Sleep, Schizophrenia, and Memory: A Connection?

Schizophrenia is a devastating mental disorder characterized by disrupted thought processes; cognitive symptoms may include hallucinations, delusions, and disorganized speech and thinking.  Patients with the disorder also show impairments of learning and memory, and difficulty in carrying out complex tasks.  A recent article by Dara Manoach and Robert Stickgold suggests that some of these symptoms may in turn be due to another, often-overlooked symptom of the disease: sleep disorders.

In healthy adults, sleep is known to affect consolidation: the process whereby information accumulated during the day is slowly integrated into the brain’s long-term networks, where it can become a lasting memory.  In research studies, volunteers who learn a new skill or memorize new facts can sometimes perform better the next morning – after a good night’s sleep allows them to consolidate the information – than they did the day before.

The relationship between a good night’s sleep and good memory in healthy adults raises the possibility that sleep deprivation in schizophrenia may be a contributing cause to some of the cognitive disturbance in that disorder.

In fact, sleep complaints are common among patients with schizophrenia, and can include difficulty falling asleep and staying asleep.  Even the type of sleep may be affected. During the course of a night, normal adults cycle through several stages of sleep, including periods of rapid eye movement (REM) sleep and “slow wave sleep” (SWS).  One theory is that SWS may help stabilize or reinforce memories, while REM sleep helps these new memories become integrated into brain networks. Some patients with schizophrenia show almost a complete abolition of SWS, and a few studies have now shown that those patients with less SWS tend to be the same ones who show the poorest recall of information learned prior to sleep.

In their review of these studies, Manoach and Stickgold suggest that healthy adults use sleep to help automate recently-learned information and skills, so that performance can be faster and less dependent on voluntary attention.  In effect, while we sleep, the brain figures out how to perform familiar tasks on “auto-pilot” so that we can focus our attention on other things.  Patients with a breakdown of normal sleep-dependent consolidation would be correspondingly less able to automate tasks, meaning that they would have to spend more attention on these tasks – making it harder to carry out complex tasks with high attentional demands.  This in turn might be the root cause of many of the cognitive deficits observed in schizophrenia.

The idea that sleep may be responsible for much of the cognitive impairment in schizophrenia is still highly theoretical. There is much more work to be done in this area, but the early results are suggesting a new way to understand at least some of the cognitive impairments in schizophrenia – which in turn may suggest that treating sleep disturbances might help provide relief from some of the symptoms of this devastating disorder.

Further reading:

D. S. Manoach and R. Stickgold (2009) Does abnormal sleep impair memory consolidation in schizophrenia? In, Frontiers in Human Neuroscience, vol. 3:21 (available online at: www.ncbi.nlm.nih.gov/pmc/articles/PMC274129).

R. Stickgold & M. P. Walker (2007) Sleep-dependent memory consolidation and reconsolidation. Sleep Medicine, vol. 8, pp. 331-343.

The Mystery of Alzheimer’s: New Clues in our Genes

Alzheimer’s disease comes in two basic variants: a common form known as late-onset AD that strikes people over age 65, and a rare early-onset form, which can strike people as young as their 30s or 40s.  Inherited variations in three genes – called the PS1, PS2, and APP genes – are known to cause the early-onset form, and about half the cases of early-onset AD may be due to presence of one or more of these genes.  But early-onset AD accounts for only about 5-10% of all AD cases.  Finding the genetic bases of the common, late-onset form has proven more elusive.  In fact, late-onset Alzheimer’s is sometimes called “sporadic” Alzheimer’s, reflecting the idea that we can’t predict whom it will strike or when.

Until recently, the only gene known to be associated with late-onset AD was APOE, a gene associated with clearing cholesterol from the bloodstream.  APOE comes in three common variants, known as E2, E3, and E4.  People carrying E4 are about three times more likely to develop late-onset AD than those carrying E3; people carrying E2 are at a slightly reduced risk for the disease.  But the link between APOE and AD is not terribly strong; many people carrying E2 still develop AD, while some carrying E4 never do.  Apparently, other genetic or environmental factors must play a role too.

