exercise

I recently reported on a finding that older adults whose life-space narrowed to their immediate home were significantly more likely to have a faster rate of global cognitive decline or develop mild cognitive impairment or Alzheimer’s.

Now there are some obvious correlates of being house-bound vs feeling able to travel out of town (such as physical disability), but this relationship between cognitive decline and confined life-space remained after such factors were taken into account. The association is thought to be related to social and mental stimulation.

But I think this association also points to something more specific: the importance of distance, and difference. Different ways of thinking; different contexts. Information (in the broadest sense of the word) that stretches your mind, that gets you out of the grooves of your familiar thoughts.

Last year I reported on a study looking at creativity in problem-solving. That study found that multicultural experiences help you become more creative in solving problems. In particular, creativity was best helped by being reminded of what you’d learned about the underlying meaning or function of behaviors in the multicultural context. In other words, what was important was truly trying to understand behavior that’s very different from your own.

While travelling undoubtedly helps, you don’t need to go to a distant place to learn about different cultures. You can read about them; you can watch movies; you can listen to other people talk about what they know. And if you have those experiences, you can then think about them at any time.

A vital tool in tackling cognitive decline in old age (including the more extreme events of mild cognitive impairment and dementia) is cognitive reserve. Cognitive reserve means that your brain can take more damage before it has noticeable effects. Many people have died with advanced Alzheimer’s pathology in their brain who showed no signs of dementia in life!

Cognitive reserve is most often associated with education, but it is also associated with occupation, bilingualism, and perhaps even music. What it comes down to is this: the more redundancy in your brain, the wider and denser the networks, the more able your brain will be to find new paths for old actions, if the old paths are damaged.

The finding that life-space can affect cognitive decline is also a reminder that we are minds in bodies. I have reported on a number of examples of what is called embodied cognition (the benefits of gesture for memory are one example of this). It’s a good general principle to bear in mind — if you fake enjoyment, you may well come to feel it; if you look at the distant hills or over the sea, your mind may think distant thoughts; if you write out your worries, the weight of them on your mind may well lighten.

I made reference to bilingualism. There have been several studies now, that point to the long-term benefits of bilingualism for fighting cognitive decline and dementia. But if you are monolingual, don’t despair. You may never achieve the fluency with another language that you would have if you’d learned it earlier in life, but it’s never too late to gain some benefit! If you feel that learning a new language is beyond you, then you’re thinking of it in the wrong way.

Learning a language is not an either-or task; you don’t have to achieve near-native fluency for there to be a point. If there’s a language you’ve always yearned to know, or a culture you’ve always been interested in, dabble. There are so many resources on the Web nowadays; there has never been a better time to learn a language! You could dabble in a language because you’re interested in a culture, or you could enhance your language learning by learning a little about an associated culture.

And don’t forget that music and math are languages too. It may be too late to become a cello virtuoso, but it’s never too late to learn a musical instrument for your own pleasure. Or if that’s not to your taste, take a music appreciation class, and enrich your understanding of the language of music.

Similarly with math: there’s a thriving little world of “math for fun” out there. Go beyond Sudoku to the world of math puzzles and games and quirky facts.

Perhaps even dance should be included in this. I have heard dance described as a language, and there has been some suggestion that dancing seems to be a physical pursuit of particular cognitive benefit for older adults.

This is not simply about ‘stimulation’. It’s about making new and flexible networks. Remember my recent report on learning speed and flexible networks? The fastest learners were those whose brains showed more flexibility during learning, with different areas of the brain being linked with different regions at different times. The key to that, I suggest, is learning and thinking about things that require your brain to forge many new paths, with speed and distance being positive attributes that you should seek out (music and dance for speed, perhaps; languages and travel for distance).

Interestingly, research into brain development has found that, as a child grows to adulthood, the brain switches from an organization based on local networks based on physical proximity to long-distance networks based on functionality. It would be interesting to know if seniors with cognitive impairment show a shrinking in their networks. Research has shown that the aging brain does tend to show reduced functional connectivity in certain high-level networks, and this connectivity can be improved with regular aerobic exercise, leading to cognitive improvement.

Don’t disdain the benefits of simply daydreaming in your armchair! Daydreaming has been found to activate areas of the brain associated with complex problem-solving, and it’s been speculated that mind wandering evokes a unique mental state that allows otherwise opposing networks to work in cooperation. Daydreaming about a more distant place has also been found to impair memory for recently learned words more than if the daydreaming concerned a closer place — a context effect that demonstrates that you can create distance effects in the privacy of your own mind, without having to venture to distant lands.

