Learning chess can improve math skills

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Twenty-two years ago to the day, on January 30, 1994, Peter Leko became the world’s youngest chess grandmaster, at the age of 14.

A proficiency in chess is often linked with higher intelligence, that is, the more intelligent you are, the more likely to be good at chess. This assumption has roots probably in the observation that chess does not allow for random chance or physical attributes, as most games do. So it follows that of you are good at it, it must be… intelligence, although there are at least an equal number of studies if not more that show that practice has more an impact on your chess ability that your native IQ score.

Personally, as one that always looks askance whenever there is talk about intelligence quotient and intelligence tests, I have serious doubts that any of these papers measured what they claimed they measured. And that is because I find the construct “intelligence” poorly defined and, as a direct consequence, hard to measure.

That being said, Sala et al. (2015) wanted to see if chess practice can enhance mathematical problem-solving abilities in young students. The authors divided 560 pupils (8 to 11 years old) into two groups: one group received chess training for 10-15 hours (1 or 2 hours per week) and an option to use a chess program, while the other group did not participate in any chess activities. The experiment took 3 months.

Both groups were tested before and after training with a mathematical problem-solving test battery and a chess ability test.

“Results show a strong correlation between chess and math scores, and a higher improvement in math in the experimental group compared with the control group. These results foster the hypothesis that even a short-time practice of chess in children can be a useful tool to enhance their mathematical abilities.” (Sala et al. (2015, Abstract).

This is all nice and well, were it not for the fact that their experimental group had significantly more pupils that already knew how to play chess (193 out of 309, 62%) compared to the control group (72 out of 251, 29%). To give credit to the authors, they acknowledge this limitation of the study, but, surprisingly, they do not run their stats without the “I-already-know-chess” subjects….

Nevertheless, even if the robustness and the arguments are a little on the shoddy side, the paper points to a possible fruitful line of research: that of additional tools to improve school performance by incorporating game and playtime into the instructors’ and parents’ teaching arsenal.

Reference: Sala G, Gorini A, & Pravettoni G (23 July 2015). Mathematical Problem-Solving Abilities and Chess. An Experimental Study on Young Pupils. SAGE Open, 1-9. DOI: 10.1177/2158244015596050. Article | FREE FULLTEXT PDF

By Neuronicus, 30 January 2016

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Mechanisms of stress resilience

71 stress - CopyLast year a new peer-reviewed journal called Neurobiology of Stress made its debut. The journal is published by Elsevier, who, in an uncharacteristic move, has provided Open Access for its first three issues. So hurry up and download the papers.

The very first issue is centered around the idea of resilience. That is, exposed to the same stressors, some people are more likely to develop stress-induced diseases, whereas others seem to be immune to the serious effects of stress.

Much research has been carried out to uncover the effects of chronic stress or of an exposure to a single severe stressor, which vary from cardiovascular disorders, obesity, irritable bowel syndrome, immune system dysfunctions to posttraumatic stress disorder, generalized anxiety, specific phobias, or depression. By comparison, there is little, but significant data on resilience: the ability to NOT develop those nasty stress-induced disorders. Without doubt, one reason for this scarcity is the difficulty in finding such rare subjects in our extremely stressful society. Therefore most of the papers in this issue focus on animal models.

Nevertheless, there is enough data on resilience to lead to no less that twenty reviews on the subject. It was difficult to choose one as most are very interesting, tackling various aspects of resilience, from sex differences to prenatal exposure to stress, from epigenetic to neurochemical modifications, from social inequalities to neurogenesis and so on.

So I chose for today a more general review of Pfau & Russo (2015), entitled “Peripheral and central mechanisms of stress resilience”. After it introduces the reader to four animal models of resilience, the paper looks at the neruoendocrine responses to stress and identifies some possible chemical mediators of resilience (like certain hormones), then at the immune responses to stress (bad, bad cytokines), and finally at the brain responses to stress (surprisingly, not focusing on amygdala, hypothalamus or hippocampus, but on the dopamine system originating from ventral tegmental area).

I catalogue the review as a medium difficulty read because it requires a certain amount of knowledge of the stress field beforehand. But do check out the other ones in the issue, too!