Now, two large-scale studies have identified three additional genes that appear to play a role in determining an individual’s risk for late-onset AD.  One study conducted by researchers in France considered over 15,000 elderly people with and without AD, and found that the people with AD were much more likely to have specific variants on genes known as CLU and CR1.  These genes may help regulate how the body clears beta amyloid, the protein that accumulates in the brains of people with AD; variants of these genes that are less effective at this task may contribute to an individual’s susceptibility to the disease.  A second study out of the UK examined over 16,000 people with and without AD, and replicated the findings with CLU as well as identifying a third genetic variant, on the PICALM gene, that also occurred more often in individuals with AD.

CLU, CR1, and PICALM join APOE as significant risk factors for the common, late-stage form of AD.  Together, the four genes may account for as much as 40-50% of AD cases.  Knowing the genetic variants associated with a disease is a long way from being able to prevent or cure that disease, but it’s an important step: now, researchers at least have some idea of where to begin targeting their efforts.

Further reading:

D Harold and others (2009). Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer’s disease. In, Nature Genetics, vol. 41, pp. 1088-1093.

JC Lambert and others (2009). Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer’s disease. In, Nature Genetics, vol. 41, pp. 1094-1099.

Thinking while driving: Why cell phones impair performance

Memory failures aren’t only a consequence of disease and brain injury; all of us experience periods when our memories aren’t quite up to par because we’re distracted.  Working memory, the memory system that holds and manages the information we need to perform the task at hand, has limited capacity – meaning it can only hold a few items at once. When distracted, working memory may be diverted to deal with the distraction, often at the expense of what we were previously doing.

There are times when such distraction can have serious consequences, such as when we’re driving a car.  The statistics are clear: car accidents are much more likely if drivers are distracted, such as by talking on a cell phone.  Now research is beginning to show us why.

A recent study examined the performance of drivers using a computerized driving simulator, while those drivers were conversing either with in-car passengers (who could see the same driving simulator), or via cell phones.  As several prior studies have shown, drivers’ performance suffered during cell phone conversations compared to in-car conversations; the cell-phone-using drivers showed slowed reaction times (such as speed of braking responses) and poorer avoidance of road and traffic hazards.  One reason appeared to be “conversation suppression”: in-car passengers tended to slow their rates of conversation as the driver approached a hazard.  This could free up attention and other brain resources, allowing the driver to focus with the hazards of the road.  In contrast, cell-phone conversants (who could not see the road, and thus could not judge approaching hazards) did not tend to suppress conversation at those critical moments.

Importantly, this particular study considered hands-free phone usage.  Several states in the US now ban or restrict drivers from using handheld cell phones, but allow hands-free phones.  But many studies now suggest the real issue isn’t whether the driver is physically holding the phone; the real issue is that a conversant who is not in the same car as the driver doesn’t suppress conversation when a road hazard appears.

The bottom line from a growing body of studies seems to be a consistent warning that cell phone usage (whether handheld or hands-free) while driving can seriously impair a driver’s performance.   The good news: talking to an in-car passenger may actually improve driver performance, because passengers often spontaneously provide alerting comments, helping the driver notice and attend to looming hazards or changes in road conditions.

Further reading:

S. G. Charlton (2009) Driving while conversing: Cell phones that distract and passengers who react. Accident Analysis and Prevention, vol. 41, pp. 160-173.

Y. Ishigami and R. M. Klein (2009) Is a hands-free phone safer than a handheld phone? Journal of Safety Research, vol. 40, pp. 157-164.

Growing Brain Cells While You Sleep

Every day, new brain cells (neurons) are born in the brains of adult mammals, a process called neurogenesis (neuro = neurons, genesis = birth).  These newborn cells appear particularly in the hippocampus – a brain area that is important for new memory formation.   Over the next few weeks, many of these newborn cells die off again.  But studies show that, if a rat has been exercising or has been exposed to new learning, more of the newborn cells survive.  The rate of survival of these new cells also depends on sleep.