I’m not saying that such daydreaming has all the benefits of actually going forth and meeting people, seeing new sights. Watching someone practice helps you learn a skill, but it’s not as good as practicing yourself. But the point is, whatever your circumstances, there is plenty you can do to stretch your mind. Why not find yourself a travel book, and get started!

Because it holds some personal resonance for me, my recent round-up of genetic news called to mind food allergies. Now food allergies can be tricky beasts to diagnose, and the reason is, they’re interactive. Maybe you can eat a food one day and everything’s fine; another day, you break out in hives. This is not simply a matter of the amount you have eaten, the situation is more complex than that. It’s a function of what we might call total allergic load — all the things you might be sensitive to (some of which you may not realize, because on their own, in the quantities you normally consume, they’re no or little problem). And then there are other factors which make you more sensitive, such as time of month (for women), and time of day. Perhaps, in light of the recent findings about the effects of environmental temperature on multiple sclerosis, temperature is another of those factors. And so on.

Now, I am not a medical doctor, nor a neuroscientist. I’m a cognitive psychologist who has spent the last 20 years reading and writing about memory. But I have taken a very broad interest in memory and cognition, and the picture I see developing is that age-related cognitive decline, mild cognitive impairment, late-onset Alzheimer’s, and early-onset Alzheimer’s, represent places on a continuum. The situation does not seem as simple as saying that these all have the same cause, because it now seems evident that there are multiple causes of dementia and cognitive impairment. I think we should start talking about Total Cognitive Burden.

Total Cognitive Burden would include genetics, lifestyle and environmental factors, childhood experience, and prenatal factors.

First, genetics.

It is estimated that around a quarter of Alzheimer’s cases are familial, that is, they are directly linked to the possession of specific gene mutations. For the other 75%, genes are likely to be a factor but so are lifestyle and environmental factors. Having said that, the most recent findings suggest that the distinction between familial and sporadic is somewhat fuzzy, so perhaps it would be fairer to say we term it familial when genetics are the principal cause, and sporadic when lifestyle and environmental factors are at least as important.

While three genes have been clearly linked to early-onset Alzheimer’s, only one gene is an established factor in late-onset Alzheimer’s — the so-called Alzheimer’s gene, the e4 allele on the APOE gene (at 19q13.2). It’s estimated that 40-65% of Alzheimer’s patients have at least one copy of this allele, and those with two copies have up to 20 times the risk of developing Alzheimer’s. Nevertheless, it is perfectly possible to have this allele, even two copies of it, and not develop the disease. It is also quite possible — and indeed a third of Alzheimer’s patients have managed it — to develop Alzheimer’s in the absence of this risky gene variant.

A recent review selected 15 genes for which there is sufficient evidence to associate them with Alzheimer’s: APOE, CLU, PICALM, EXOC3L2, BIN1, CR1, SORL1, TNK1, IL8, LDLR, CST3, CHRNB2, SORCS1, TNF, and CCR2. Most of these are directly implicated in cholesterol metabolism, intracellular transport of beta-amyloid precursor, and autophagy of damaged organelles, and indirectly in inflammatory response.

For example, five of these genes (APOE; LDLR; SORL1; CLU; TNF) are implicated in lipid metabolism (four in cholesterol metabolism). This is consistent with evidence that high cholesterol levels in midlife is a risk factor for developing Alzheimer’s. Cholesterol plays a key role in regulating amyloid-beta and its development into toxic oligomers.

Five genes (PICALM; SORL1; APOE; BIN1; LDLR) appear to be involved in the intracellular transport of APP, directly influencing whether the precursor proteins develop properly.

Seven genes (TNF; IL8; CR1; CLU; CCR2; PICALM; CHRNB2) were found to interfere with the immune system, increasing inflammation in the brain.

If you’re interested you can read more each of these genes in that review, but the point I want to make is that genes can’t be considered alone. They interact with each other, and they interact with other factors (for example, there is some evidence that SORL1 is a risk factor for women only; if you have always kept your cholesterol levels low, through diet and/or drugs, having genes that poorly manage cholesterol will not be so much of an issue). It seems reasonable to assume that the particular nature of an individual’s pathway to Alzheimer’s will be determined by the precise collection of variants on several genes; this will also help determine how soon and how fast the Alzheimer’s develops.

