Speed reading apps blow away comprehension.

Schotter et al. make a demonstration that being able to glance back during reading (not allowed under speed reading conditions) significantly enhances comprehension...readers' control over their eye movements is important.

Recent Web apps have spurred excitement around the prospect of achieving speed reading by eliminating eye movements (i.e., with rapid serial visual presentation, or RSVP, in which words are presented briefly one at a time and sequentially). Our experiment using a novel trailing-mask paradigm contradicts these claims. Subjects read normally or while the display of text was manipulated such that each word was masked once the reader’s eyes moved past it. This manipulation created a scenario similar to RSVP: The reader could read each word only once; regressions (i.e., rereadings of words), which are a natural part of the reading process, were functionally eliminated. Crucially, the inability to regress affected comprehension negatively. Furthermore, this effect was not confined to ambiguous sentences. These data suggest that regressions contribute to the ability to understand what one has read and call into question the viability of speed-reading apps that eliminate eye movements (e.g., those that use RSVP).

Watching the physical correlate of memory improvement during sleep.

Euston and Steenland do a perspective on nice work by Yang et al. that probes the role of sleep in altering mouse brain structures. I pass on their summary figure (click to enlarge) and some context comments.:

Figure Legend. Three phenomena that occur during sleep have been linked to memory enhancement—slow-wave oscillations in brain electrical activity, reactivation of recent experiences, and changes in synaptic connectivity but the strength of the evidence (indicated by arrow thickness) varies. As shown in red, Yang et al. link both reactivation and slow-wave sleep to changes in synaptic connectivity that enhance learning.

To address whether synaptic strength increases or decreases during sleep, Yang et al. used a powerful technique to visualize dendritic spines in the motor cortex of live mice. The mice were genetically engineered to express a fluorescent protein in a subset of cortical cells. A small window was created in the skull, allowing microscopic imaging of dendritic spines repeatedly over the course of hours or even days. This technique was previously used to show that training mice to stay atop a rotating rod—an acquired skill—induced the formation of new dendritic spines in the motor cortex. Further, the rate of new spine formation was correlated with the degree of task improvement. These findings provided direct evidence that synaptic change in the mammalian cortex underlies learning. Yang et al. extend these findings, showing that learning-induced spine changes are segregated on specific dendritic branches. After learning, when two branches on the same dendritic arbor were examined, one typically showed many more new spines than the other. If mice were subsequently trained on a different skill (i.e., running backward on the spinning rod), the new spines induced by the second task grew selectively on the previously underproductive branch. Hence, different skills seem to be localized on different dendritic branches.

To test the role of sleep in spine formation, Yang et al. repeated their experiment with and without an 8-hour period of sleep deprivation immediately after training. Sleep deprivation markedly decreased the number of new spines. This effect also was branch-specific in that sleep deprivation reduced spine formation primarily on the dendritic branch with the higher number of new spines. Importantly, sleep had no effect on the rate of spine elimination. The authors also observed that sleep made newly formed spines much more likely to still be present 1 day later, consistent with the idea that consolidated memories are less sensitive to decay. In other words, sleep gives spines staying power.

When being a control-freak doesn't help....

Bocanegra and Hommel note limits to the usefulness of cognitive control, showing, in particular, how overcontrol (induced by task instructions) can prevent the otherwise automatic exploitation of statistical stimulus characteristics needed to optimize behavior. They describe how they set up the experiment:

Participants performed a two-alternative forced-choice task on a foveally presented stimulus that could vary on a subset of binary perceptual features, such as color (red, green), shape (diamond, square), size (large, small), topology (open, closed), and location (up, down). Unbeknownst to the participants, we manipulated the statistical informativeness of an additional feature that was not part of the task, such that this feature always predicted the correct response in one condition (the predictive condition) but not in the other condition (the baseline condition). Because the cognitive system is known to exploit statistical stimulus-response contingencies automatically, performance was expected to be better in the predictive than in the baseline condition.

