at this task by giving them multiple examples of object descriptions written from memory and descriptions written from the imagination, with each labelled as such. Feedback also boosted performance during blind testing – that is, telling participants whether each memory/imagination judgment they made was accurate or not."Although the current results are curious," the researchers said, "they only begin to explain how participants made their judgments. Future experimental work investigating the characteristics and decision processes that aid in resolving the source of others' memories will increase the applicability of these findings."_________________________________  Clark-Foos, A., Brewer, G., & Marsh, R. (2015). Judging the reality of others' memories Memory, 23 (3), 427-436 DOI: 10.1080/09658211.2014.893364 Post written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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  • March 30, 2015
  • 03:20 AM

Asthma and ADHD (again)

by Paul Whiteley in Questioning Answers

"Asthmatic children had a higher risk of also having ADHD."That was the conclusion reached by Kirsten Holmberg and colleagues [1] based on their analysis of rates of ADHD, and other variables found "through the Swedish Twin Register, linked to the Swedish Medical Birth Register, the National Patient Register and the Prescribed Drug Register." Said data came from over 20,000 twins who's parents were questioned when children were aged 9 or 12 years.For those unfamiliar with the proposed connection [2] between the respiratory condition(s) headed under the label of asthma and the presentation of attention-deficit hyperactivity disorder (ADHD), this is not the first time that peer-reviewed research has hinted at some kind of relationship. The 'big data' studies coming out of Taiwan for example, have similarly reported an association (see here). That part of any relationship between asthma and ADHD might also be mediated by the comorbid appearance of autism (see here) has also been proposed, although the the idea that autism (singularly) and asthma might overlap has been recently questioned (see here).Holmberg et al also reported that: "The association [between asthma and ADHD] was not restricted to either of the two dimensions of ADHD" following their analysis of the 'inattentive' and 'hyperactive/impulsive' domains that made up ADHD. They did find that asthma severity might however mediate the association with ADHD as per their reporting on an increased odds ratio (OR) "for >4 asthma attacks in the last 12 months."What's more to say about this possible connection? Well, preferential screening for ADHD when a diagnosis of asthma is received might be something for healthcare professionals to consider first and foremost. Acknowledging also that there may be several facets to ADHD including those related to sleep for example (see here) one might also entertain some further clinical investigations here also in light of what asthma can also do to sleeping patterns and routines [3]."Asthma medication seems not to increase the risk of ADHD" was another conclusion from Holmberg et al so to some degree allaying any fears that pharmacotherapy for asthma is 'causative' of ADHD. That being said, the idea that certain medicines might be 'linked' to both asthma and/or ADHD [4] is still deserving of further research consideration as has been previously mentioned on this blog (see here and see here). I might also put forward the idea that when it comes to overlapping variables potentially spanning asthma and ADHD, one might have a look at issues such as vitamin D availability (see here and see here) or even food (see here and see here) as potentially showing some shared involvement for some.For whatever reason, the evidence linking asthma and ADHD is growing...Music: Some Might Say from Oasis.----------[1] Holmberg K. et al. Impact of asthma medication and familial factors on the association between childhood asthma and ADHD A combined twin- and register-based study. Clin Exp Allergy. 2015 Mar 13.[2] Chou CJ. et al. Asthma in patients with attention-deficit/hyperactivity disorder: a nationwide population-based study. Ann Clin Psychiatry. 2014 Nov;26(4):254-60.[3] Teodorescu M. et al. Association between asthma and risk of developing obstructive sleep apnea. JAMA. 2015 Jan 13;313(2):156-64.[4] Tiegs G. et al. New problems arising from old drugs: second-generation effects of acetaminophen. Expert Rev Clin Pharmacol. 2014 Sep;7(5):655-62.----------Holmberg K, Lundholm C, Anckarsäter H, Larsson H, & Almqvist C (2015). Impact of asthma medication and familial factors on the association between childhood asthma and ADHD A combined twin- and register-based study. Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology PMID: 25772649... Read more »