[I say ‘Alzheimer’s’, but Alzheimer’s is not, of course, the only path to dementia, and vascular dementia in particular is closely associated. Moreover, my focus on Alzheimer’s isn’t meant to limit the discussion. When I talk about the pathway to dementia, I am thinking about all these points on the continuum: age-related cognitive decline, mild cognitive impairment, senile dementia, and early dementia.]

It also seems plausible to suggest that the precise collection of relevant genes will determine not only which drug and neurological treatments might be most effective, but also which lifestyle and environmental factors are most important in preventing the development of the disease.

I have reported often on lifestyle factors that affect cognitive decline and dementia — factors such as diet, exercise, intellectual and social engagement — factors that may mediate risk through their effects on cardiovascular health, diabetes, inflammation, and cognitive reserve. We are only beginning to understand how childhood and prenatal environment might also have effects on cognitive health many decades later — for example, through their effects on head size and brain development.

You cannot do anything about your genes, but genes are not destiny. You cannot, now, do anything about your prenatal environment or your early years (but you may be able to do something about your children’s or your grandchildren’s). But you can, perhaps, be aware of whether you have vulnerabilities in these areas — vulnerabilities which will add to your Total Cognitive Burden. More easily, you can assess your lifestyle — over the course of your life — in these terms. Here are the sorts of questions you might ask yourself:

Do you have any health issues such as diabetes, cardiovascular disease, multiple sclerosis, positive HIV status?

Do you have a sleep disorder?

Have you, at any point in your life, been exposed to toxic elements (such as lead or severe air pollution) for a significant length of time?

Did you experience a lot of stress in childhood? Stress might come from a dangerous living environment (such as a violent neighborhood), warring parents, a dysfunctional parent, or a personally traumatic event (to take some examples).

Did you do a lot of drugs, or indulge in binge drinking, in college?

Have you spent many years eating an unhealthy diet — one heavy in fats and sugars?

Do you drink heavily?

Do you have ongoing stress in your life, or have experienced significant amounts of stress at some period during middle-age?

Do you rarely engage in exercise?

Do you spend most evenings blobbed out in front of the TV?

Do you experience little in the way of mental stimulation from your occupation or hobbies?

These questions are just off the top of my head, the ones that came most readily to mind. But they give you, I hope, some idea of the range of factors that might go to make up your TCB. The next step from there is to see what factors you can do something about. While you can’t do anything about your past, the good news is that, at any age, some benefit accrues from engaging in preventative strategies (such as improving your sleeping, reducing your stress, eating healthily, exercising regularly, engaging in mentally and socially stimulating activities). How much benefit will depend on how much effort you put into these preventative strategies, and on which and how many TCB factors are pushing you and how far you are along on the path. But it’s never too late to do something.

On the up-side, you might be relieved by such an exercise, realizing that your risk of dementia is smaller than you feared! If so, you might use this knowledge to motivate you to aspire to an excellent old age — with no cognitive decline. We tend to assume that declining faculties are an inevitable consequence of getting older, but this doesn’t have to be true. Some ‘super-agers’ have shown us that it is possible to grow very old and still perform as well as those decades younger. If your TCB is low, why don’t you make it even lower, and aspire to be one of those!

There was an alarming article recently in the Guardian newspaper. It said that in the UK, diabetes is now nearly four times as common as all forms of cancer combined. Some 3.6 million people in the UK are thought to have type 2 diabetes (2.8 are diagnosed, but there’s thought to be a large number undiagnosed) and nearly twice as many people are at high risk of developing it. The bit that really stunned me? Diabetes costs the health service roughly 10% of its entire budget. In north America, one in five men over 50 have diabetes. In some parts of the world, it’s said as much as a quarter of the population have diabetes or even a third (Nauru)! Type 2 diabetes is six times more common in people of South Asian descent, and three times in people of African and African-Caribbean origin.

Why am I talking about diabetes in a blog dedicated to memory and learning? Because diabetes, if left untreated, has a number of complications, several of which impinge on brain function.

For example, over half of those with type 2 diabetes will die of cardiovascular disease, and vascular risk factors not only increase your chances of heart problems and stroke (diabetes doubles your risk of stroke), but also of cognitive impairment and dementia.

Type 2 diabetes is associated with obesity, which can bring about high blood pressure and sleep apnea, both of which are cognitive risk factors.

Both diabetes and hypertension increases the chances of white-matter lesions in the brain (this was even evident in obese adolescents with diabetes), and the degree of white-matter lesions in the brain is related to the severity of age-related cognitive decline and increased risk of Alzheimer’s.