We embedded these predictive and baseline conditions into two different tasks, which we thought would induce different cognitive-control states. The control task included instructions intended to emphasize the need for top-down control: Participants were instructed to classify the stimulus according to a feature-conjunction rule (e.g., size and topology: left response key for large and open or small and closed shapes, right response key for small and open or large and closed shapes). The automatic task included instructions intended to deemphasize the need for control: Participants were instructed to classify the stimulus according to a single feature (e.g., shape: left response key for a diamond and right response key for a square). In the automatic task, the features were mapped consistently on responses and thus allowed automatic visuomotor translation. In contrast, the stimulus-response mapping in the control task required the attention-demanding integration of two features before the response could be determined.

As expected, the predictive feature improved performance when participants performed the task automatically. Counterintuitively, however, the predictive feature impaired performance when subjects were performing the exact same task in a top-down, controlled manner.

Their abstract:

In order to engage in goal-directed behavior, cognitive agents have to control the processing of task-relevant features in their environments. Although cognitive control is critical for performance in unpredictable task environments, it is currently unknown how it affects performance in highly structured and predictable environments. In the present study, we showed that, counterintuitively, top-down control can impair and interfere with the otherwise automatic integration of statistical information in a predictable task environment, and it can render behavior less efficient than it would have been without the attempt to control the flow of information. In other words, less can sometimes be more (in terms of cognitive control), especially if the environment provides sufficient information for the cognitive system to behave on autopilot based on automatic processes alone.

Another Poulenc offering: Improvisation No. 13

Another Monday morning post of a recent piano recording I've done.

  

Brain initiative meets physics….Opps!

Scientists leading the much-heralded Obama Brain Initiative initially providing $100 million (now NIH is seeking 4.5 billion for their part of the project) to craft new tools for measuring brain activity may have been insufficiently aware that some of their ideas:

“violated either a physical law or some very significant engineering constraint or biological constraint,”

I want to pass on the text of this article noting a meeting sponsored by the National Science Foundation at Cold Spring Harbor Laboratory.

The goal is to have a realistic discussion of what the physical limits are, he says, so “scientists who want to make devices will not make crazy proposals,” or, “if a proposal is crazy, one could recognize it as such” and look for other ways to make the idea work.

One such “fanciful” idea is to build nanosized radios that could snuggle up to individual neurons to record and transmit information about their activity, says physicist Peter Littlewood, director of Argonne National Laboratory in Lemont, Illinois. But any radio small enough to be injected into the brain without causing significant harm would not be able to transmit any information out through tissue and bone, he says. Make the devices any more powerful, he adds, and they'd likely cook the surrounding brain. Another aspiration that is likely doomed is to get microscopes that probe the brain with pulses of light to penetrate much further than they already do, Mitra says. A little more than 1 mm is possible, he adds, but even 1 cm is “out of the question, since the signal to background [noise] ratio decreases exponentially with depth.”

But physicists and engineers shouldn't simply shoot down outlandish proposals—or gripe about the intrinsic messiness of the brain's biology. They should model themselves as “fancy technicians” who can help develop revolutionary tools, Littlewood says. There are precedents for such collaboration, he notes: He, Mitra, and their colleagues at Bell Labs, for example, helped develop functional magnetic resonance imaging in the 1990s.

One area where physical scientists can help today is in fashioning small, strong, conductive wires that can record from many different neurons simultaneously, says neuro physicist David Kleinfeld of the University of California, San Diego. For decades, neuro scientists have relied largely on electrodes fashioned from fragile glass pipettes. But only a small number of these sensors will fit in a given brain region without disrupting connections between cells or killing them outright. Biophysicist Timothy Harris at the Janelia Farm Research Campus in Ashburn, Virginia, and others have had some success at making much smaller ones for fish and fly brains—some, made of silicon, are roughly 3 microns wide, about 25 times thinner than a human hair.

These probes are by no means the tiniest possible—polymer-coated carbon nanotubes, for example, can be 0.1 microns or smaller across and are highly conductive. Such thin wires tend to be very short and too flexible to get into the brain easily, however—when pushed, they simply buckle. One question Harris plans to pose at the meeting is whether the probes could be magnetized, then pulled, rather than pushed, into the brain with a powerful magnet.

