the brain is so very awesome…

http://www.nature.com/ncomms/2014/140411/ncomms4687/full/ncomms4687.html

more awesomeness in neuroscience…

Brain Scans Can Detect Children’s Reading Ability

BY AMBER MOORE

Stanford researchers say that brain scans can help detect whether or not a child will develop reading-related problems in the future, a discovery that opens up possibility of intervention programs for helping children improve their reading ability.  In a study, conducted over a period of three years, researchers at Stanford University assessed children’s reading skills with the help of standardized tests. They observed and analyzed the participants’ brain scans taken during the study.

Researchers found that in each of the 39 children, the rate of development in the white matter region accurately predicted the child’s score on a reading test. The white matter regions of the brain are associated with reading; the rate of development in the brain region is measured by fractional anisotropy, or FA.

Further, children who displayed above-average reading skills had FA in two regions, the left hemisphere arcuate fasciculus and the left hemisphere inferior longitudinal fasciculus. Interestingly, in children who develop good reading skills, the initial FA was lower but increased over time. In children that had lower reading abilities, the FA was higher initially but declined afterwards.

According to researchers, a child’s ability to read at seven years of age can predict hisor her reading ability at 17 years of age. But, detecting if the child has problems with reading can be a challenge. “By the time kids reach elementary school, we’re not great at finding ways of helping them catch up,” said Jason D. Yeatman, a doctoral candidate in psychology at Stanford and the lead author on the study.

The great news is the study could one day lead to an early warning system for struggling students and this could help children improve their reading ability as the brain is young and is still developing.

“Once we have an accurate model relating the maturation of the brain’s reading circuitry to children’s acquisition of reading skills, and once we understand which factors are beneficial, I really think it will be possible to develop early intervention protocols for children who are poor readers, and tailor individualized lesson plans to emphasize good development. Over the next five to 10 years, that’s what we’re really hoping to do,” Yeatman said.

The study was published in the Proceedings of the National Academy of Sciences.

Retrieved from: http://www.medicaldaily.com/articles/12666/20121012/brain-scans-detect-childrens-reading-ability.htm#go5H3ZzSAe1jtK0g.99

Development of white matter and reading skills

PNAS Plus – Biological Sciences – Psychological and Cognitive Sciences

Jason D. Yeatman, Robert F. Dougherty, Michal Ben-Shachar, and Brian A. Wandell

White matter tissue properties are highly correlated with reading proficiency; we would like to have a model that relates the dynamics of an individual’s white matter development to their acquisition of skilled reading. The development of cerebral white matter involves multiple biological processes, and the balance between these processes differs between individuals. Cross-sectional measures of white matter mask the interplay between these processes and their connection to an individual’s cognitive development. Hence, we performed a longitudinal study to measure white-matter development (diffusion-weighted imaging) and reading development (behavioral testing) in individual children (age 7–15 y). The pattern of white-matter development differed significantly among children. In the left arcuate and left inferior longitudinal fasciculus, children with above-average reading skills initially had low fractional anisotropy (FA) that increased over the 3-y period, whereas children with below-average reading skills had higher initial FA that declined over time. We describe a dual-process model of white matter development comprising biological processes with opposing effects on FA, such as axonal myelination and pruning, to explain the pattern of results.

PNAS Plus: Development of white matter and reading skillsPNAS 2012 ; published ahead of print October 8, 2012,doi:10.1073/pnas.1206792109

Retrieved from: http://www.pnas.org/search?fulltext=reading&go.x=0&go.y=0&go=GO&submit=yes

 

 

Neurogenesis and Depression/Stress

http://www.functionalneurogenesis.com/blog/

Impaired adult neurogenesis leads to depression – is it realistic?

Jason Snyder | 08/31/2012

About a year ago we published a paper linking adult neurogenesis to depression. A causal sort of ‘linking’, right? I mean, we found that, when adult neurogenesis was eliminated, mice had elevated glucocorticoids in response to stress and showed depressive-like behaviours¹. So doesn’t this mean that impaired adult neurogenesis could lead to depression in humans, in the real world?

Well, it could…and we did end our paper with the following:

Because the production of new granule neurons is itself strongly regulated by stress and glucocorticoids, this system forms a loop through which stress, by inhibiting adult neurogenesis, could lead to enhanced responsiveness to future stress. This type of programming could be adaptive, predisposing animals to behave in ways best suited to the severity of their particular environments. However, maladaptive progression of such a feed-forward loop could potentially lead to increased stress responsiveness and depressive behaviours that persist even in the absence of stressful events.

We had to end it somehow – I was just happy that after 3 years of work we were DONE²! But our final speculation makes it clear that, while this chapter may be done, the story is not. And this fact was rightly pointed out in a recent commentary by Lucassen et al. in Molecular Psychiatry³, where they continue the discussion and bring up some good points. Here is a loose elaboration on some of the outstanding issues they bring up.