As we sleep, we (like rats) cycle through several “stages,” including rapid-eye movement (REM) sleep, which is believed to be when we dream, and several kinds of non-REM sleep.

A recent study has suggested that REM is particularly important for neurogenesis in the hippocampus.  One group of rats were given four days of REM deprivation, by putting the rats in a small chamber where the floor was a treadmill that automatically activated whenever the rats entered REM sleep – forcing them to step forward to avoid being carried into the wall of the chamber.  (Non-REM sleep didn’t activate the treadmill.) For comparison, a group of control rats were placed in the same type of chamber, but treadmill activation was unrelated to sleep cycle.

The REM-deprived rats showed much less neurogenesis than controls. Both groups showed similar amounts of total sleep, and similar levels of stress hormones, indicating that the stress of being periodically awoken was similar for the REM-deprived and control rats. This study therefore suggests that REM sleep is particularly important for the birth and survival of new neurons in the adult brain.

There are two important implications of this study.  The first is that it adds to a growing literature suggesting that relatively short-term periods of sleep deprivation (equivalent to a few nights’ insomnia or intentional wakefulness) can significantly affect the brain.  This is a cautionary finding for those of us who routinely don’t get a full night’s sleep.

The second implication is that not all sleep is equal.  This study also adds to a growing literature suggesting that REM sleep has some special functions, particularly contributing to learning and memory.  Many medications, including some over-the-counter sleeping aids, disrupt REM sleep.  If REM sleep is indeed important for neurogenesis, then disrupting REM may disrupt neurogenesis – which might in turn have consequences for a person’s learning and memory abilities.

 

Further Reading:

R. Guzman-Marin et al. (2008). Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat. Sleep, 31(2):167-175.

Society for Neuroscience Meeting: Brain Research Past, Future, and Present

This past week, I traveled to Chicago to attend the annual meeting of the Society for Neuroscience, the association for researchers studying all aspects of the brain, from biochemical processes, genetics, and anatomy, to animal behavior, to human disorders such as schizophrenia, Alzheimer’s and epilepsy – and everything in between.  There were over 30,000 attendees, all in Chicago at the same time – more than the population of some small cities.  The SfN meeting is a chance for colleagues from around the world to gather, report on their latest findings, and exchange ideas.

Two of the keynote lectures stick in my mind.  The first was a talk by Richard Morris, the eminent British researcher who studies how brains form new memories.  Since 2009 marks SfN’s 40^th anniversary, Morris gave a brief overview of SfN’s history, reminding us all how far the science of neuroscience has come in that time.  Some of the researchers attending the 2009 meeting had not yet been born in 1969, and many of the seminal papers which we now take for granted had not yet been published. A salient example is Bliss & Lømo’s (1973) article documenting long-term changes in neurons as a result of experience: a phenomenon termed long-term potentiation (LTP) which is now generally believed to be one of the fundamental ways in which the brain encodes new learning.  Modern research methods such as functional neuroimaging (fMRI and PET) and genetic mapping, not to mention information-sharing via the Internet, were not yet available in 1969. In the past 40 years, we’ve developed new tools to diagnose diseases and new methods to treat them, as well as a broader understanding of how the brain works and why it sometimes doesn’t. Looking back now on how much we’ve learned in the last 40 years, one can’t help but wonder what we might learn in the next 40 years – and whether some of today’s most terrifying and incurable disorders, such as schizophrenia, Alzheimer’s, and epilepsy, could join polio and smallpox as relics of the past.

Against this vision of past and future, SfN attendees face a present reality in which competition for research funding is perhaps as fierce as it has ever been.  At the National Institutes of Health (NIH), the federal institution that is the major funder of biomedical research in the US, only about 20% of submitted research proposals actually receive funding.  The situation would have been much worse during the economic downturn, but for a large injection of stimulus funds provided by the Recovery Act (ARRA), which allowed many labs to continue their research (and to maintain and hire laboratory staff).  There is concern about what will happen when that infusion of money runs out. Francis Collins, NIH’s director, addressed SfN attendees and stressed that researchers themselves have a responsibility not only to conduct research, but also to communicate to the broader public why that research matters, and why in times of budgetary crisis, scientific research is an investment in the future of our species and our planet that our society must continue to support.  With luck, this year’s SfN meeting attendees came away charged with that vision as much as with inspiration for new and exciting research directions.