Ultimately, researchers hope to measure neural activity inside the brain without poking wires into living tissue, and there, too, physics can help. Harris has his eye on light-sheet microscopy, which shines a plane of light across a living brain tissue, illuminating neurons engineered to fluoresce green or red when they are flooded by calcium during neuronal firing. Last year, neuroscientist Misha Ahrens and colleagues at Janelia Farm used this technique to produce the first “real” whole-brain activity map of a zebrafish larva, Harris says.

A larval zebrafish brain is 1000 times smaller than a mouse brain, however. It is also conveniently transparent, while mouse and human brain tissue scatter and blur light. Using the same optical techniques that astronomers employ to discern very faint or close-together stars with a telescope, researchers such as physicist Na Ji, also at Janelia Farm, have discovered ways to distinguish between hard-to-see neurons in murky brain tissue.

In preparation for the meeting, Mitra has brushed off an old copy of Principles of Optics by Emil Wolf and Max Born, one of the most venerable and difficult physics tomes. Getting back to basics, he hopes, will help him and his BRAIN project colleagues determine which rules must be followed to the letter, and which might be cleverly circumvented.

Gratitude reduces economic impatience.

Whenever I come across yet another self-help laundry list of useful tricks for feeling better, and try a few, I repeatedly find that briefly following instructions to practice feeling gratitude has a very salutary, calming, effect...taking the edge off any impatience I might be feeling. DeSteno et al. look at this in a more systematic way, distinguishing the effect of gratitude from more positive global emotions of happiness with respect impatience, or short-term gratification. 75 study participants were split in three groups with different emotion-induction conditions: being asked to write brief essays on experiences of feeling grateful, happy, or neutral. They then made choices between receiving smaller cash amounts (ranging from $11 to $80) immediately and larger cash amounts (ranging from $25 to $85) at a point from 1 week to 6 months in the future. Their results clearly revealed that gratitude reduces excessive economic impatience (the temporal discounting of future versus immediate rewards) compared with the neutral and happy conditions, which were about equal. Here is their abstract:

The human mind tends to excessively discount the value of delayed rewards relative to immediate ones, and it is thought that “hot” affective processes drive desires for short-term gratification. Supporting this view, recent findings demonstrate that sadness exacerbates financial impatience even when the sadness is unrelated to the economic decision at hand. Such findings might reinforce the view that emotions must always be suppressed to combat impatience. But if emotions serve adaptive functions, then certain emotions might be capable of reducing excessive impatience for delayed rewards. We found evidence supporting this alternative view. Specifically, we found that (a) the emotion gratitude reduces impatience even when real money is at stake, and (b) the effects of gratitude are differentiable from those of the more general positive state of happiness. These findings challenge the view that individuals must tamp down affective responses through effortful self-regulation to reach more patient and adaptive economic decisions.

Childhood bullying predicts adult inflammation.

How is this for a chilling finding? Childhood bullying leaves bullies with lower, and victims with higher, levels of chronic inflammation than those uninvolved in bullying. From Copeland et al. :

Bullying is a common childhood experience that involves repeated mistreatment to improve or maintain one’s status. Victims display long-term social, psychological, and health consequences, whereas bullies display minimal ill effects. The aim of this study is to test how this adverse social experience is biologically embedded to affect short- or long-term levels of C-reactive protein (CRP), a marker of low-grade systemic inflammation. The prospective population-based Great Smoky Mountains Study (n = 1,420), with up to nine waves of data per subject, was used, covering childhood/adolescence (ages 9–16) and young adulthood (ages 19 and 21). Structured interviews were used to assess bullying involvement and relevant covariates at all childhood/adolescent observations. Blood spots were collected at each observation and assayed for CRP levels. During childhood and adolescence, the number of waves at which the child was bullied predicted increasing levels of CRP. Although CRP levels rose for all participants from childhood into adulthood, being bullied predicted greater increases in CRP levels, whereas bullying others predicted lower increases in CRP compared with those uninvolved in bullying. This pattern was robust, controlling for body mass index, substance use, physical and mental health status, and exposures to other childhood psychosocial adversities. A child’s role in bullying may serve as either a risk or a protective factor for adult low-grade inflammation, independent of other factors. Inflammation is a physiological response that mediates the effects of both social adversity and dominance on decreases in health.

Added note: I just came across this related article by Raposa et. al. on the developmental pathway from early life stress to inflammation.

