prefrontal cortex

is the area of the brain at the very front of the frontal lobes. It is involved in "executive functions", such as working memory, decision-making, planning and judgment. Prefrontal regions appear to be particularly sensitive to the effects of aging. It is thought that the reduced ability to recall the context of memories that occurs with advancing age, is evidence that the prefrontal cortex is also critical for context processing - a process involved in many cognitive functions. A recent study has also revealed that emotional stimuli and attentional functions are integrated in a specific part of the prefrontal cortex - the anterior cingulate (located between the right and left halves).

Attention warps memory space

A recent study reveals that when we focus on searching for something, regions across the brain are pulled into the search. The study sheds light on how attention works.

In the experiments, brain activity was recorded as participants searched for people or vehicles in movie clips. Computational models showed how each of the roughly 50,000 locations near the cortex responded to each of the 935 categories of objects and actions seen in the movie clips.

05/2013

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Re-organization more important than changes in brain size

A new finding points to brain reorganization, rather than brain size, as the driver in primate brain evolution. Data from 17 anthropoid primate species (including humans) across 40 million years has found that around three quarters of differences between the brains of species of monkeys and apes are due to internal reorganization that is independent of size. The prefrontal cortex in particular appears to have played the biggest role in explaining the evolutionary changes in primate brains.

04/2013

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Social isolation decreases myelin

December, 2012

A mouse study demonstrates that prolonged social isolation can lead to a decrease in myelin, an effect implicated in a number of disorders, including age-related cognitive decline.

Problems with myelin — demyelination (seen most dramatically in MS, but also in other forms of neurodegeneration, including normal aging and depression); failure to develop sufficient myelin (in children and adolescents) — are increasingly being implicated in a wide range of disorders. A new animal study adds to that evidence by showing that social isolation brings about both depression and loss of myelin.

In the study, adult mice were isolated for eight weeks (which is of course longer for a mouse than it is to us) to induce a depressive-like state. They were then introduced to a mouse they hadn’t seen before. Although typically very social animals, those who had been socially isolated didn’t show any interest in interacting with the new mouse — a common pattern in human behavior as well.

Analysis of their brains revealed significantly lower levels of gene transcription for oligodendrocyte cells (the components of myelin) in the prefrontal cortex. This appeared to be caused by a lower production of heterochromatin (tightly packed DNA) in the cell nuclei, producing less mature oligodendrocytes.

Interestingly, even short periods of isolation were sufficient to produce changes in chromatin and myelin, although behavior wasn’t affected.

Happily, however, regardless of length of isolation, myelin production went back to normal after a period of social integration.

The findings add to the evidence that environmental factors can have significant effects on brain development and function, and support the idea that socializing is good for the brain.

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Exercise may be best way to protect against brain shrinkage

November, 2012

A large study of older adults shows that physical exercise is associated with less brain atrophy and fewer white matter lesions. A small study shows that frail seniors benefit equally from exercise.

A study using data from the Lothian Birth Cohort (people born in Scotland in 1936) has analyzed brain scans of 638 participants when they were 73 years old. Comparing this data with participants’ earlier reports of their exercise and leisure activities at age 70, it was found that those who reported higher levels of regular physical activity showed significantly less brain atrophy than those who did minimal exercise. Participation in social and mentally stimulating activities, on the other hand, wasn’t associated with differences in brain atrophy.

Regular physical exercise was also associated with fewer white matter lesions. While leisure activity was also associated with healthier white matter, this was not significant after factors such as age, social class, and health status were taken into account.

Unfortunately, this study is reported in a journal to which I don’t have access. I would love to have more details about the leisure activities data and the brain scans. However, although the failure to find a positive effect of stimulating activities is disappointing, it’s worth noting another recent study, that produced two relevant findings. First, men with high levels of cognitive activity showed a significant reduction in white matter lesions, while women did not. Women with high levels of cognitive activity, on the other hand, showed less overall brain atrophy — but men did not.

Secondly, both genders showed less atrophy in a particular region of the prefrontal cortex, but there was no effect on the hippocampus — the natural place to look for effects (and the region where physical exercise is known to have positive effects).

In other words, the positive effects of cognitive activity on the brain might be quite different from the positive effects of physical exercise.