Mild cognitive impairment is more likely to develop into Alzheimer’s if vascular risk factors such as high blood pressure, diabetes, cerebrovascular disease and high cholesterol are present, especially if untreated. Indeed it has been suggested that Alzheimer’s memory loss could be due to a third form of diabetes. And Down syndrome, Alzheimer's, diabetes, and cardiovascular disease, have been shown to share a common disease mechanism.

So diabetes is part of a suite of factors that act on the heart and the brain.

But treatment of such risk factors (e.g. by using high blood pressure medicines, insulin, cholesterol-lowering drugs and diet control, giving up smoking or drinking) significantly reduces the risk of developing Alzheimer’s. Bariatric surgery has been found to improve cognition in obese patients. And several factors have been shown to make a significant difference as to whether a diabetic develops cognitive problems.

Older diabetics are more likely to develop cognitive problems if they:

• have higher (though still normal) blood pressure,
• have gait and balance problems,
• report themselves to be in bad health regardless of actual problems (this may be related to stress and anxiety),
• have higher levels of the stress hormone cortisol,
• don’t manage their condition (poor glucose control),
• have depression,
• eat high-fat meals.

Glucose control / insulin sensitivity may be a crucial factor even for non-diabetics. A study involving non-diabetic middle-aged and elderly people found that those with impaired glucose tolerance (a pre-diabetic condition) had a smaller hippocampus and scored worse on tests for recent memory. And some evidence suggests that a link found between midlife obesity and increased risk of cognitive impairment and dementia in old age may have to do with poorer insulin sensitivity.

Exercise and dietary changes are of course the main lifestyle factors that can turn such glucose impairment around, and do wonders for diabetes too. In fact, a recent small study found that an extreme low-calorie diet (don’t try this without medical help!) normalized pre-breakfast blood sugar levels and pancreas activity within a week, and may even have permanently cured some diabetics after a couple of months.

Diabetes appears to affect two cognitive domains in particular: executive functioning and speed of processing.

You can read all the research reports on diabetes that I’ve made over the years in my new topic collection.

Let’s talk about the cognitive benefits of learning and using another language.

In a recent news report, I talked about the finding that intensive learning of a very novel language significantly grew several brain regions, of which two were positively associated with language proficiency. These regions were the right hippocampus and the left superior temporal gyrus. Growth of the first of these probably reflects the learning of a great many new words, and the second may reflect heavy use of the phonological loop (a part of working memory).

There are several aspects to this study that are worth discussing in the context of using language learning as a means of protecting against age-related cognitive decline.

First of all, let me start with a general reminder. We now know that, analogous to muscles, we can ‘grow’ specific brain regions by working them. But an adult brain is confined by the skull — growth in one part is generally at the expense of another part. So, unlike body-building, you can’t just grow your whole brain!

This suggests that it pays to think about the areas you want to improve (which goes right back to the first chapter of The Memory Key: it’s no good talking about improving ‘your memory’ — rather, you should pick the memory tasks you want to improve).

One of the big advantages of growing the parts of the brain involved in language is that language is so utterly critical to our intellectual ability. Most of us use language to think and to communicate. There’s a reason why so many studies of older adults’ cognitive performance use verbal fluency as the measure!

But, in the same way that the increase in London cab drivers’ right posterior hippocampus appears to be at the expense of the anterior hippocampus, the growth in the right hippocampus may be at the expense of other functions (perhaps spatial navigation).

Is this a reason for not learning? Certainly not! But it is perhaps a reminder that we should be aiming for two things in preventing cognitive decline. The first is in ‘growing’ brain tissue: making new neurons, and new connections. This is to counteract the shrinkage (brain atrophy) that tends to occur with age.

The second concerns flexibility. Retaining the brain’s plasticity is a vital part of fighting cognitive decline, even more vital, perhaps, than retaining brain tissue. To keep this plasticity, we need to keep the brain changing.

Here’s a question we don’t yet know the answer to: how much age-related cognitive decline is down to people steadily experiencing fewer and fewer novel events, learning less, thinking fewer new thoughts?

But we do know it matters.

So let’s go back to our intensive language learners growing parts of their brain. Does the growth in the right hippocampus (unfortunately we don’t know how much that growth was localized within the right hippocampus) mean that it will now remain that size, at the expense, presumably, of some other area (and function)?

No, it doesn’t. As far as language is concerned, the hippocampus is primarily a short-term processor. As those new words are consolidated, they’ll move into long-term memory, in the language network across the cortex. Once the interpreters stop acquiring new vocabulary at this rate, I would expect to see this region reduce. Indeed (and I am speculating here), I would expect this to happen once a solid ‘semantic network’ for the new language was established in long-term memory. At this point, new vocabulary will be more and more encoded in terms of that network, and reliance on the short-term processes of the hippocampus will become less (although still important!).