Reference: Pfau ML & Russo SJ (1 Jan 2015). Peripheral and central mechanisms of stress resilience. Neurobiology of Stress, 1:66-79. PMID: 25506605, PMCID: PMC4260357, DOI: 10.1016/j.ynstr.2014.09.004. Article | FREE FULLTEXT PDF

By Neuronicus, 24 January 2016

The Firsts: Anandamide (1992)

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Cannabis, the plant whose psychoactive tetrahydrocannabinol (THC) binds to the same receptors in the brain as anandamide.

A rare tragedy took place in France a few days ago when a Phase I clinical trial for a new drug destined to improve mood and alleviate pain has resulted in one person dead and five other hospitalized. Phase I means that the drug successfully passed all animal tests and was being tried for the first time in humans to test its safety (efficacy and potency are tested in phase II and III, respectively).

The trial has been suspended and an investigation is on the way. So far, it appears that both the manufacturer (Bial) and the testing company (Biotrial) have followed all the guidelines and regulations. The running hypothesis is that the drug (BIA 10-2474) is acting on an unexpected target. What does that mean?

BIA 10-2474 is a FAAH inhibitor (fatty acid amide hydrolase). This enzyme breaks down anandamide, which is an endocannabinoid. In other words, is a neurotransmitter in the brain that binds to the same receptors as THC, the main active component of marijuana. So, if you give someone BIA 10-2474, the result would be an increase in the availability of anandamide, presumably with anxiolytic and analgesic effects (yes, similar to smoking weed).

There are other FAAH inhibitors out there that had been previously tried in humans and they were never marketed not because they were unsafe, but because they were ineffective in producing the desired results, i.e. less pain and/or anxiety.

So we don’t know yet why BIA 10-2474 killed people, but the bet is that in addition to FAAH, it also binds to some other protein. Why they didn’t discover this in animal trials, is a mystery; perhaps the unknown protein is unique to humans? By the looks of the drug’s structure, I think is computer generated, meaning is composed of a bunch of functional groups that someone put together in the hopes that it would fit neatly on the target binding site; but so many functional groups thrown in together might bind unexpectedly to other places than the intended. More on the story in Nature.

Anyway, that was the very long intro to today’s featured paper: the discovery of anandamide. Which happened very recently, in 1992, by the Mechoulam group at the Hebrew University of Jerusalem, Israel. Anandamide is the first endocannabinoid to be isolated. Mechoulam’s postodcs, William Devane and Lumir Hanus, used mass spectroscopy and NMR (nuclear magnetic resonance, MRI is an application of the same principles) to identify and isolate the molecule in a pig brain. And then they named it, fittingly, the “amide of bliss”…

Of note, members of the same Mechoulam group identified two more of the six known endocannabinoids. The three pages paper is highly technical, but I am assured (by a chemist) that is an easy-peasy read for any organic chemist.

Reference: Devane WA, Hanus L, Breuer A, Pertwee RG, Stevenson LA, Griffin G, Gibson D, Mandelbaum A, Etinger A, & Mechoulam R (18 Dec 1992). Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science, 258(5090):1946-9. PMID: 1470919, DOI: 10.1126/science.1470919.  Article | Research Gate Full Text

By Neuronicus, 18 January 2016

No CPU required for integrating data from different senses

69 PD star-209371_1920Most of the time the brain receives information from different senses about the same object or event. For example, to localize an object that makes noise we use both visual and auditory information – if these are available to us -, process called multisensory information integration (MSII).

It is generally believed that the way this integration happens in a physical sense is by getting all these data in a special brain region dedicated to integrate information from multiple senses. And that there are several regions like that in the brain; for example superior colliculi integrate the visual and auditory information from the example above. This belief is not without empirical support. Indeed, many experiments both in vivo (i.e. in the awake behaving animal) and in silico (i.e. simulated on a computer program by building neural networks) have strengthened this idea.

But Zhang et al. (2016) claim there is some data that doesn’t fit the model. So let’s build a different model. Which is exactly what they have done using continuous attractor neural networks (CANN) as the building blocks for a neural network that seems to be biologically realistic. The output of their experiments shows that instead of having a central processing area in the brain that integrates data from multiple senses, optimal processing can be achieved by a decentralized network with neurons that are reciprocally connected.

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Excerpt from the Methods section of Zhang et al. (2016, doi: 10.1523/JNEUROSCI.0578-15.2016.)

Today, uncharacteristically, I am covering a paper that I have not read in its entirety. That is because, frankly, they lost me after the first Methods paragraph where they describe the way they built the neural network. In my defense, I don’t think there are many people in the world outside the neural networks field that can follow the mathematical formulae (see the Excerpt pic).