Tonics for a long life?

I've recently come across two articles relevant to life extension (work done with mice and worms, to be sure, but a human who reads these papers might well be trying to get their hands on some of the stuff described to give it a try!). Dubai et al. report their work on Klotho, an aging regulator that, when overexpressed, extends lifespan in mice and nematode worms, and, when disrupted, accelerates aging phenotypes. (A lifespan expanding human variant of the KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers.) Here is their summary:

Aging is the primary risk factor for cognitive decline, an emerging health threat to aging societies worldwide. Whether anti-aging factors such as klotho can counteract cognitive decline is unknown. We show that a lifespan-extending variant of the human KLOTHO gene, KL-VS, is associated with enhanced cognition in heterozygous carriers. Because this allele increased klotho levels in serum, we analyzed transgenic mice with systemic overexpression of klotho. They performed better than controls in multiple tests of learning and memory. Elevating klotho in mice also enhanced long-term potentiation, a form of synaptic plasticity, and enriched synaptic GluN2B, an N-methyl-D-aspartate receptor (NMDAR) subunit with key functions in learning and memory. Blockade of GluN2B abolished klotho-mediated effects. Surprisingly, klotho effects were evident also in young mice and did not correlate with age in humans, suggesting independence from the aging process. Augmenting klotho or its effects may enhance cognition and counteract cognitive deficits at different life stages.

And, Ye et al. have done a screen, using nematodes, of over 1200 drugs active on human cells, including drugs approved for human use, finding ~60 that increase C. elegans lifespan up to 43%. They mainly act on proteins that function in signaling pathways between cells relevant to oxidative stress resistance - hormone or neurotransmitter receptors, particularly those for adrenaline and noradrenaline, serotonin, dopamine, histamine, and serotonin. This suggests and narrows down a list of drugs that might be tested for life extension in mammals.

One goal of aging research is to find drugs that delay the onset of age-associated disease. Studies in invertebrates, particularly Caenorhabditis elegans, have uncovered numerous genes involved in aging, many conserved in mammals. However, which of these encode proteins suitable for drug targeting is unknown. To investigate this question, we screened a library of compounds with known mammalian pharmacology for compounds that increase C. elegans lifespan. We identified 60 compounds that increase longevity in C. elegans, 33 of which also increased resistance to oxidative stress. Many of these compounds are drugs approved for human use. Enhanced resistance to oxidative stress was associated primarily with compounds that target receptors for biogenic amines, such as dopamine or serotonin. A pharmacological network constructed with these data reveal that lifespan extension and increased stress resistance cluster together in a few pharmacological classes, most involved in intercellular signaling. These studies identify compounds that can now be explored for beneficial effects on aging in mammals, as well as tools that can be used to further investigate the mechanisms underlying aging in C. elegans.

Rapidity of human brain and muscle evolution - the downside of smarts?

Roberts does a summary of fascinating work by Bozak et al. He sets the context: 

Somewhat narcissistically, one of the spectacular changes in phenotype that we tend to be most interested in is the enhancement in our own brain power which has occurred over the 6 million years that separate us from our last shared ancestor with chimpanzees. The chimp genome is famously very similar to our own, but the technological, linguistic, and cultural phenotype is clearly profoundly different. Several studies have asked open-ended questions as to what happens between the genotype and phenotype to make us so different from our cousins, finding differences in levels, splicing, and editing of gene transcripts, for example. Now a paper just published in PLOS Biology by Katarzyna Bozek, Philipp Khaitovich, and colleagues looks at another intermediate phenotype—the metabolome—with some intriguing and unexpected answers...The metabolome is the set of small molecules (metabolites) that are found in a given tissue; by “small” we mean those with a molecular weight of less than 1,500 Daltons, which includes fats, amino acids, sugars, nucleotides, and vitamins (vitamin B12, for example, is near the top end of this range).  

...the metabolomes of human prefrontal cortex (and of combined brain regions) have changed four times as rapidly in the last 6 million years as those of chimps. While gratifying, this largely confirms for metabolites what was already known for transcripts. 