Red wine and the brain: Cheers!

A growing body of studies on the interactions between diet, behavior and health suggest that individuals who consume moderate amounts of alcohol (particularly wine) are statistically less likely to die from cardiovascular disease.  One possibility is that chemical compounds in wine (particularly red wine) may protect against heart disease.  An alternate theory is socioeconomic: in the US, wine is often considered a “high-class” form of alcohol – compared with, say, beer or whisky – and wine drinkers as a group tend to be more highly educated, to exercise more often, and to be more healthy overall.  In this case, wine drinking might not directly protect against heart health, but wine drinkers as a group might show reduced risk of heart disease because of these other factors.

In the last few years, there have been intriguing suggestions that low-to-moderate alcohol consumption may also protect against age-related cognitive decline, and even against Alzheimer’s disease.  One study considered mice that had been specially bred to develop beta amyloid plaques in their brains; beta amyloid plaques are a hallmark of Alzheimer’s disease in humans.  Some of the mice were given moderate amounts of cabernet sauvignon in their water supply for a period of about 7 months; others were given plain water. The group given wine showed less accumulation of plaques in their brain, and also showed much less decline in memory function than their counterparts.  The implication is that some (or some combination) of the chemical compounds in wine – specifically red wine – helps the brain combat plaque accumulation. 

And what about in humans?  A study published late last year in the Journal of the American Geriatric Society followed nearly 6,000 community-dwelling elderly adults for three years.  Each individual’s baseline alcohol consumption was recorded at the start of the study: about 42% of the women and 71% of the men were alcohol drinkers.  As would be expected, most of the volunteers showed some mild cognitive decline over the course of the study.  But female drinkers showed less decline than female nondrinkers on the Mini-Mental Status Exam or MMSE, a standard test of general cognitive function.  No such differences were observed between male drinkers and non-drinkers.  The authors’ conclusion: low-to-moderate alcohol consumption may help slow cognitive decline in elderly women.  This echoes an earlier study from 2005 which found a similar effect: that elderly women who drink about one serving of alcohol a day may have a slightly reduced risk of cognitive decline.  It’s not clear why women appear to benefit more than men, although one possibility is that, since women are at greater statistical risk of Alzheimer’s then men, more of the women are in a position to benefit from the plaque-busting properties of red wine.

There’s an obvious and serious caveat: the current findings do not represent an invitation to heavy drinking.  Long-term intake of large amounts of alcohol damages the brain, and is associated with a host of other health complications.  Current US guidelines suggest that women drink no more than two to three units a day (one unit is approximately one small glass of wine), while men (who typically have larger body weights) should drink no more than three or four units per day.  (These are general guidelines, and don’t apply to everyone; some individuals should drink much less or not at all.)

Nevertheless, for those who enjoy an occasional glass of wine, there now seems to be a reasonable cause to rejoice: modest amounts of red wine may not only pleasure the palate, but may also help protect the aging brain.

 

Further Reading:

J. Wang and others (2006). “Moderate consumption of cabernet sauvignon attenuates Abeta neuropathology in a mouse model of Alzheimer’s disease.” In, “FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology,” vol. 20, no. 13, pp. 2313-2320.

D. J. Stott and others (2008). “Does low to moderate alcohol intake protect against cognitive decline in older people?”In, Journal of the American Geriatric Society, vol. 56, no. 12, pp. 2217-2224.

M. J. Stampfer and others (2005). “Effects of moderate alcohol consumption on cognitive function in women.” In, New England Journal of Medicine, vol. 352, no. 3, pp. 245-253.

Eat less, remember more?

Researchers studying the effects of diet in animals have long known that caloric restriction (abbreviated CR) can improve longevity.  That is, lab rats fed a special, low-calorie diet tend to live longer than their comrades given a “normal” diet.  The same is true in other species, including dogs, fish, and yeast.  We don’t know yet if CR would also improve longevity in humans.