Anyway, my gut instinct is that both hypotheses have merit in that the brain uses both specialized multisensory areas, like superior colliculi and decentralized, distributed reciprocal connections, like the model proposed by Zhang et al. (2016).

Reference: Zhang WH, Chen A, Rasch MJ, & Wu S (13 Jan 2016). Decentralized Multisensory Information Integration in Neural Systems. Journal of Neuroscience, 36(2):532-47. doi: 10.1523/JNEUROSCI.0578-15.2016. Article | FREE Fulltext PDF

By Neuronicus, 14 January 2016

Ebola survivors can still transmit the disease

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Ebola patient treated in isolation. License: PD

Ebola is a nasty, nasty disease, incurable, extremely virulent, and with a high mortality rate. Its last devastating outbreak in West Africa in the past couple of years compelled the governments and pharmaceutical agencies to invest heavily in the search of a cure or a vaccine. As a result, there are already a dozen or so of possible vaccines being tested in various phases of drug development. Some hold real promise and, hopefully, one would breed true very soon.

But that’s not what today article is about. It is about the Ebola survivors. If the patient is still alive after two weeks from symptoms onset, there are very good chances s/he will survive it. Depending on the country, the survival rates vary between 10% up to 75%, with the average being about 50% (that is, you got one chance in two to survive Ebola).

It is very difficult to conduct thorough testing on Ebola survivors, mainly due to poor accessibility to them. However, Thorson et al. (2016) looked at all the available evidence, from published articles to non-peer-reviewed papers, from WHO data (World Health Organization) to personal communications and Internet feeds to see if Ebola survivors can still transmit the disease.

In short: yes, they can, unfortunately. Primarily through sexual transmission, as the authors found reports of Ebola being present in the sperm up to 284 days after symptom onset (and possibly even longer). Also, there are reports of sexual partners being infected by an Ebola survivor.

The authors (and the WHO) recommend that the survivors should be tested every 3 months and declared free of Ebola only when RT-PCR (reverse transcription polymerase chain reaction, a method that detects RNA expression) is negative twice. Meanwhile, Ebola survivors should practice abstinence. Or, use condoms, although the virus is really small (80 nm), therefore a condom may not present an impenetrable barrier.

Reference: Thorson A, Formenty P, Lofthouse C, & Broutet N (Jan 2016). Systematic review of the literature on viral persistence and sexual transmission from recovered Ebola survivors: evidence and recommendations. BMJ Open, 6:e008859. doi:10.1136/bmjopen-2015-008859.  Article | FREE Fulltext PDF

By Neuronicus, 10 January 2016

CCL11 found in aged but not young blood inhibits adult neurogenesis

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Portion of Fig. 1 from Villeda et al. (2011, doi: 10.1038/nature10357) describing the parabiosis procedure. Basically, under complete anesthesia, the peritoneal membranes and the skins of the two mice were sutured together. The young mice were 3–4 months (yellow) and old mice were 18–20 months old (grey).

My last post was about parabiosis and its sparse revival as a technique in physiology experiments. Parabiosis is the surgical procedure that joins two living animals allowing them to share their circulatory systems. Here is an interesting paper that used the method to tackle blood’s contribution to neurogenesis.

Adult neurogenesis, that is the birth of new neurons in the adult brain, declines with age. This neurogenesis has been observed in some, but not all brain regions, called neurogenic niches.

Because these niches occur in blood-rich areas of the brain, Villeda et al. (2011) wondered if, in addition with the traditional factors required for neurogenesis like enrichment or running, blood factors may also have something to do with neurogenesis. The authors made a young and an old mouse to share their blood via parabiosis (see pic.).

Five weeks after the parabiosis procedure, the young mouse had decreased neurogenesis and the old mouse had increased neurogenesis compared to age-matched controls. To make sure their results are due to something in the blood, they injected plasma from an old mouse into a young mouse and that also resulted in reduced neurogenesis. Moreover, the reduced neurogenesis was correlated with impaired learning as shown by electrophysiological recordings from the hippocampus and from behavioral fear conditioning.