  • March 29, 2015
  • 08:05 PM

UK Researchers find parental perception of child’s weight is skewed

by Dr. Jekyll in Lunatic Laboratories

Childhood obesity affects more than double the amount of children it did 30 years ago, according to the Centers for Disease Control and Prevention(CDC). To figure out why the rate is increasing researchers studied the relationship between parents and their obese children to determine how to improve pediatric health. The study actually reveals how poorly parents rate their own child’s weight issues — at least until they reach extreme levels of obesity.... Read more »

Black et al. (2015) Child obesity cut-offs as derived from parental perceptions: cross-sectional questionnaire. British Journal of General Practice. info:/10.3399/bjgp15X684385

  • March 29, 2015
  • 04:39 AM

Sera from children with autism inducing autistic features in rats?

by Paul Whiteley in Questioning Answers

"The autism sera injected rats demonstrated developmental delay and deficits in social communication, interaction, and novelty."That was one of the findings reported in the paper by Syed Faraz Kazim and colleagues [1] (open-access) who, among other things, injected intracerebroventricularly sera collected from children with autism into newborn rats and examined behavioural effects compared with injections of sera from asymptomatic controls. Actually, that was only one part of the research from Kazim et al but it does invite some further interesting questions...In brief, and bearing in mind the paper is open-access, a few details:A caveat first: "Based on studies described in this manuscript, the authors submitted a patent application to the United States Patent and Trademark Office on 12/11/2014, entitled: “Treatment of Autism Spectrum Disorders with Ciliary Neurotrophic Factor Peptide Mimetic”; application number US62/083,570; Inventors: Khalid Iqbal and Inge Grundke-Iqbal." The authors report a potential competing interest and good on them for doing so.As noted, there were several aspects to this research focused to a large extent around neurotrophins including something called ciliary neurotrophic factor (CNTF) or rather "a CNTF small peptide mimetic, P6" which might have the ability to increase levels of BDNF (brain derived neurotrophic factor ), a compound that has cropped up before on this blog (see here).So: sera from children with autism were initially added to "mouse primary cultured cortical neurons grown for 72 hours in medium" and resulted in "gross morphological changes". Pretreatment of said mouse neurons with P6 - "which corresponds to amino acid residues 146–156 of human CNTF" - seemed to have an effect that: "resulted in a significant reduction in cell death in cultured neurons treated with sera from autistic children." Another detail derived from this experiment: "Primary cortical neurons grown in the presence of autistic sera showed higher levels of oxidative stress." Interesting in light of other research in this area with autism in mind (see here)...Next: what was it in the sera from autistic children which seemed to be having effects on mouse neurons which weren't seen in control sera? Well it's possible that: "the presence of neurotrophic abnormalities in the sera from autistic children that could have contributed to altered development of neurons and increase in cell death and oxidative stress found." By neurotrophic abnormalities, the authors meant issues with "mature CNTF and BDNF" among other things.Next were the results from those studies where rat pups were injected with autism or control sera "with or without P6". More quotes: "alterations in the levels of neurotrophic factors in the sera from autistic individuals could contribute to neurobehavioral phenotype of autism in rats". By that the authors reported some potential differences in rat behaviour focused on things like grooming behaviour (repetitive behaviour) and ultrasonic calls (akin to social communication). P6 potentially rescuing functions was also reported for some of the tests.Conclusion: with the caveats of much more investigation required and that rats are rats and not humans (see here) "this study provides evidence regarding the neurotrophic abnormalities in autism and the potential role they play in the pathophysiology" of the condition. Further: "Ameliorating the neurotrophic imbalance during early stages of brain development can serve as a potential therapeutic approach for autism. P6 represents a new class of neurotrophic peptide mimetics that has potential therapeutic value for ASD and related conditions."I'm rather interested in this work and the potential for at least some cases of autism as and when replicative work is undertaken. I note in other patents from this group (see here) the idea that peptides with a neurotrophic link might have some application to "neural pathologies where BDNF levels are dysregulated" is one that has been embraced.The authors, the late Inge Grundke-Iqbal & Khalid Iqbal, have a pretty impressive peer-reviewed track record based to a large extent on their work on neurodegeneration and "abnormally hyperphosphorylated tau" as the main component of the tangles in Alzheimer's disease. Indeed, these findings have particular relevance recently (see here). Applying their, and their research groups, expertise to autism is most definitely an asset, albeit with the requirement for quite a bit more research in this area.To close: The Stone Roses - She Bangs the Drums.---------- [1] Kazim SF. et al. Sera from Children with Autism Induce Autistic Features Which Can Be Rescued with a CNTF Small Peptide Mimetic in Rats. PLoS ONE. 2015; 10(3): e0118627.----------Kazim, S., Cardenas-Aguayo, M., Arif, M., Blanchard, J., Fayyaz, F., Grundke-Iqbal, I., & Iqbal, K. (2015). Sera from Children with Autism Induce Autistic Features Which Can Be Rescued with a CNTF Small Peptide Mimetic in Rats PLOS ONE, 10 (3) DOI: 10.1371/journal.pone.0118627... Read more »

