hippocampus

means "sea horse", and is named for its shape. It is one of the oldest parts of the brain, and is buried deep inside, within the limbic lobe. The hippocampus is important for the forming, and perhaps long-term storage, of associative and episodic memories. Specifically, the hippocampus has been implicated in (among other things) the encoding of face-name associations, the retrieval of face-name associations, the encoding of events, the recall of personal memories in response to smells. It may also be involved in the processes by which memories are consolidated during sleep.

What transient amnesia tells us about autobiographical memory and brain plasticity

November, 2011
  • Brain scans of those suffering from transient global amnesia indicate a permanent role of the hippocampus in autobiographical memory, and demonstrate the brain’s ability to self-repair.

When a middle-aged woman loses her memory after sex, it naturally makes the headlines. Many might equate this sort of headline to “Man marries alien”, but this is an example of a rare condition — temporary, you will be relieved to hear — known as transient global amnesia. Such abrupt, localized loss of autobiographical memory is usually preceded by strenuous physical activity or stressful events. It generally occurs in middle-aged or older adults, but has been known to occur in younger people. In those cases, there may be a history of migraine or head trauma.

Following an earlier study in which 29 of 41 TGA patients were found to have small lesions in the CA1 region of the hippocampus, scanning of another 16 TGA patients has revealed 14 had these same lesions. It seems likely that all the patients had such lesions, but because they are very small and don’t last long, they’re easy to miss. The lesion is best seen after 24-72 hours, but is gone after 5-6 days.

At the start of one of these attacks, memory for the first 30 years of life was significantly impaired, but still much better than memory for the years after that. There was a clear temporal gradient, with memory increasingly worse for events closer in time. There was no difference between events in the previous year and events in the previous five years, but a clear jump at that five-year point.

The exact location of the lesions was significant: when the lesion was in the anterior part of the region, memory for recent events was more impaired.

The hippocampus is known to be crucially involved in episodic memory (memory for events), and an integral part of the network for autobiographical memory. In recent years, it has come to be thought that such memories are only hosted temporarily by the hippocampus, and over a few years come to be permanently lodged in the neocortex (the standard consolidation model). Evidence from a number of studies of this change at the five-year mark has been taken as support for this theory. According to this, then, older memories should be safe from hippocampal damage.

An opposing theory, however, is that the hippocampus continues to be involved in such memories, with both the neocortex and the hippocampus involved in putting together reconsolidated memories (the multiple trace model). According to this model, each retrieval of an episodic memory creates a new version in the hippocampus. The more versions, the better protected a memory will be from any damage to the hippocampus.

The findings from this study show that while there is indeed a significant difference between older and more recent memories, the CA1 region of the hippocampus continues to be crucial for retrieving older memories, and for our sense of self-continuity.

Interestingly, some studies have also found a difference between the left and right hemispheres, with the right hippocampus showing a temporal gradient and the left hippocampus showing constant activation across all time periods. Such a hemisphere difference was not found in the present study. The researchers suggest that the reason may lie in the age of the participants (average age was 68), reflecting a reduction in hemispheric asymmetry with age.

There’s another message in this study. In these cases of TGA, memory function is restored within 24 hours (and generally sooner, within 6-10 hours). This shows how fast the brain can repair damage. Similarly, the fact that such tiny lesions have temporary effects so much more dramatic than the more lasting effects of larger lesions, is also a tribute to the plasticity of the brain.

The findings are consistent with findings of a preferential degeneration of CA1 neurons in the early stages of Alzheimer's disease, and suggest a target for treatment.

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Common health complaints increase Alzheimer's risk

October, 2011

Two large studies respectively find that common health complaints and irregular heartbeat are associated with an increased risk of developing Alzheimer’s, while a rat study adds to evidence that stress is also a risk factor.

A ten-year study involving 7,239 older adults (65+) has found that each common health complaint increased dementia risk by an average of about 3%, and that these individual risks compounded. Thus, while a healthy older adult had about an 18% chance of developing dementia after 10 years, those with a dozen of these health complaints had, on average, closer to a 40% chance.

It’s important to note that these complaints were not for serious disorders that have been implicated in Alzheimer’s. The researchers constructed a ‘frailty’ index, involving 19 different health and wellbeing factors: overall health, eyesight, hearing, denture fit, arthritis/rheumatism, eye trouble, ear trouble, stomach trouble, kidney trouble, bladder control, bowel control, feet/ankle trouble, stuffy nose/sneezing, bone fractures, chest problems, cough, skin problems, dental problems, other problems.

