Monday, February 22, 2016

Running and neurogenesis; the plastic brain

A new paper online in the Journal of Physiology ("Physical exercise increases adult hippocampal neurogenesis in male rats provided it is aerobic and sustained," Nokia et al.), and described here by the NYT, reports that running is good for the brain.  At least the rat brain.

From the paper (emphasis mine):
Adult hippocampal neurogenesis (AHN) is a continuous process through which cells proliferate in the subgranular zone of the dentate gyrus, mature into granule cells, and ultimately become incorporated into hippocampal neuronal networks. In rodents, adult-born hippocampal neurons seem crucial for a variety of adaptive behaviors such as learning, pattern separation, and responses to stress. Aerobic exercise, e.g. running, increases AHN and improves cognitive performance in both male and female adult rodents. The increase in AHN in response to running is reported to be in part due to an increase in the number of surviving neuronal precursor cells (type 2) rather than to the shortening of the cell cycle. There are also studies indicating that running increases the survival and incorporation of newly divided hippocampal cells, born days before commencing training, to increase net neurogenesis. [See the paper for citations for reported findings, which I've removed here for length.]
It has already been well-established that aerobic exercise is associated with an increase in adult hipocampal neurogenesis, the number of neurons in the hippocampus, the region of the brain associated with producing long-term memory among other functions.  But, Nokia et al. wondered if it was only aerobic exercise, or whether other kinds of exercise have the same effect.

So they compared the number of neuronal cells of mice subjected to high-intensity interval training, resistance training and distance running.  They found no increase in the rats who did resistance training compared to sedentary rats, and a smaller than expected increase in rats that did the interval training.  It was only in the brains of the rats who did aerobic exercise that neurogenesis was significantly increased.  The authors hypothesize that this is because running stimulates the production of  brain-derived neurotrophic factor and insulin-like growth factor, which are associated with neurogenesis. The more aerobic exercise the animal does, the more of these the animal produces, and thus the more neurons.

Currently the best advice for preventing dementia in old age is to maintain a social life, quit smoking, and exercise.  And, if this rat study can be applied to humans, this should at least qualify that as aerobic exercise; running or biking, say.  As with all such lifestyle advice, this surely won't work for everyone, but the evidence is increasingly in its favor, at least on a population basis.

But there are deeper implications of this work, I think.  If exercise changes the architecture of the brain in ways that can affect learning, even in adults, and, as has been repeatedly demonstrated, stimulating children by reading to them, using lots of words, playing music to them, and so on, or the reverse, growing up in poverty,  or with disease, or amid famine all can affect brain architecture and thus cognitive ability for better or for worse, why do so many continue to privilege genes and genes alone -- or even more, a single gene -- for the creation of intelligence?

Source: "Effects on brain development leading to cognitive impairment:  A worldwide epidemic," Olness,
Journal of Developmental & Behavioral Pediatrics:
April 2003 - Volume 24 - Issue 2 - pp 120-130

It seems that the brain responds to experience at all ages, but it's possible that there's a 'sensitive period' for cognition.  As just one example, the cognitive abilities of children reared in institutions in Bucharest were compared to that of children never placed in an institution to those whose lives began there but who moved to foster care before age two.  Those who were reared entirely in institutions had much lower cognitive ability than the other two groups; the cognitive abilities of those who were moved to foster care before age two significantly improved.  The authors of this study suggest that there may be a sensitive period for developing cognitive ability, just as there is one for learning language, and many other aspects of brain function.

Of course, as with any trait, genes play a crucial role in the development of the brain.  But they don't do it alone.  E.g., a 2010 paper in Child Development describes the genetic underpinnings of the developing brain, but its plasticity as well.
The foundations of brain architecture are established early in life through a continuous series of dynamic interactions between genetic influences and environmental conditions and experiences (Friederici, 2006; Grossman, 2003; Hensch, 2005; Horn, 2004; Katz & Shatz, 1996; Majdan & Shatz, 2006; Singer, 1995). There is increasing evidence that environmental factors play a crucial role in coordinating the timing and pattern of gene expression, which in turn determines initial brain architecture. Because specific experiences potentiate or inhibit neural connectivity at key developmental stages, these time points are referred to as sensitive periods (Hess, 1973; Knudsen, 2004). Each one of our perceptual, cognitive, and emotional capabilities is built upon the scaffolding provided by early life experiences. Examples can be found in both the visual and auditory systems, where the foundation for later cognitive architecture is laid down during sensitive periods for basic neural circuitry.  
Genetic determinists might acknowledge the plasticity of the brain but then say that how the brain responds to experience is what's genetically determined, and thus that there are children who just aren't genetically equipped to be the next Einstein, or even to learn calculus.  We know this is true at least at one extreme of the distribution of intelligence, because there are many alleles known to be associated with low cognitive ability.  These usually cause syndromic conditions, however, so aren't related only to how quickly synapses are crossed, or memories made, or whatever it is that underlies -- or defines -- intelligence.  As with many other trait distributions, what happens at the extremes doesn't necessarily represent what's going on in the middle, so I think the jury is still out as to the overriding importance of single or even a small number of alleles in the development of normal or above normal intelligence (again, whatever that is -- for the moment, let's call it the ability to score well on IQ tests).  And indeed no genes with large effects on intelligence have yet been identified, despite decades of looking.  That has so far included comparison of the tails of the distribution among individuals without a clear-cut pathology.

So, of course there are genes involved in how quickly people think, or make connections between ideas, or memorize, or invent things, or remember -- how people learn.  But it's not either mainly genes or environment.  It's both, interacting, and molding the reactive brain.  There is enough evidence now to show that the brain is a hungry organ, soaking up and responding to experience at all times, throughout life.  Whether or not we believe that society should be investing in optimizing the environment of every child to maximize their potential is a social and political decision, not a scientific one.

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