  • March 28, 2015
  • 08:20 PM

The neurobiological underpinnings of suicidal behavior

by neurosci in Neuroscientifically Challenged

When you consider that so much of our energy and such a large portion of our behavioral repertoire is devoted to ways of ensuring our survival, suicide appears to be perhaps the most inexplicable human behavior. What would make this human machine--which most of the time seems to be resolutely programmed to scratch, claw, and fight to endure through even the most dire situations--so easily decide to give it all up, even when the circumstances may not objectively seem all that desperate? Suicide is a difficult behavior to justify rationally, and yet it is shockingly common. More people throughout the world end their lives by suicide each year than are killed by homicide and wars combined.The multitudinous influences that are thought to contribute to suicidal behavior are also very convoluted and difficult to untangle. Clearly, among different individuals the factors that lead to an act of suicide will vary considerably; nevertheless, there are some variables that are thought to generally increase the risk of suicidal behavior. A number of studies have, for example, demonstrated that genetic factors are associated with a predisposition to suicidal behavior. Also, early-life adversity--like sexual abuse, physical abuse, or severe neglect--has been strongly linked to suicide. However, even among groups with higher suicide risk there is a great deal of variability, which adds to the complexity of the issue. For example, personality traits like impulsiveness and aggression have been associated with an increased risk of suicide--but this relationship is seen primarily in younger people. It is not as apparent in older individuals who display suicidal behavior; they are often characterized by higher levels of harm avoidance instead of risk-taking.While there are a number of predisposing factors involving personal characteristics or previous life events that make suicidal ideation and behavior more likely, there are also factors that immediately precede a suicide attempt which are thought to be directly linked to the transition from thinking about suicide to acting on those thoughts. Of course, some of those factors are likely to involve changes in neurobiology and neurochemistry that cause suicide--which may have previously just been an occasional thought--to become the focus of a present-moment plan that is sometimes borne out with great urgency and determination. And, while it is important to be able to identify influences that predispose individuals to suicidal thinking in general, an understanding of the neurobiological factors that precipitate a suicide attempt might open the door for treatments designed to protect an individual from acting on (or experiencing) sudden impulses to complete a suicide.While the distally predisposing factors for suicidal behavior are difficult to identify due to the myriad influences involved, however, the proximal neurobiological influences are hard to pinpoint due both to their complexity and the fact that a suicidal crisis is often short-lived and difficult to study. The most direct way to investigate changes in the suicidal brain would be to look at brains of individuals who are suicide completers (i.e. those who are now deceased due to suicide). One reason for focusing on suicide completers is that we can expect some neurochemical--and possibly psychological--differences between suicide completers and those who attempted suicide but are still alive. However, working with postmortem brains has its own limitations: obtaining accurate background information may be challenging without the ability to interview the patient, there may be effects on the brain (e.g. from the process of death and its associated trauma or from drugs/medications taken before death) that may make it hard to isolate factors involved in provoking one towards suicide, and the limitation of only being able to examine the brain at one time makes causal interpretations difficult.Regardless, investigations into irregularities in the brains of those who exhibit suicidal behavior (both attempters and completers) have identified several possible contributing factors that may influence the decision to act on suicidal thoughts. Many of these factors are also implicated in depressed states, as most suicidal