The findings do, of course, add to the now-compelling evidence for the benefits of regular physical activity in fighting cognitive decline.

It’s good news, then, that a small study has found that even frail seniors can derive significant benefits from exercise.

The study involved 83 older adults (61-89), some of whom were considered frail. Forty-three took part in group exercises (3 times a week for 12 weeks), while 40 were wait-listed controls. Participants were assessed for physical capacity, quality of life and cognitive health a week before the program began, and at the end.

Those who took part in the exercise program significantly improved their physical capacity, cognitive performance, and quality of life. These benefits were equivalent among frail and non-frail participants.

Frailty is associated with a higher risk of falls, hospitalizations, cognitive decline and psychological distress, and, of course, increases with age. In the U.S, it’s estimated that 7% of seniors aged 65 to 74, 18% of those aged 75 to 84, and 37% of seniors over the age of 85 are frail.

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The importance of cognitive control for intelligence

October, 2012

Brain imaging points to the importance of cognitive control, mediated by the connectivity of one particular brain region, for fluid intelligence.

What underlies differences in fluid intelligence? How are smart brains different from those that are merely ‘average’?

Brain imaging studies have pointed to several aspects. One is brain size. Although the history of simplistic comparisons of brain size has been turbulent (you cannot, for example, directly compare brain size without taking into account the size of the body it’s part of), nevertheless, overall brain size does count for something — 6.7% of individual variation in intelligence, it’s estimated. So, something, but not a huge amount.

Activity levels in the prefrontal cortex, research also suggests, account for another 5% of variation in individual intelligence. (Do keep in mind that these figures are not saying that, for example, prefrontal activity explains 5% of intelligence. We are talking about differences between individuals.)

A new study points to a third important factor — one that, indeed, accounts for more than either of these other factors. The strength of the connections from the left prefrontal cortex to other areas is estimated to account for 10% of individual differences in intelligence.

These findings suggest a new perspective on what intelligence is. They suggest that part of intelligence rests on the functioning of the prefrontal cortex and its ability to communicate with the rest of the brain — what researchers are calling ‘global connectivity’. This may reflect cognitive control and, in particular, goal maintenance. The left prefrontal cortex is thought to be involved in (among other things) remembering your goals and any instructions you need for accomplishing those goals.

The study involved 93 adults (average age 23; range 18-40), whose brains were monitored while they were doing nothing and when they were engaged in the cognitively challenging N-back working memory task.

Brain activity patterns revealed three regions within the frontoparietal network that were significantly involved in this task: the left lateral prefrontal cortex, right premotor cortex, and right medial posterior parietal cortex. All three of these regions also showed signs of being global hubs — that is, they were highly connected to other regions across the brain.

Of these, however, only the left lateral prefrontal cortex showed a significant association between its connectivity and individual’s fluid intelligence. This was confirmed by a second independent measure — working memory capacity — which was also correlated with this region’s connectivity, and only this region.

In other words, those with greater connectivity in the left LPFC had greater cognitive control, which is reflected in higher working memory capacity and higher fluid intelligence. There was no correlation between connectivity and crystallized intelligence.

Interestingly, although other global hubs (such as the anterior prefrontal cortex and anterior cingulate cortex) also have strong relationships with intelligence and high levels of global connectivity, they did not show correlations between their levels of connectivity and fluid intelligence. That is, although the activity within these regions may be important for intelligence, their connections to other brain regions are not.

So what’s so important about the connections the LPFC has with the rest of the brain? It appears that, although it connects widely to sensory and motor areas, it is primarily the connections within the frontoparietal control network that are most important — as well as the deactivation of connections with the default network (the network active during rest).

This is not to say that the LPFC is the ‘seat of intelligence’! Research has made it clear that a number of brain regions support intelligence, as do other areas of connectivity. The finding is important because it shows that the left LPFC supports cognitive control and intelligence through a mechanism involving global connectivity and some other as-yet-unknown property. One possibility is that this region is a ‘flexible’ hub — able to shift its connectivity with a number of different brain regions as the task demands.

In other words, what may count is how many different connectivity patterns the left LPFC has in its repertoire, and how good it is at switching to them.