I think that intensity is important. Intensity by its very nature is rarely maintained. People at the top of their field — champion sportspeople, top-ranking musicians, ‘geniuses’, and so on —they have to maintain that intensity as long as they want to stay at the top, and I would expect their brains to show more enduring changes (that is, particular regions that are unusually large, and others that are smaller than average). For the rest of us, any enduring changes are less marked.

But making those changes is important!

In recent years, research has come to suggest that, although regular moderate exercise is highly beneficial for physical and mental health, short bouts of intense activity have their own specific benefits above and beyond that. I think the same might be true for mental activity.

This may be particularly (or differently) true as we get older, when it does tend to get harder to learn — making (relatively) short bouts of intensive study/learning/activity so vital. We need that concentrated practice more than we did when we were young and learning came easier. And concentrated practice may be exactly the way to produce significant change in our brains.

But we don’t need to worry about becoming ‘muscle-bound’ — if we learn thousands of new words in a few months (an excellent step in acquiring a new language), we will then go on to acquire grammar and practice reading and writing whole sentences. The words will consolidate; different language skills will build different parts of the brain; those areas no longer being intensively worked will diminish (a little).

Moreover, it’s not only about growing particular regions, it’s also very much about building new or stronger connections between regions — building new networks. Because language learning involves so many regions, it may be especially good for that aspect too (see, for example, another recent news report, on how language learning grows white matter and reorganizes brain structures).

The important thing is that your brain is changing; the important thing is that your brain keeps changing. I think intensive periods of new learning are the way to achieve this, interspersed with consolidation periods.

As I’ve said before, variety is key. By providing variety in learning and experiences across tasks and domains, you can keep your brain flexible. By providing intense focus for a period, you can better build specific ‘mental muscles’.

What is neurogenesis?

Neurogenesis — the creation of new brain cells — occurs of course at a great rate in the very young. For a long time, it was not thought to occur in adult brains — once you were grown, it was thought, all you could do was watch your brain cells die!

Adult neurogenesis (the creation of new brain cells in adult brains) was first discovered in 1965, but only recently has it been accepted as a general phenomenon that occurs in many species, including humans (1998).

Where does adult neurogenesis occur?

It's now widely accepted that adult neurogenesis occurs in the subgranular zone of the dentate gyrus within the hippocampus and the subventricular zone (SVZ) lining the walls of the lateral ventricles within the forebrain. It occurs, indeed, at a quite frantic rate — some 9000 new cells are born in the dentate gyrus every day in young adult rat brains — but under normal circumstances, at least half of those new cells will die within one or two months.

The neurons produced in the SVZ are sent to the olfactory bulb, while those produced in the dentate gyrus are intended for the hippocampus.

Adult neurogenesis might occur in other regions, but this is not yet well-established. However, recent research has found that small, non-pyramidal, inhibitory interneurons are being created in the cortex and striatum. These new interneurons appear to arise from a previously unknown class of local precursor cells. These interneurons make and secrete GABA (see below for why GABA is important), and are thought to play a role in regulating larger types of neurons that make long-distance connections between brain regions.

How does neurogenesis occur?

New neurons are spawned from the division of neural precursor cells — cells that have the potential to become neurons or support cells. How do they decide whether to remain a stem cell, turn into a neuron, or a support cell (an astrocyte or oligodendrocyte)?

Observation that neuroblasts traveled to the olfactory bulb from the SVZ through tubes formed by astrocytes has led to an interest in the role of those support cells. It's now been found that astrocytes encourage both precursor cell proliferation and their maturation into neurons — precursor cells grown on glia divide about twice as fast as they do when grown on fibroblasts, and are about six times more likely to become neurons.

Adult astrocytes are only about half as effective as embryonic astrocytes in promoting neurogenesis.

It’s been suggested that the role of astrocytes may help explain why neurogenesis only occurs in certain parts of the brain — it may be that there’s something missing from the glial cells in those regions.

The latest research suggests that the astrocytes influence the decision through a protein that it secretes called Wnt3. When Wnt3 proteins were blocked in the brains of adult mice, neurogenesis decreased dramatically; when additional Wnt3 was introduced, neurogenesis increased.