Caloric restriction also improves learning and memory in animal.  For example, a standard test of learning in rats is to place the rat in a shallow pool. Somewhere in the pool is a little platform, hidden just below the surface of the water. Rats are actually quite competent swimmers, and will swim around until they stumble across the platform; then they’ll climb out of the water.  With repeated trials, healthy rats learn the location of the platform quickly, and as soon as they’re placed in the pool, they rapidly swim to the platform and climb up.  It’s a skill that declines with age, so that older rats have a harder time learning to locate the hidden platform than younger rats do. Rats given lifelong CR – provided with only 60% as much food as a healthy rat would normally choose to eat – show less decline with age than animals given free access to food. 

A recent study suggests that caloric restriction might improve learning and memory in humans, too.  Two groups of healthy elderly individuals were assigned to follow either a “standard” diet or a calorie-restricted diet for 3 month.  At the end of that period, unsurprisingly, the CR group had lost weight.  More surprisingly, the CR group showed a significant improvement – almost 30% — in their memory scores.  The group on a regular diet showed no change from their baseline scores.

So, should we all start cutting back drastically on our caloric intake?  Here, the question gets complicated.  Obviously, there are many health benefits to maintaining a healthy diet, managing our cholesterol levels and keeping blood pressure in check.  But severe caloric restriction, with caloric reductions as dramatic as in the studies above, can have risks. The obvious risk is malnutrition. When reducing caloric intake, there may also be reduced intake of nutrients and vitamins that the body needs to function; as a result, calorie-restricted diets should only be attempted under medical supervision and with proper care to ensure that the body is still getting adequate supplies of nutrients and vitamins. 

Anecdotally, I’ve talked to two people who study caloric restriction in animals, and after seeing the dramatic positive effects, they had decided to attempt extending their own longevity in the same way. (They both had the medical background needed to attempt CR responsibly, without risking their health.) They reported feeling continually hungry, irritable, overtired, and cold.  In the end, they decided, a longer life wasn’t worth it if one was going to be miserable the whole time.

Instead, these and other researchers are focusing on the mechanisms involved – trying to understand exactly why CR produces the cognitive benefits it does.  Maybe, if we understood that, there would be a way to produce the same effects – in a more painless way than near-starvation.

Further reading:

J. Stewart and others (1989). The effects of life-long food restriction on spatial memory in young and aged Fischer 344 rats measured in the 8-arm radial and the Morris water mazes. In, Neurobiology of Aging, vol. 10, pp. 669-675.

A. V. Witte and others (2009). “Caloric restriction improves memory in elderly humans.” In, Proceedings of the National Academy of Sciences (USA), vol. 106, no. 4, pp. 1255-1260.

Diabetes and the Brain

It’s been well-established that type II diabetes (also called adult-onset diabetes) is linked with cognitive decline.  In type II diabetes, there is a reduction in the production or effectiveness of insulin, a hormone that the body uses to break down glucose so that our cells can take it in and use it for energy.  Less insulin (or insensitivity to insulin) means the cells can’t absorb glucose properly.  Over time, this can cause a host of medical complications – and can also damage the brain.  Several studies have now shown that individuals with type II diabetes – particularly elderly patients – perform worse than would be expected for their age group on a number of cognitive tests, and may have an increased risk of dementia.

The reason for the relationship between diabetes and cognitive impairment has been less clear, but a popular hypothesis has been that type II diabetes is associated with a heightened risk of cardiovascular disease, which in turn reduces the amount of blood flow to the brain, limiting the supply of oxygen and nutrients to brain cells.  Over time, this reduced supply could cause brain cells to malfunction and even die.

But a recent study has suggested a second way in which diabetes could damage the brain, and specifically the hippocampus, a part of the brain that is critical for our ability to lay down new memories.  William Wu and colleagues used magnetic resonance imaging (MRI) to examine of the brains of elderly individuals with type II diabetes.  Compared to individuals of the same age but without diabetes, the patients showed abnormalities in the dentate gyrus, a small region within the hippocampus.  Across individuals, the higher the blood glucose levels, the more abnormality in the dentate gyrus. 