An association between negative connections with the default network and fluid intelligence also adds to evidence for the importance of inhibiting task-irrelevant processing.

All this emphasizes the role of cognitive control in intelligence, and perhaps goes some way to explaining why self-regulation in children is so predictive of later success, apart from the obvious.

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Effect of blood pressure on the aging brain depends on genetics

July, 2012

For those with the Alzheimer’s gene, higher blood pressure, even though within the normal range, is linked to greater brain shrinkage and reduced cognitive ability.

I’ve reported before on the evidence suggesting that carriers of the ‘Alzheimer’s gene’, APOE4, tend to have smaller brain volumes and perform worse on cognitive tests, despite being cognitively ‘normal’. However, the research hasn’t been consistent, and now a new study suggests the reason.

The e4 variant of the apolipoprotein (APOE) gene not only increases the risk of dementia, but also of cardiovascular disease. These effects are not unrelated. Apoliproprotein is involved in the transportation of cholesterol. In older adults, it has been shown that other vascular risk factors (such as elevated cholesterol, hypertension or diabetes) worsen the cognitive effects of having this gene variant.

This new study extends the finding, by looking at 72 healthy adults from a wide age range (19-77).

Participants were tested on various cognitive abilities known to be sensitive to aging and the effects of the e4 allele. Those abilities include speed of information processing, working memory and episodic memory. Blood pressure, brain scans, and of course genetic tests, were also performed.

There are a number of interesting findings:

  • The relationship between age and hippocampal volume was stronger for those carrying the e4 allele (shrinkage of this brain region occurs with age, and is significantly greater in those with MCI or dementia).
  • Higher systolic blood pressure was significantly associated with greater atrophy (i.e., smaller volumes), slower processing speed, and reduced working memory capacity — but only for those with the e4 variant.
  • Among those with the better and more common e3 variant, working memory was associated with lateral prefrontal cortex volume and with processing speed. Greater age was associated with higher systolic blood pressure, smaller volumes of the prefrontal cortex and prefrontal white matter, and slower processing. However, blood pressure was not itself associated with either brain atrophy or slower cognition.
  • For those with the Alzheimer’s variant (e4), older adults with higher blood pressure had smaller volumes of prefrontal white matter, and this in turn was associated with slower speed, which in turn linked to reduced working memory.

In other words, for those with the Alzheimer’s gene, age differences in working memory (which underpin so much of age-related cognitive impairment) were produced by higher blood pressure, reduced prefrontal white matter, and slower processing. For those without the gene, age differences in working memory were produced by reduced prefrontal cortex and prefrontal white matter.

Most importantly, these increases in blood pressure that we are talking about are well within the normal range (although at the higher end).

The researchers make an interesting point: that these findings are in line with “growing evidence that ‘normal’ should be viewed in the context of individual’s genetic predisposition”.

What it comes down to is this: those with the Alzheimer’s gene variant (and no doubt other genetic variants) have a greater vulnerability to some of the risk factors that commonly increase as we age. Those with a family history of dementia or serious cognitive impairment should therefore pay particular attention to controlling vascular risk factors, such as hypertension and diabetes.

This doesn’t mean that those without such a family history can safely ignore such conditions! When they get to the point of being clinically diagnosed as problems, then they are assuredly problems for your brain regardless of your genetics. What this study tells us is that these vascular issues appear to be problematic for Alzheimer’s gene carriers before they get to that point of clinical diagnosis.

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Group settings hurt expressions of intelligence, especially in women

March, 2012

Comparing performance on an IQ test when it is given under normal conditions and when it is given in a group situation reveals that IQ drops in a group setting, and for some (mostly women) it drops dramatically.

This is another demonstration of stereotype threat, which is also a nice demonstration of the contextual nature of intelligence. The study involved 70 volunteers (average age 25; range 18-49), who were put in groups of 5. Participants were given a baseline IQ test, on which they were given no feedback. The group then participated in a group IQ test, in which 92 multi-choice questions were presented on a monitor (both individual and group tests were taken from Cattell’s culture fair intelligence test). Each question appeared to each person at the same time, for a pre-determined time. After each question, they were provided with feedback in the form of their own relative rank within the group, and the rank of one other group member. Ranking was based on performance on the last 10 questions. Two of each group had their brain activity monitored.