...brain is not the most spectacular outlier here. The real surprise is that the human muscle metabolome has experienced more than eight times as much change as its chimp counterpart. Indeed, metabolomically speaking, human muscle has changed more in the last 6 million years than mouse muscle has since we parted company from mice back in the Early Cretaceous.  

...the authors compared the performance of humans, chimps, and macaques in a strength test that involved pulling a handle to raise a weight. Human strength, as measured by this test, was barely half that of the non-human primates. Amazingly, untrained chimps and macaques raised in captivity easily outperformed university-level basketball players and professional mountain climbers. The authors speculate that the fates of human brain and muscle may be inextricably entwined, and that weak muscle may be the price we pay for the metabolic demands of our amazing cognitive powers.

A Monday musical offering - Poulenc Improvisation No. 7

This is recorded on the Steinway B at my Twin Valley Rd. residence in Middleton, WI.  I used to regularly post my piano work on MindBlog, and will try to return to the habit.

First direct evidence for human sex pheromones.

Here is a clever experiment by Zhou et al., who digitally morph the gender of moving point light displays of walking from male to female while subjects are exposed to two human steroids that they can not discriminate. Here is their summary and abstract:

•Human steroid androstadienone conveys masculinity to straight women and gay men
•Human steroid estratetraenol conveys femininity to straight men
•The effects take place in the absence of awareness
•Human gender perception draws on subconscious chemosensory biological cues

Recent studies have suggested the existence of human sex pheromones, with particular interest in two human steroids: androstadienone (androsta-4,16,-dien-3-one) and estratetraenol (estra-1,3,5(10),16-tetraen-3-ol). The current study takes a critical step to test the qualification of the two steroids as sex pheromones by examining whether they communicate gender information in a sex-specific manner. By using dynamic point-light displays that portray the gaits of walkers whose gender is digitally morphed from male to female, we show that smelling androstadienone systematically biases heterosexual females, but not males, toward perceiving the walkers as more masculine. By contrast, smelling estratetraenol systematically biases heterosexual males, but not females, toward perceiving the walkers as more feminine. Homosexual males exhibit a response pattern akin to that of heterosexual females, whereas bisexual or homosexual females fall in between heterosexual males and females. These effects are obtained despite that the olfactory stimuli are not explicitly discriminable. The results provide the first direct evidence that the two human steroids communicate opposite gender information that is differentially effective to the two sex groups based on their sexual orientation. Moreover, they demonstrate that human visual gender perception draws on subconscious chemosensory biological cues, an effect that has been hitherto unsuspected.

Social attention and our ventromedial prefrontal cortex.

Ralph Adolphs points to an interesting article by Wolf et al. showing that bilateral ventromedial prefrontal cortex damage impairs visual attention to the eye regions of faces, particularly for fearful faces. From Adolphs summary:

Failing to look at the eyes. Shown in each image are the regions of a face at which different groups of subjects look, as measured using eye-tracking. The hottest colours (red regions) denote those regions of the face where people look the most. Whereas this corresponds to the eye region of the face in healthy controls (far left), it is abnormal in certain clinical populations, including individuals with lesions of the vmPFC (top right) or amygdala (bottom right) and individuals with autism spectrum disorder (bottom centre) Top row: from Wolf et al. 2014. Bottom row: data from Michael Spezio, Daniel Kennedy, Ralph Adolphs. All images represent spatially smoothed data averaged across multiple fixations, multiple stimuli and multiple subjects within the indicated group.

Blue Mind - looking at water improves your health and calm

I just spend three days this past weekend in a guesthouse cabin in Door County, Wisconsin - three days of seeing mainly gorgeous green forests and the blue expanses of Lake Michigan on both sides of the Door County peninsula. Over those days, just looking at the water, I could feel a calm growing that quieted my normally chattering mind. Now, back in my university office, what do I stumble across but an article (on stress) that mentions this calming effect of water, a review by Michael Gross titled "Chronic stress means we’re always on the hunt", which first notes that one relief described for chronic stress (dubbed "Red Mind") is to give the stress system some real exercise (doing something like sky diving) to put the more mundane stresses of daily life in perspective. But then, in a second portion of his article, he points to work of Wallace J. Nichols and others who use the phrase "Blue mind" to describe the interface between our psychology and natural environment, particularly water, the largest feature of that environment. Gross notes that Nichols has put his ideas

...in a new book, called Blue Mind: How Water Makes You Happier, More Connected, and Better at What You Do, which is due to appear in June. In his book, Nichols discusses a spate of recent psychology papers showing that the proximity of “blue nature” can improve people’s physical and mental health and counterbalance the damaging effects of the chronic stress and the permanent engagement of the red mind. While the opportunity to exercise plays a part, several studies have shown that the positive effect of being near water can be separated from that aspect.