Combined with other emerging data, this is relatively convincing proof that chronic high levels of blood glucose can directly damage the brain, and particularly the dentate gyrus. And – because this part of the brain is so critical for memory –  this could be one key reason why individuals with type II diabetes so often show memory impairments.

Why should the dentate gyrus be so sensitive?  That’s not clear. But it’s intriguing to note that the dentate gyrus is one of the few places in the adult brain that continues to generate newborn brain cells throughout life.  One might speculate that these newborn cells are particularly delicate – and particularly easy to destroy when glucose levels get out of balance.

If there’s any good news here, it’s that type II diabetes can often be controlled by a combination of diet, medication, and exercise.  For anyone who needed it, the recent results provide one more reason to try and do just that.

Further reading:

William Wu and others (2009). “The brain in the age of old: The hippocampal formation is targeted differentially by diseases of late life.”  In, Annals of Neurology, vol. 64, issue 6, pp. 698-706.

G. J. Biessels and others (2006). “Risk of dementia in diabetes mellitus: A systematic review.” In, The Lancet Neurology, vol. 5, no. 1, pp. 64-74.

T. Cukierman and others (2005). “Cognitive decline and dementia in diabetes – Systematic overview of prospective observational studies.”  In, Diabetologia, vol. 48, no. 12, pp. 2460-2469.

Ginkgo and Memory: Not So Fast

Dietary supplements – products like vitamins and herbal supplements – form a multibillion-dollar industry in the US.  Under current US law, dietary supplements are regulated as foods, rather than as drugs, which means that they’re exempt from some of the strict Federal regulations that apply to drugs.  In particular, makers of dietary supplements are not required to obtain FDA approval, proving that their products are either safe or effective, before they’re allowed to start putting those products on the shelves of supermarkets and drug stores. This makes it very hard for a consumer to know what’s effective – and what’s safe.

One of the top-selling dietary supplements in the US is ginkgo, a compound extracted from the leaves of the ginkgo biloba tree.  Gingko extracts have long been marketed for their supposed memory-boosting powers.  However, the hard science to back up this claim has been lacking.

One study, published in the prestigious Journal of the American Medical Association (JAMA) in 2002, examined cognitive function in healthy elderly individuals given ginkgo supplements, compared to peers who were given a placebo (an inactive sugar pill).  The study found no significant benefits of ginkgo on memory.  Another placebo-controlled study, published around the same time in a different journal, came to a different conclusion – that gingko could indeed enhance some kinds of memory and attention – but this study was funded by a company that markets a ginkgo supplement, which raised some red flags in the scientific community about whether the results were truly objective.  Most scientists now believe that there is little evidence that ginkgo improves memory in healthy adults.

Another possibility is that, even if ginkgo has little effect in boosting the memory power of healthy adults, it might be useful in helping to prevent dementia, including Alzheimer’s disease.  That claim now appears to have been overturned too.  In a study published in JAMA last year, over 3000 non-demented elderly individuals were given daily supplements of either ginkgo or a placebo.  This was a large, carefully-designed and well-controlled study, meant to provide definitive evidence about ginkgo’s effects. The study lasted for six years, and during this time about 20% of the participants developed dementia.  This included 246 of the participants who’d been taking the placebo, and 277 of those who’d been taking the ginkgo.  Statistically, this means that the people taking ginkgo were just as likely to develop dementia (including Alzheimer’s) as people taking the placebo.

This is the biggest, longest study of gingko so far, and it’s hard to argue with the results, although some have tried – for example, suggesting that ginkgo may have an effect that only emerges after people have been taking the supplements for more than six years, or that the particular dosage (or brand of ginkgo supplement) used in the study may not have been optimal.  Still, the burden of proof now seems to be on those who promote the supplement to provide compelling evidence that it has some measurable benefit.