Here’s the remarkable thing. If you gather together individuals on the basis of similar baseline IQ, then you can watch their IQ diverge over the course of the group IQ task, with some dropping dramatically (e.g., 17 points from a mean IQ of 126). Moreover, even those little affected still dropped some (8 points from a mean IQ of 126).

Data from the 27 brain scans (one had to be omitted for technical reasons) suggest that everyone was initially hindered by the group setting, but ‘high performers’ (those who ended up scoring above the median) managed to largely recover, while ‘low performers’ (those who ended up scoring below the median) never did.

Personality tests carried out after the group task found no significant personality differences between high and low performers, but gender was a significant variable: 10/13 high performers were male, while 11/14 low performers were female (remember, there was no difference in baseline IQ — this is not a case of men being smarter!).

There were significant differences between the high and low performers in activity in the amygdala and the right lateral prefrontal cortex. Specifically, all participants had an initial increase in amygdala activation and diminished activity in the prefrontal cortex, but by the end of the task, the high-performing group showed decreased amygdala activation and increased prefrontal cortex activation, while the low performers didn’t change. This may reflect the high performers’ greater ability to reduce their anxiety. Activity in the nucleus accumbens was similar in both groups, and consistent with the idea that the students had expectations about the relative ranking they were about to receive.

It should be pointed out that the specific feedback given — the relative ranking — was not a factor. What’s important is that it was being given at all, and the high performers were those who became less anxious as time went on, regardless of their specific ranking.

There are three big lessons here. One is that social pressure significantly depresses talent (meetings make you stupid?), and this seems to be worse when individuals perceive themselves to have a lower social rank. The second is that our ability to regulate our emotions is important, and something we should put more energy into. And the third is that we’ve got to shake ourselves loose from the idea that IQ is something we can measure in isolation. Social context matters.

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Reviving a failing sense of smell through training

January, 2012

A rat study reveals how training can improve or impair smell perception.

The olfactory bulb is in the oldest part of our brain. It connects directly to the amygdala (our ‘emotion center’) and our prefrontal cortex, giving smells a more direct pathway to memory than our other senses. But the olfactory bulb is only part of the system processing smells. It projects to several other regions, all of which are together called the primary olfactory cortex, and of which the most prominent member is the piriform cortex. More recently, however, it has been suggested that it would be more useful to regard the olfactory bulb as the primary olfactory cortex (primary in the sense that it is first), while the piriform cortex should be regarded as association cortex — meaning that it integrates sensory information with ‘higher-order’ (cognitive, contextual, and behavioral) information.

Testing this hypothesis, a new rat study has found that, when rats were given training to distinguish various odors, each smell produced a different pattern of electrical activity in the olfactory bulb. However, only those smells that the rat could distinguish from others were reflected in distinct patterns of brain activity in the anterior piriform cortex, while smells that the rat couldn’t differentiate produced identical brain activity patterns there. Interestingly, the smells that the rats could easily distinguish were ones in which one of the ten components in the target odor had been replaced with a new component. The smells they found difficult to distinguish were those in which a component had simply been deleted.

When a new group of rats was given additional training (8 days vs the 2 days given the original group), they eventually learned to discriminate between the odors the first animals couldn’t distinguish, and this was reflected in distinct patterns of brain activity in the anterior piriform cortex. When a third group were taught to ignore the difference between odors the first rats could readily distinguish, they became unable to tell the odors apart, and similar patterns of brain activity were produced in the piriform cortex.

The effects of training were also quite stable — they were still evident after two weeks.

These findings support the idea of the piriform cortex as association cortex. It is here that experience modified neuronal activity. In the olfactory bulb, where all the various odors were reflected in different patterns of activity right from the beginning (meaning that this part of the brain could discriminate between odors that the rat itself couldn’t distinguish), training made no difference to the patterns of activity.

Having said that, it should be noted that this is not entirely consistent with previous research. Several studies have found that odor training produces changes in the representations in the olfactory bulb. The difference may lie in the method of neural recording.

How far does this generalize to the human brain? Human studies have suggested that odors are represented in the posterior piriform cortex rather than the anterior piriform cortex. They have also suggested that the anterior piriform cortex is involved in expectations relating to the smells, rather than representing the smells themselves. Whether these differences reflect species differences, task differences, or methodological differences, remains to be seen.