individuals display some characteristics of a depressed mood even if they don't meet the criteria for a diagnosis of major depressive disorder. (This, of course, adds another layer of complexity to interpretation as it is difficult to determine if suicide-related factors are simply characteristics of a depressed mood and not solely related to suicidal actions.) The role of each of these factors in suicidal behavior is still hypothetical, and the relative contribution of each is unknown. However, it is thought that some--or all--of them may be implicated in bringing about the brain state associated with suicidal actions.Alterations in neurotransmitter systemsAbnormalities in the serotonin system have long been linked to depressive behavior, despite more recent doubts about the central role of serotonin in the etiology of depression. Similarly, there appear to be some anomalies in the serotonin system in the brains of suicidal individuals. In an early study on alterations in the serotonin system in depressed patients, Asberg et al. found that patients with lows levels of 5-hydroxyindoleacetic acid, the primary metabolite of serotonin (and thus often used as a proxy measure of serotonin levels), were significantly more likely to attempt suicide. Additionally, those who survive a suicide attempt display a diminished response to the administration of fenfluramine, which is a serotonin agonist that in a typical brain prompts increased serotonin release. A number of neuroimaging studies have also detected reduced serotonin receptor availability in the brains of suicidal patients. This evidence all suggests that abnormalities in the serotonin system play some role in suicidal behavior, although the specifics of that role remain unknown.As we have learned from investigations of depression, however, it is important to avoid focusing too much on one-neurotransmitter explanations of behavior. Accordingly, a number of other neurotransmitter abnormalities have been detected in suicidal patients as well. For example, gene expression analyses in postmortem brains of individuals who died by suicide have identified altered expression of genes encoding for GABA and glutamate receptors in various areas of the brain. Although the consequences of these variations in gene expression is unknown, abnormalities in GABA and glutamate signaling have both also been hypothesized to play a role in depression. Abnormalities in the stress responseIrregularities in the stress response have long been implicated in depression, and thus it may not be surprising that stress system anomalies have been observed in patients exhibiting suicidal behavior as well. The hypothalamic-pituitary-adrenal (HPA) axis is a network that connects the hypothalamus, pituitary gland, and adrenal glands; it is activated during stressful experiences. When the HPA axis is stimulated, corticotropin-releasing hormone is secreted from the hypothalamus, which causes the pituitary gland to secrete adrenocorticotropic hormone, which then prompts the adrenal glands to release the stress hormone cortisol. In depressed patients, cortisol levels are generally higher than normal, suggesting the HPA axis is hyperactive; this may be indicative of the patient being in a state of chronic stress.In suicidal individuals, the HPA axis seems to be dysregulated as well. For example, in one study the HPA activity of a group of psychiatric inpatients was tested using what is known as the ... Read more »

Turecki, G. (2014) The molecular bases of the suicidal brain. Nature Reviews Neuroscience, 15(12), 802-816. DOI: 10.1038/nrn3839  

  • March 28, 2015
  • 01:46 PM

Too much attention can be a deficit

by Dr. Jekyll in Lunatic Laboratories

Sometimes being too focused on a task is not a good thing. During tasks that require our attention, we might become so engrossed in what we are doing that we fail to notice there is a better way to get the job done. For example, let’s say you are coming out of a New York City subway one late afternoon and you want to find out which way is west. You might begin to scan street signs and then suddenly realize that you could just look for the setting sun.... Read more »

Nicolas W. Schuck, Robert Gaschler, Dorit Wenke, Jakob Heinzle, Peter A. Frensch, John-Dylan Haynes, & Carlo Reverberi. (2015) Medial Prefrontal Cortex Predicts Internally Driven Strategy Shifts. Neuron. info:/Link