It’s also worth noting that ginkgo, like all drugs, has some side effects.  In particular, ginkgo appears to improve blood flow and to reduce clotting; as such, it may have some uses related to cardiovascular health or other medical conditions – but this also means that it may increase the risk of stroke in people who are taking anticoagulant medication (including some heart medications and aspirin or ibuprofen).  There’s also been some concern that certain kinds of antidepressants may interact dangerously with ginkgo.  For many people, the possible risks of ginkgo may outweigh any, as-yet-unproven, benefits to the brain.

 

Further reading:

 

P. R. Solomon and others (2002). “Ginkgo for memory enhancement: A randomized controlled trial.” JAMA, vol. 288, no. 7, pp. 835-840.

J. A. Mix & W. D. Crews (2002). “A double-blind, placebo-controlled, randomized trial of Ginkgo biloba extract EGb 761® in a sample of cognitively intact older adults: Neuropsychological findings.” Human Psychopharmacology: Clinical and Experimental, vol. 17, no. 6, pp. 267-277.

S. T. DeKosky and others (2008). “Ginkgo biloba for prevention of dementia: A randomized controlled trial.” JAMA, vol. 300, no. 19, pp. 2253-2262.

Teaching Old Dogs New Tricks

The old folk wisdom – that it’s hard to teach an old dog (or an old human) new tricks – has some grounding in science.  Namely, humans and other animals have “sensitive periods” in brain development, windows of opportunity for new learning that close after a certain age.

One example is language learning: children can learn new languages more easily than adults do.  Human languages have about 25-40 sounds – but not all languages use the same sounds. For example, the sounds /l/ and /r/ are meaningfully different in English (so that “lay” and “ray” are different words with different meanings) but these sounds are not meaningfully different in Japanese, so that native Japanese speakers often have difficulty hearing the difference between these two sounds.  But Japanese infants younger than 6-8 months old can distinguish them – an ability that is lost by the time the infants reach about 11 months old (unless those infants are exposed to English as well as to their native language).  Similarly, an “English-speaking” baby can distinguish between sounds such as the soft /p/ and sharp /p/ of the Thai language, or the Hindi /ta/ vs. /Ta/ — even though most adult English speakers can’t tell these sounds apart.  Apparently, there is a “sensitive period” early in life during which the brain learns the sounds of language.  This period lasts until about age 10-11 months — and then the window closes.

The phenomenon of sensitive periods is widespread.  Other species have sensitive periods for learning their own “languages.”  For example, male sparrows raised in the wild learn their characteristic birdsongs from listening to other males of the same species. If young birds are raised in isolation, but allowed to hear birdsong, they can still learn to sing normally – but only if exposure to birdsong occurs within the first 30-100 days of their life; after that, the window of opportunity is closed.  

And sensitive periods don’t only apply to hearing and producing sounds: vision has a sensitive period too. Human infants born with cataracts blocking their vision in one eye will see normally if corrective surgery is performed within a few months of birth, but if the surgery is delayed a few years, normal vision never develops.  Apparently, within the first few months of life, the brain learns how to see — how to interpret information coming from the eyes — and if that learning isn’t set up early in life, the window of opportunity closes.  

In all these examples, the message is the same: early learning is easy and natural; later learning may be harder if not impossible.

But newer research, while not overturning the idea of sensitive periods, is challenging the idea that they are immutable.  The truth may be more subtle.  Although adults may have more trouble than children in mastering the sounds of a new language, many can learn to speak a new language quite fluently. And the adults may learn faster – even if their final level of proficiency is not as high as someone who learned the language as a child.  Language is a complex phenomenon that may require many subskills – some of which may have sensitive periods that “close” later than others, and some of which may never close at all.  

Perhaps the best news of all is that, although language learning is harder after childhood, there is no good evidence that the ability to learn a new language drops off significantly after that.  In language learning as with anything else, it appears that you can teach a new dog new tricks… it just takes a little longer.

 

Further reading on sensitive periods:

M. Thomas and M. Johnson (2008). “New advances in understanding sensitive periods in brain development.” In, Current Directions in Psychological Science, vol. 17, pp. 1-5.