But whether or not the same exact regions are involved, there are practical implications we can consider. The findings do suggest that one road to olfactory impairment is through neglect — if you learn to ignore differences between smells, you will become increasingly less able to do so. An impaired sense of smell has been found in Alzheimer’s disease, Parkinson's disease, schizophrenia, and even normal aging. While some of that may well reflect impairment earlier in the perception process, some of it may reflect the consequences of neglect. The burning question is, then, would it be possible to restore smell function through odor training?

I’d really like to see this study replicated with old rats.

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Poverty-related stress affects cognitive ability

November, 2011

Stress in the lives of young children from low-income homes negatively affects their executive function and IQ, and these associations are mediated through parenting behavior and household risk.

The study involved 1,292 children followed from birth, whose cortisol levels were assessed at 7, 15, and 24 months. Three tests related to executive functions were given at age 3. Measures of parenting quality (maternal sensitivity, detachment, intrusiveness, positive regard, negative regard, and animation, during interaction with the child) and household environment (household crowding, safety and noise levels) were assessed during the home visits.

Earlier studies have indicated that a poor environment in and of itself is stressful to children, and is associated with increased cortisol levels. Interestingly, in one Mexican study, preschool children in poor homes participating in a conditional cash transfer scheme showed reduced cortisol levels.

This study found that children in lower-income homes received less positive parenting and had higher levels of cortisol in their first two years than children in slightly better-off homes. Higher levels of cortisol were associated with lower levels of executive function abilities, and to a lesser extent IQ, at 3 years.

African American children were more affected than White children on every measure. Cortisol levels were significantly higher; executive function and IQ significantly lower; ratings of positive parenting significantly lower and ratings of negative parenting significantly higher. Maternal education was significantly lower, poverty greater, homes more crowded and less safe.

The model derived from this data shows executive function negatively predicted by cortisol, while the effect on IQ is marginal. However, both executive function and IQ are predicted by negative parenting, positive parenting, and household risk (although this last variable has a greater effect on IQ than executive function). Neither executive function nor IQ was directly predicted by maternal education, ethnicity, or poverty level. Cortisol level was inversely related to positive parenting, but was not directly related to negative parenting or household risk.

Indirectly (according to this best-fit model), poverty was related to executive function through negative parenting; maternal education was related to executive function through negative parenting and to a lesser extent positive parenting; both poverty and maternal education were related to IQ through positive parenting, negative parenting, and household risk; African American ethnicity was related to executive function through negative parenting and positive parenting, and to IQ through negative parenting, positive parenting, and household risk. Cortisol levels were higher in African American children and this was unrelated to poverty level or maternal education.

Executive function (which includes working memory, inhibitory control, and attention shifting) is vital for self-regulation and central to early academic achievement. A link between cortisol level and executive function has previously been shown in preschool children, as well as adults. The association partly reflects the fact that stress hormone levels affect synaptic plasticity in the prefrontal cortex, where executive functions are carried out. This is not to say that this is the only brain region so affected, but it is an especially sensitive one. Chronic levels of stress alter the stress response systems in ways that impair flexible regulation.

What is important about this study is this association between stress level and cognitive ability at an early age, that the effect of parenting on cortisol is associated with positive aspects rather than negative ones, and that the association between poverty and cognitive ability is mediated by both cortisol and parenting behavior — both positive and negative aspects.

A final word should be made on the subject of the higher cortisol levels in African Americans. Because of the lack of high-income African Americans in the sample (a reflection of the participating communities), it wasn’t possible to directly test whether the effect is accounted for by poverty. So this remains a possibility. It is also possible that there is some genetic difference. But it also might reflect other sources of stress, such as that relating to prejudice and stereotype threat.

Based on mother’s ethnic status, 58% of the families were Caucasian and 42% African American. Two-thirds of the participants had an income-to-need ratio (estimated total household income divided by the 2005 federal poverty threshold adjusted for number of household members) less than 200% of poverty. Just over half of the mothers weren’t married, and most of them (89%) had never been married. The home visits at 7, 15, and 24 months lasted at least an hour, and include a videotaped free play or puzzle completion interaction between mother and child. Cortisol samples were taken prior to an emotion challenge task, and 20 minutes and 40 minutes after peak emotional arousal.