  • March 28, 2015
  • 11:00 AM

Misbeliefs, evolution and games: a positive case

by Sergio Graziosi in Evolutionary Games Group

A recurrent theme here in TheEGG is the limits and reliability of knowledge. These get explored from many directions: on epistemological grounds, from the philosophy of science angle, but also formally, through game theory and simulations. In this post, I will explore the topic of misbeliefs as adaptations. Misbeliefs will be intended as ideas about […]... Read more »

Kaznatcheev, A., Montrey, M., & Shultz, T.R. (2014) Evolving useful delusions: Subjectively rational selfishness leads to objectively irrational cooperation. Proceedings of the 36th annual conference of the Cognitive Science Society. arXiv: 1405.0041v1

  • March 28, 2015
  • 04:27 AM

Screening for autism in preterm infants

by Paul Whiteley in Questioning Answers

"A positive screen on the M-CHAT [Modified Checklist for Autism in Toddlers] occurs more commonly in very preterm infants than those born at term."So said the study by Peter Gray and colleagues [1] as the topic of preterm status - that is, babies born alive before 37 weeks of pregnancy - potentially being linked to a greater risk of autism or at least, increased risk of screening positive for autism, crops up yet again on this blog (see here).Gray et al examined a cohort of children born at the very boundaries of the definition of preterm ("≤30weeks gestation") when aged 2 years old, questioning mums of preterm children (n=97) and mums of term infants (n=77) with a whole range of questionnaires / schedules including the M-CHAT and the Child Behaviour Checklist (CBCL) among other things. "Previously collected data from the mothers at 12months - the Edinburgh Postnatal Depression Scales (EPDS)" were also analysed.Authors reported that a higher percentage of preterm kids "screened positive on the M-CHAT" compared with term controls (13.4% vs. 3.9% respectively). These statistics decreased somewhat as a consequence of "an M-CHAT follow-up interview by phone" with only one child with membership of the preterm group subsequently receiving a diagnosis of autism from the entire cohort. The authors discuss some of the whys and wherefores of those pretermers who initially screened positive on the M-CHAT and how they were: "born to younger, non-Caucasian mothers and were of lower birth weight and had a higher incidence of being small for gestational age."As per my discussion on the paper by Alexa Guy and colleagues [2] (see here again), the message coming through about using M-CHAT with the preterm population is again one of 'use with caution'. Indeed, the Gray paper illustrates how the follow-up consultation is a pretty important part of M-CHAT, something further developed on by the findings from Diana Robins and colleagues [3] and the whole M-CHAT-R/F thing (see here). I wouldn't necessarily say that M-CHAT is completely useless as a screen for autism under certain conditions. Merely that looking for the early red flags that might denote autism is very much still a work in progress potentially confounded by length of gestation. YouTube video anyone?Music: PJ Harvey- The Words That Maketh Murder.----------[1] Gray PH. et al. Screening for autism spectrum disorder in very preterm infants during early childhood. Early Hum Dev. 2015 Mar 9;91(4):271-276.[2] Guy A. et al. Infants Born Late/Moderately Preterm Are at Increased Risk for a PositiveAutism Screen at 2 Years of Age. J Pediatrics. 2014. 5 December.[3] Robins DL. et al. Validation of the modified checklist for Autism in toddlers, revised with follow-up (M-CHAT-R/F). Pediatrics. 2014 Jan;133(1):37-45.----------Gray PH, Edwards DM, O'Callaghan MJ, & Gibbons K (2015). Screening for autism spectrum disorder in very preterm infants during early childhood. Early human development, 91 (4), 271-276 PMID: 25766314... Read more »