Crowdsourcing our brain’s wiring.

You too can be be a neuroscientist! I have to join in the general chorus of press pointing to the efforts of Sebastian Seung, now moving from MIT to Princeton Univ. Detailed analysis of serial ultra-thin electron microscope sections of brain neurons is extremely laborious - tracing one cells takes about 50 hours. Seung has asked for help from the general public ("citizen neuroscientists") in doing this with neurons in the mouse retina. The data on how bipolar cells connect to amacrine motion detecting cells in the retina has suggested a model for motion detection. This animation of their results is a treat to watch:

The science of inequality.

The May 23 issue of Science Magazine has a large section devoted the origins and analysis of economic inequality. And, the general gist of virtually all the articles is that inequality is here to stay, predicted by social and also simple physical models of exchange. A weekly chaos and complexity discussion group that I attend just this past Tuesday discussed the economic Yard-Sale Model of wealth redistribution, in which power-law-like distributions result even when all individuals are identical and playing by the same rules. In a previous post, I have passed on a simple model illustrated by Clint Sprott, organizer of the seminars.

The monkey business illusion.

Many people have by now viewed the famous "Gorilla Video" made by Daniel Simons over fifteen years ago, in which most viewers asked to count how many times students are passing a basketball to each other completely miss the fact that a gorilla walks through the middle of the scene halfway through the exercise. I'm passing on Simons' update of his original demonstration, which shows further how we see what we want or expect to see. It has been viewed over 4 million times, and gives links to his other work and publications. (The video is public on youtube, but copyrighted, so I hope Mr. Simons doesn't mind this advertisement for his work.)

 

How social equality is represented in the brain.

Interesting work from Aoki, Adolphs, and collaborators:

A distinct aspect of the sense of fairness in humans is that we care not only about equality in material rewards but also about equality in nonmaterial values. One such value is the opportunity to choose freely among many options, often regarded as a fundamental right to economic freedom. In modern developed societies, equal opportunities in work, living, and lifestyle are enforced by antidiscrimination laws. Despite the widespread endorsement of equal opportunity, no studies have explored how people assign value to it. We used functional magnetic resonance imaging to identify the neural substrates for subjective valuation of equality in choice opportunity. Participants performed a two-person choice task in which the number of choices available was varied across trials independently of choice outcomes. By using this procedure, we manipulated the degree of equality in choice opportunity between players and dissociated it from the value of reward outcomes and their equality. We found that activation in the ventromedial prefrontal cortex (vmPFC) tracked the degree to which the number of options between the two players was equal. In contrast, activation in the ventral striatum tracked the number of options available to participants themselves but not the equality between players. Our results demonstrate that the vmPFC, a key brain region previously implicated in the processing of social values, is also involved in valuation of equality in choice opportunity between individuals. These findings may provide valuable insight into the human ability to value equal opportunity, a characteristic long emphasized in politics, economics, and philosophy.

Note: The same issue of Journal of Neuroscience has a related article by Matthew Apps and Ramnani showing that activity in the anterior cingulate gyrus covaries with the net value of rewards that someone else will receive when that person is required to exert effort for the reward.