How are these new neurons then integrated into existing networks? Mouse experiments have found that the brain chemical called GABA is critical. Normally, GABA inhibits neuronal signals, but it turns out that with new neurons, GABA has a different effect: it excites them, and prepares them for integration into the adult brain. Thus a constant flood of GABA is needed initially; the flood then shifts to a more targeted pulse that gives the new neuron specific connections that communicate using GABA; finally, the neuron receives connections that communicate via another chemical, glutamate. The neuron is now ready to function as an adult neuron, and will respond to glutamate and GABA as it should.

The creation and development of new neurons in the adult brain is very much a "hot" topic right now — it's still very much a work-in-progress. However, it is clear that other brain chemicals are also involved. An important one is BDNF (brain-derived neurotrophic factor), which seems to be needed during the proliferation of hippocampal precursor cells to trigger their transformation into neurons.

Other growth factors have been found to stimulate proliferation of hippocampal progenitor cells: FGF-2 (fibroblast growth factor-2) and EGF (epidermal growth factor).

Recently it has been discovered that the normal form of the prion protein which, when malformed, causes mad cow disease, is also involved in neurogenesis. These proteins, in their normal form, are found throughout our bodies, and particularly in our brains. Now it seems that the more of these prion proteins that are available, the faster neural precursor cells turn into neurons.

The immune system's T cells (which recognize brain proteins) are also critically involved in enabling neurogenesis to occur. Among mice given environmental enrichment, only those with healthy T-cells had their production of new neurons boosted.

Factors that influence neurogenesis

A number of factors have been found to affect the creation and survival of new neurons. For a start, damage to the brain (from a variety of causes) can provoke neurogenesis.

Moderate alcohol consumption over a relatively long period of time can also enhance the formation of new nerve cells in the adult brain (this may be related to alcohol's enhancement of GABA's function). Excess alcohol, however, has a detrimental effect on the formation of new neurons in the adult hippocampus. But although neurogenesis is inhibited during alcohol dependency, it does recover. A pronounced increase in new neuron formation in the hippocampus was found within four-to-five weeks of abstinence. This included a twofold burst in brain cell proliferation at day seven of abstinence.

Most drugs of abuse such as nicotine, heroine, and cocaine suppress neurogenesis, but a new study suggests that cannabinoids also promote neurogenesis. The study involved a synthetic cannabinoid, which increased the proliferation of progenitor cells in the hippocampal dentate gyrus of mice, in a similar manner as some antidepressants have been shown to do. The cannabinoid also produced similar antidepressant effects. Further research is needed to confirm this early finding.

If antidepressants promote neurogenesis, it won't be surprising to find that chronic stress, anxiety and depression are associated with losing hippocampal neurons. A rat study has also found that stress in early life can permanently impair neurogenesis in the hippocampus.

Showing the other side of this picture, perhaps, an intriguing rat study found that status affected neurogenesis in the hippocampus, with high-status animals having around 30% more neurons in their hippocampus after being placed in a naturalistic setting with other rats.

Also, a study into the brains of songbirds found that birds living in large groups have more new neurons and probably a better memory than those living alone.

Both physical activity and environmental enrichment (“mental stimulation”) have been shown to affect both how many cells are born in the dentate gyrus of rats and how many survive. Learning that uses the hippocampus has also been shown to have a positive effect, although results here have been inconsistent.

Inconsistent results from studies looking at neurogenesis are, it is suggested, largely because of a confusion between proliferation and survival. Neurogenesis is measured in terms of these two factors, which researchers often fail to distinguish between: the generation of new brain cells, and their survival. But these are separate factors, that are independently affected by various factors.

The inconsistency found in the effects of learning may also be partly explained by the complex nature of the effects. For example, during the later phase of learning, when performance is starting to plateau, neurons created during the late phase were more likely to survive, but neurons created during the early phase of more rapid learning disappeared. It’s speculated that that this may be a “pruning” process by which cells that haven’t made synaptic connections are removed from the network.

And finally, rodent studies suggest a calorie-restricted diet may also be of benefit.

It's not all about growing new neurons

A few years ago, we were surprised by news that new neurons could be created in the adult brain. However, it’s remained a tenet that adult neurons don’t grow — this because researchers have found no sign that any structural remodelling takes place in an adult brain. Now a mouse study using new techniques has revealed that dramatic restructuring occurs in the less-known, less-accessible inhibitory interneurons. Dendrites (the branched projections of a nerve cell that conducts electrical stimulation to the cell body) show sometimes dramatic growth, and this growth is tied to use, supporting the idea that the more we use our minds, the better they will be.