  • March 27, 2015
  • 03:18 PM

Why it's important that employers let staff personalise their workspaces

by BPS Research Digest in BPS Research Digest

The sparring mitt, yellow stitches spelling "SLUGGER" casually lying on the desk. The Mathlete trophy on a high shelf. A Ganesha statue, slightly chipped. Why do people bring these kinds of personal objects into the workplace?Researchers Kris Byron and Gregory Laurence found answers by consulting 28 people in a range of jobs and workplaces. They used the "grounded theory" approach, starting with a clutch of more open-ended interviews and then pursuing the lines of inquiry that emerged, in every case inventorying the person’s workspace and exploring the significance of each object.The conventional understanding is that personal objects are territorial markers used to communicate who we are to co-workers. And indeed many interviewees emphasised this function, a "unique fingerprint" that expresses difference. This might be an indicator of character –  I’m a happy-go-lucky person – but participants also used objects to emphasise their organisational roles. A framed MBA certificate reminds others that this cubicle bunny is made of management material, thank you, whereas doodles show that the person is part of the creative class. An event planner explained that the thank-you notes pinned to their board were to reassure others of her reliability – a core requirement in her role.As well as showing differences, personalisation can also affirm shared identity. Star Wars memorabilia across multiple desks shows that "a lot of us have, you know, that techie background". Similarly, some items were inside jokes, with meaning only apparent to those sharing in its history. And although personalisation could emphasise status – think of that MBA certificate – some managers attempted to de-emphasise status differences by presenting everyday objects that made themselves more approachable.Interviewees raised another reason for personalisation: to build relationships. These items were seen as icebreakers or ways to find "common ground", whether through the contents of a bookshelf, or a photo denoting parenthood. Byron and Laurence photographed every desk-setup from the perspective of an outside visitor, and found that 75 per cent of such conversation-starters were positioned to be clearly visible from that view. Many participants felt that these personalisation functions were vital and companies prevent them at their peril: "They want to have such strong relationships with customers but they’re taking away the personal elements that I think can lend towards building those types of relationships with clients."In contrast, a certain proportion of personalisation objects – about a third in all – were positioned to only be visible to the owner themselves. These exemplify a final function of personalisation – not to communicate to others, but to remind ourselves of our identity.This could be an aspirational symbol – the poster put up by a designer that showed "the kind of design I eventually want to do", or the gift from an inspiring role model. Or it might be a way to put work into a larger context, so on the tough days, "you can look at your picture [of children] and realize this is only a job."Many objects had multiple functions – communicating difference, starting conversations, and reminding oneself of identity. Byron and Laurence conclude that "organizations would be unwise to put excessive limits on employees’ personalization of their workspaces," as an innocuous paperweight may turn out to carry a lot inside._________________________________ Byron, K., & Laurence, G. (2015). Diplomas, Photos, and Tchotchkes as Symbolic Self-Representations: Understanding Employees' Individual Use of Symbols Academy of Management Journal, 58 (1), 298-323 DOI: 10.5465/amj.2012.0932 --further reading--The supposed benefits of open-plan offices do not outweigh the costsPost written by Alex Fradera (@alexfradera) for the BPS Research Digest.

... Read more »

  • March 27, 2015
  • 09:06 AM

The ABCs of Alphabet-Magnet Synesthesia

by Elizabeth Preston in Inkfish

Is it cool or existentially disturbing to think that your personal brain quirks might come from the toys you played with as a toddler?

In a study published earlier this month, psychologists asked 6,588 American synesthetes what colors they associate with each letter of the alphabet. Then they compared these associations to a certain vintage set of Fisher-Price alphabet magnets. They found that at least 6% of their synesthetes had improbably close matches to the colors of the magnets.

T... Read more »

  • March 27, 2015
  • 07:02 AM

Fire-setters: Psychotic and non-psychotic 

by Rita Handrich in The Jury Room

There is a lot of literature on fire-setters but not, apparently, on how psychotic fire-setters differ from those who are not psychotic. As it turns out, there are some significant differences. Researchers in The Netherlands examined the records of 124 fire-setters (30 psychotic and 94 non-psychotic) sent for pretrial forensic mental health assessments between 2000 […]

Related posts:
But, your honor! That witness was drunk!
Can you trust the results of forensic evaluations on legal sanity?
A new question for the jury: Did my brain implant make me do it?