Brain correlates of expertise in musical improvisation

Pihno et al. show that expertise in musical improvisation is associated with increased connectivity between premotor and prefrontal areas, suggesting that the ability to produce novel output can be automated by training:

Musicians have been used extensively to study neural correlates of long-term practice, but no studies have investigated the specific effects of training musical creativity. Here, we used human functional MRI to measure brain activity during improvisation in a sample of 39 professional pianists with varying backgrounds in classical and jazz piano playing. We found total hours of improvisation experience to be negatively associated with activity in frontoparietal executive cortical areas. In contrast, improvisation training was positively associated with functional connectivity of the bilateral dorsolateral prefrontal cortices, dorsal premotor cortices, and presupplementary areas. The effects were significant when controlling for hours of classical piano practice and age. These results indicate that even neural mechanisms involved in creative behaviors, which require a flexible online generation of novel and meaningful output, can be automated by training. Second, improvisational musical training can influence functional brain properties at a network level. We show that the greater functional connectivity seen in experienced improvisers may reflect a more efficient exchange of information within associative networks of importance for musical creativity.

Brain correlates of "the good life" ??

Lewis et al. offer another example of the class of experiments correlating the volume of a specific brain area with a specific behavior, in this case eudaimonic well-being, which is positively correlated with volume in the right insular cortex. Eudaimonia is fundamentally linked to notions of agency, and recent work has identified insular cortex as a source of agentic control. The insula has also been linked to facilitation of self-awareness, as well as to the regulation of bodily states and modulation of decision making based on interoceptive information about these bodily states.

Whether the behavior causes the larger insular volume or vice versa can’t be determined. These particular experiments did not control for simple subjective (hedonic) well-being, so the observed volume increase in the insula may not be a unique correlate of eudaimonia. Here is their abstract, and the entire text of the article is open source.

Eudaimonic well-being reflects traits concerned with personal growth, self-acceptance, purpose in life and autonomy (among others) and is a substantial predictor of life events, including health. Although interest in the aetiology of eudaimonic well-being has blossomed in recent years, little is known of the underlying neural substrates of this construct. To address this gap in our knowledge, here we examined whether regional gray matter (GM) volume was associated with eudaimonic well-being. Structural magnetic resonance images from 70 young, healthy adults who also completed Ryff’s 42-item measure of the six core facets of eudaimonia, were analysed with voxel-based morphometry techniques. We found that eudaimonic well-being was positively associated with right insular cortex GM volume. This association was also reflected in three of the sub-scales of eudaimonia: personal growth, positive relations and purpose in life. Positive relations also showed a significant association with left insula volume. No other significant associations were observed, although personal growth was marginally associated with left insula, and purpose in life exhibited a marginally significant negative association with middle temporal gyrus GM volume. These findings are the first to our knowledge linking eudaimonic well-being with regional brain structure.

Stress can protect from Alzheimer's disease

Yanker and his collaborators have found that levels of a neuro-protective protein called REST (repressor element 1-silencing transcription factor) are increased in the brain by any form of cellular stress (oxidative, immune, etc.) It acts by repressing genes involved in cell death and Alzheimer's dementia. REST levels in prefrontal cortical neurons are positively correlated with a measure of global cognition, and also separate measures of episodic, semantic and working memory. Measurements of autopsied brains of elderly people who have died of Alzheimer's are three times lower than in the brains of people the same age without dementia. Here is their abstract:

Human neurons are functional over an entire lifetime, yet the mechanisms that preserve function and protect against neurodegeneration during ageing are unknown. Here we show that induction of the repressor element 1-silencing transcription factor (REST; also known as neuron-restrictive silencer factor, NRSF) is a universal feature of normal ageing in human cortical and hippocampal neurons. REST is lost, however, in mild cognitive impairment and Alzheimer’s disease. Chromatin immunoprecipitation with deep sequencing and expression analysis show that REST represses genes that promote cell death and Alzheimer’s disease pathology, and induces the expression of stress response genes. Moreover, REST potently protects neurons from oxidative stress and amyloid β-protein toxicity, and conditional deletion of REST in the mouse brain leads to age-related neurodegeneration. A functional orthologue of REST, Caenorhabditis elegans SPR-4, also protects against oxidative stress and amyloid β-protein toxicity. During normal ageing, REST is induced in part by cell non-autonomous Wnt signalling. However, in Alzheimer’s disease, frontotemporal dementia and dementia with Lewy bodies, REST is lost from the nucleus and appears in autophagosomes together with pathological misfolded proteins. Finally, REST levels during ageing are closely correlated with cognitive preservation and longevity. Thus, the activation state of REST may distinguish neuroprotection from neurodegeneration in the ageing brain.