Is a feed-forward cascade plausible? In other words, is it possible that stress reduces neurogenesis, which leads to a hyperactive HPA response, which further reduces neurogenesis, thereby additionally increasing the stress response etc etc, eventually damaging the brain and leading to depression? As Lucassen et al point out, stress typically reduces neurogenesis by only ~30% which is much smaller than the 100% reduction seen in our transgenic mice. Could a 30% reduction be enough to initiate this vicious cycle? What if it was chronic? People have looked in the past and not observed HPA alterations after smaller (but also equally large) reductions in neurogenesis, so the answer might appear to be negative. But there are many important differences between studies, including when stress hormones were measured (e.g. baseline or after stress) as well as factors such as life history, genetic makeup, and stressor controllability, as is suggested in the commentary. Of course, in reality, chronic stress has multiple effects throughout the hippocampus (and brain) and so the development of depression is certainly due to additive effects (this is both their sentiment and mine). And so perhaps in the real world a more modest reduction in neurogenesis does have the potential to tip the scales towards depression, if it is coupled with other (which?) pathologies.

How could so few adult-born neurons regulate the HPA axis? Depending on my mood, my thoughts on this question fluctuate quite a bit. Half of the time I think “This is ridiculous” and the other half of the time I look at the evidence and think “Heck yeah. Maybe⁴.” (see our recent review for more detailed arguments on the heck yeah side of things). In our study we reduced neurogenesis for up to 12 weeks, preventing about 50,000 cells from being added or 10% of the total population. More important than sheer numbers, however, is the ever-increasing evidence that adult-born neurons are different from mature neurons – more plastic, more excitable, uniquely neuromodulated. Some of the most intriguing evidence comes from one of the authors themselves who has shown that even 4 month old neurons (but potentially older?) undergo extensive structural modification following learning whereas perinatal-born cells do not. We have estimated that ~40% of the total granule cell population is added in adulthood in the rat and so my point is that in the real world we have to consider that there are probably cumulative effects of adult neurogenesis over years, and even decades in humans. And so the population of adult-born cells, and its functionality, may not be so small in the end.

Do new neurons sense detect stress through glucocorticoids? One common assumption is that glucocorticoid receptors are necessary for inhibition of the HPA axis…but must that always be the case? By 1-2 weeks of age the majority of adult-born neurons do express MRs and GRs and therefore certainly could directly detect glucocorticoid levels and initiate a shutting down of the HPA axis. But perhaps new neurons process stressful information that is relayed through glutamatergic pathways. In this scenario new neurons might not be required for sensing glucocorticoids and initiating negative feedback. Instead, after being stressed, they could be required for biasing the animal away from the negative experience (akin to perceiving a change in context, similar Opendak & Gould’s proposal for reconciling stress and memory hypotheses of new neuron function) which might reduce CNS drive on the HPA axis. This opens the door to the possibility that the HPA and behavioural roles of adult neurogenesis are somewhat dissociable, in which case a role for new neurons in the development of depression is not (only) through the feedforward cascade hypothesis but through direct effects on behaviour. This might also help explain the inconsistent links between stress hormones, hippocampal volume, and depression that plague the stress-depression literature.

So, we showed that adult-born neurons are required (in mice) for normal stress responses and emotional behaviour. Our final speculation was, well, just that – a leap towards the next big question. Maybe realistic, maybe not. Maybe a component of the real picture. In any case, the route has been mapped.

—————————————————————–

References
Lucassen PJ, Fitzsimons CP, Korosi A, Joels M, Belzung C, & Abrous DN (2012). Stressing new neurons into depression? Molecular psychiatry PMID: 22547116

Snyder JS, Soumier A, Brewer M, Pickel J, & Cameron HA (2011). Adult hippocampal neurogenesis buffers stress responses and depressive behaviour. Nature, 476 (7361), 458-61 PMID: 21814201

Footnotes

¹You thought this footnote was going to be some comment on human depression vs. depressive-like behaviour in animal models but instead I just wanted to mention that, now that I’ve moved back to Canada, I feel compelled to use ‘behaviour’ instead of ‘behavior’ and it feels silly because the same people read this stuff no matter which country I’m in when I write it.

²Is there an emoticon for dusting the dirt off your hands, blowing smoke away from the tip of a revolver, or enjoying a refreshing beverage after chopping a bunch of wood or giving birth? Insert it here.

³One of the authors having actually commented on this blog (!), and who is 1st author on what looks to be a very interesting paper that is related to this whole discussion.

⁴I may be a pessimist. Realist? A guy with a healthy amount of skepticism?

⁵The photo? It’s a depression.

Neurogenesis…never ceases to amaze me.

We have come very far from the faulty belief that the birth of new neurons only occurred in developing organisms.  Now, it is a fairly known phenomenon.  One we probably would have eschewed years ago.

Neurons, neurons…how they do grow!

I like this blog about neurogenesis and hope you do as well!

http://www.functionalneurogenesis.com/blog/