... Read more »

  • March 27, 2015
  • 06:02 AM

Inflammation impairs social cognitive processing

by Paul Whiteley in Questioning Answers

A quote to begin: "acute inflammation can lead to decreases in the ability to accurately and reliably comprehend emotional information from others."It comes from the article published by Mona Moieni and colleagues [1] who examined a concept familiar to many people with a connection to autism either personally or professionally: Theory of Mind (ToM). Rather interestingly, Moieni et al "examined whether exposure to an experimental inflammatory challenge led to changes in ToM." Inflammatory challenge refers to the artificial induction of a state of inflammation via the use of something called endotoxin, something I've covered under another name previously on this blog (see here).As part of a larger research project on inflammation-induced depressed mood (see here) researchers set about looking at social cognition under inflammatory-inducing and placebo conditions specifically based on the "Reading the Mind in the Eyes (RME) test". The RME test has quite a firm foundation in autism research [2]. Their results indicated that using the RME test as a sort of measure of ToM "endotoxin (vs. placebo) led to decreases in performance on the RME test from baseline to the peak of inflammatory response, indicating that acute inflammation can lead to decreases in the ability to accurately and reliably comprehend emotional information from others."With the caveats that (a) this wasn't a study of people with autism (or at least not those diagnosed with autism) and (b) acute inflammation may not be the same as chronic inflammation, these are intriguing results potentially overlaying onto several other research areas. Autism and inflammation is something that I'm quite interested in on this blog as per the idea that physiology and psychology might not be some far apart in certain cases/types of autism (see here). That other somatic manifestations might also be linked to inflammatory processes with autism in mind (see here) is something else to mention.I hold back from saying that all those with autism who 'fail' ToM tasks are somehow in a state of inflammation given that this is a complicated area (see here). As per my previous ramblings, I'm also not necessarily the greatest fan of the sweeping generalisations made about ToM when it comes to autism (see here). Particularly when one looks at the way that ToM is examined in relation to autism [3] and how ToM issues cross quite a few different labels [4] some of which might overlap with autism (see here).Still, if there is the remotest possibility that the physiological state of acute inflammation might correlate with issues with mentalising or completing mentalising tasks, I'd be minded to suggest that future work on ToM might be minded to take this into account. Likewise, in all those studies looking at inflammatory processes linked to something like autism, measuring ToM before and after could represent an interesting parameter when looking at potential interventions...Some music then... The Wedding Present and My Favourite Dress.----------[1] Moieni M. et al. Inflammation impairs social cognitive processing: A randomized controlled trial of endotoxin. Brain, Behavior, and Immunity. 2015. May 10.[2] Baron-Cohen S. et al. The "Reading the Mind in the Eyes" Test revised version: a study with normal adults, and adults with Asperger syndrome or high-functioning autism. J Child Psychol Psychiatry. 2001 Feb;42(2):241-51.----------Moieni M, Irwin MR, Jevtic I, Breen EC, & Eisenberger NI (2015). Inflammation impairs social cognitive processing: a randomized controlled trial of endotoxin. Brain, behavior, and immunity PMID: 25770082... Read more »

  • March 27, 2015
  • 01:22 AM

Is a trauma focus truly needed in PTSD treatment?

by Eva Alisic in Trauma Recovery

For treatment of Posttraumatic Stress Disorder to be effective, is it really necessary to focus on the trauma itself? ... Read more »

Barlow DH, Bullis JR, Comer JS, & Ametaj AA. (2013) Evidence-based psychological treatments: an update and a way forward. Annual review of clinical psychology, 1-27. PMID: 23245338  

Watts BV, Schnurr PP, Mayo L, Young-Xu Y, Weeks WB, & Friedman MJ. (2013) Meta-analysis of the efficacy of treatments for posttraumatic stress disorder. The Journal of clinical psychiatry. PMID: 23842024  

Wampold BE, Imel ZE, Laska KM, Benish S, Miller SD, Flückiger C, Del Re AC, Baardseth TP, & Budge S. (2010) Determining what works in the treatment of PTSD. Clinical psychology review, 923-33. PMID: 20638168  

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