Long-term genetic effects of childhood environment

The long-term effects of getting off to a poor start are deeper than you might believe. A DNA study of forty 45-year-old males in a long-running UK study has found clear differences in gene methylation between those who experienced either very high or very low standards of living as children or adults (methylation of a gene at a significant point in the DNA reduces the activity of the gene). More than twice as many methylation differences were associated with the combined effect of the wealth, housing conditions and occupation of parents (that is, early upbringing) than were associated with the current socio-economic circumstances in adulthood (1252 differences as opposed to 545).

The findings may explain why the health disadvantages known to be associated with low socio-economic position can remain for life, despite later improvement in living conditions. The methylation profiles associated with childhood family living conditions were clustered together in large stretches of DNA, which suggests that a well-defined epigenetic pattern is linked to early socio-economic environment. Adult diseases known to be associated with early life disadvantage include coronary heart disease, type 2 diabetes and respiratory disorders.

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[2589] Blair C, Granger DA, Willoughby M, Mills-Koonce R, Cox M, Greenberg MT, Kivlighan KT, Fortunato CK, the Investigators FLP. Salivary Cortisol Mediates Effects of Poverty and Parenting on Executive Functions in Early Childhood. Child Development [Internet]. 2011 :no - no. Available from: http://dx.doi.org/10.1111/j.1467-8624.2011.01643.x

Fernald, L. C., & Gunnar, M. R. (2009). Poverty-alleviation program participation and salivary cortisol in very low-income children. Social Science and Medicine, 68, 2180–2189.

[2590] Borghol N, Suderman M, McArdle W, Racine A, Hallett M, Pembrey M, Hertzman C, Power C, Szyf M. Associations with early-life socio-economic position in adult DNA methylation. International Journal of Epidemiology [Internet]. 2011 . Available from: http://ije.oxfordjournals.org/content/early/2011/10/18/ije.dyr147.abstract

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Cannabis disrupts synchronized brain activity

November, 2011

Effects of a cannabis-like drug on rats explain why cannabis is linked to schizophrenia and how it might impair cognition, as well as supporting our understanding of how working memory works.

Research into the effects of cannabis on cognition has produced inconsistent results. Much may depend on extent of usage, timing, and perhaps (this is speculation) genetic differences. But marijuana abuse is common among sufferers of schizophrenia and recent studies have shown that the psychoactive ingredient of marijuana can induce some symptoms of schizophrenia in healthy volunteers.

Now new research helps explain why marijuana is linked to schizophrenia, and why it might have detrimental effects on attention and memory.

In this rat study, a drug that mimics the psychoactive ingredient of marijuana (by activating the cannabinoid receptors) produced significant disruption in brain networks, with brain activity becoming uncoordinated and inaccurate.

In recent years it has become increasingly clear that synchronized brainwaves play a crucial role in information processing — especially that between the hippocampus and prefrontal cortex (see, for example, my reports last month on theta waves improving retrieval and the effect of running on theta and gamma rhythms). Interactions between the hippocampus and prefrontal cortex seem to be involved in working memory functions, and may provide the mechanism for bringing together memory and decision-making during goal-directed behaviors.

Consistent with this, during decision-making on a maze task, hippocampal theta waves and prefrontal gamma waves were impaired, and the theta synchronization between the two was disrupted. These effects correlated with impaired performance on the maze task.

These findings are consistent with earlier findings that drugs that activate the cannabinoid receptors disrupt the theta rhythm in the hippocampus and impair spatial working memory. This experiment extends that result to coordinated brainwaves beyond the hippocampus.

Similar neural activity is observed in schizophrenia patients, as well as in healthy carriers of a genetic risk variant.

The findings add to the evidence that working memory processes involve coordination between the prefrontal cortex and the hippocampus through theta rhythm synchronization. The findings are consistent with the idea that items are encoded and indexed along the phase of the theta wave into episodic representations and transferred from the hippocampus to the neocortex as a theta phase code. By disrupting that code, cannabis makes it more difficult to retain and index the information relevant to the task at hand.

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