So what in the blood does it? The authors looked at 66 proteins found in the blood (I don’t know the blood make-up, so I can’t tell if 66 is a lot or not ) and noticed that 6 of these had increased levels in the blood of ageing mice whether linked by parabiosis or not. Out of these six, the authors focus on CCL11 (unclear to me why that one, my bet is that they tried the others too but didn’t have enough data). CCLL11 is a small signaling protein involved in allergies. So the authors injected it into young mice and Lo and Behold! there was decreased neurogenesis in their hippocampus. Maybe the vampires were onto something, whadda ya know? Just kidding… don’t go around sucking young people’s blood!

This paper covers a lot of work and, correspondingly, has no less than 23 authors and almost 20 Mb of supplemental documents! The story it tells is very interesting and as complete as it gets, covering many aspects of the problems investigated and many techniques to address those problems. Good read.

Reference: Villeda SA, Luo J, Mosher KI, Zou B, Britschgi M, Bieri G, Stan TM, Fainberg N, Ding Z, Eggel A, Lucin KM, Czirr E, Park JS, Couillard-Després S, Aigner L, Li G, Peskind ER, Kaye JA, Quinn JF, Galasko DR, Xie XS, Rando TA, Wyss-Coray T. (31 Aug 2011). The ageing systemic milieu negatively regulates neurogenesis and cognitive function. Nature. 477(7362):90-94. doi: 10.1038/nature10357. Article | FREE Fulltext PDF

By Neuronicus, 6 January 2016

Your blood is better than my blood

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Siamese tomatoes. Taken from here.

Parabiosis is a surgical procedure that lets two animals to share the same blood; it’s a case of reverse conjoined twins restricted to the circulatory system.

The procedure is over 150 years old and is a useful technique in physiology, though rarely used, probably due to the perceived cruelty towards the animals, although today is performed under anesthesia and aseptic condition. It delivered good data; for example, it was a parabiosis experiment with rodents that showed is not the sugar in the blood that causes cavities but the sugar in the mouth. Similarly, parabiosis has been proven useful in cancer, diabetes, and ageing research.

Scudellari (2015) wrote a News piece for Nature describing some advancements in the ageing field using the parabiosis technique. Namely, by joining the circulatory systems of a young and an old mouse, researchers have observed that the old mouse is faster, smarter, with rejuvenated muscles and glossier fur. Now the race is to find out what in the blood does it. Researchers caution that the young blood is not effectively reversing ageing, but may have factors circulating in it that promote tissue repair. Already a muscle-rejuvenating protein has been identified.

I am not going through the original papers themselves as I usually do (they are provided as links in the Reference paper). Instead, I am featuring the news piece by Scudellari because in addition of looking at parabiosis and ageing result, it also provides a nice historical account of the use of parabiosis. Enjoy!

Reference: Scudellari, M. (22 Jan 2015). Ageing research: Blood to blood. Nature, 517: 426-429. Article | FREE Fulltext PDF

By Neuronicus, 4 January 2015

Yeast can make morphine

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Opiates like morphine and heroin can be made at home by anybody with a home beer-brewing kit and the right strain of yeast. In 2015, two published papers and a Ph.D. dissertation described the relatively easy way to convince yeast to make morphine from sugar (the links are provided in the Reference paper). That is the bad news.

The good news is that scientists have been policing themselves (well, most of them, anyway) long before regulations are put in place to deal with technological advancements by, for example, limiting access to the laboratory, keeping things under lock and key, publishing incomplete data, and generally being very careful with what they’re doing.

Complementing this behavior, an article published by Oye et al. (2015) outlines other measures that can be put in place so that this new piece of knowledge doesn’t increase the accessibility to opiates, thereby increasing the number of addicts, which is estimated to more than 16 million people worldwide. For example, researchers can make the morphine-producing yeast dependent on unusual nutrients or engineer the existing strain to produce less-marketable varieties of opiates or prohibit the access to made-to-order DNA sequences for this type of yeast and so on.

You may very well ask “Why did the scientists made this kind of yeast anyway?”. Because some medicines are either very expensive or laborious to produce by the pharmaceutical companies, the researchers have sought a method to make these drugs more easily and cheaply by engineering bacteria, fungi, or plants to produce them for us. Insulin is a good example of an expensive and hard-to-get-by drug that we managed to engineer yeast strains to produce it for us. And opiates are still the best analgesics out there.

Reference: Oye KA, Lawson JC, & Bubela T (21 May 2015). Drugs: Regulate ‘home-brew’ opiates. Nature, 521(7552):281-3. doi: 10.1038/521281a. Article | FREE Fulltext PDF

By Neuronicus, 2 January 2016