Not all complaints are created equal. The most common complaint — arthritis/rheumatism —was only slightly higher among those with dementia. Two of the largest differences were poor eyesight (3% of the non-demented group vs 9% of those with dementia) and poor hearing (3% and 6%).

At the end of the study, 4,324 (60%) were still alive, and of these, 416 (9.6%) had Alzheimer's disease, 191 (4.4%) had another sort of dementia and 677 (15.7%) had other cognitive problems (but note that 1,023 were of uncertain cognitive ability).

While these results need to be confirmed in other research — the study used data from broader health surveys that weren’t specifically designed for this purpose, and many of those who died during the study will have probably had dementia — they do suggest the importance of maintaining good general health.

Common irregular heartbeat raises risk of dementia

In another study, which ran from 1994 to 2008 and followed 3,045 older adults (mean age 74 at study start), those with atrial fibrillation were found to have a significantly greater risk of developing Alzheimer’s.

At the beginning of the study, 4.3% of the participants had atrial fibrillation (the most common kind of chronically irregular heartbeat); a further 12.2% developed it during the study. Participants were followed for an average of seven years. Over this time, those with atrial fibrillation had a 40-50% higher risk of developing dementia of any type, including probable Alzheimer's disease. Overall, 18.8% of the participants developed some type of dementia during the course of the study.

While atrial fibrillation is associated with other cardiovascular risk factors and disease, this study shows that atrial fibrillation increases dementia risk more than just through this association. Possible mechanisms for this increased risk include:

  • weakening the heart's pumping ability, leading to less oxygen going to the brain;
  • increasing the chance of tiny blood clots going to the brain, causing small, clinically undetected strokes;
  • a combination of these plus other factors that contribute to dementia such as inflammation.

The next step is to see whether any treatments for atrial fibrillation reduce the risk of developing dementia.

Stress may increase risk for Alzheimer's disease

And a rat study has shown that increased release of stress hormones leads to cognitive impairment and that characteristic of Alzheimer’s disease, tau tangles. The rats were subjected to stress for an hour every day for a month, by such means as overcrowding or being placed on a vibrating platform. These rats developed increased hyperphosphorylation of tau protein in the hippocampus and prefrontal cortex, and these changes were associated with memory deficits and impaired behavioral flexibility.

Previous research has shown that stress leads to that other characteristic of Alzheimer’s disease: the formation of beta-amyloid.

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Timing of estrogen therapy is crucial

October, 2011

A rat study provides further evidence that the conflicting findings on the benefit of estrogen therapy stem from the importance of timing.

The very large and long-running Women's Health Initiative study surprised everyone when it produced its finding that hormone therapy generally increased rather than decreased stroke risk as well as other health problems. But one explanation for that finding might be that many of the women only received hormone replacement therapy years after menopause. There are indications that timing is crucial.

This new rat study involved female rats equivalent to human 60-65 year olds, about a decade past menopause.  An enzyme called CHIP (carboxyl terminus of Hsc70 interacting protein) was found to increase binding with estrogen receptors, resulting in about half the receptors getting hauled to the cell's proteosome to be chopped up and degraded. When some of the aged rats were later treated with estrogen, mortality increased. When middle-aged rats were treated with estrogen, on the other hand, results were positive.

In other words, putting in extra estrogen after the number of estrogen receptors in the brain has been dramatically decreased is a bad idea.

While this study focused on mortality, other research has produced similar conflicting results as to whether estrogen therapy helps fight age-related cognitive impairment in women (see my report). It’s interesting to note that this effect only occurred in the hippocampus — estrogen receptors in the uterus were unaffected.

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One cause of damage in older brains, and how exercise can help

September, 2011

Two mice studies indicate that an increase in a protein involved in immune response may be behind the reduced ability of older brains to create new neurons, and that exercise produces a protein that helps protect against damage caused by illness, injury, surgery and pollutants.

In the first mouse study, when young and old mice were conjoined, allowing blood to flow between the two, the young mice showed a decrease in neurogenesis while the old mice showed an increase. When blood plasma was then taken from old mice and injected into young mice, there was a similar decrease in neurogenesis, and impairments in memory and learning.

Analysis of the concentrations of blood proteins in the conjoined animals revealed the chemokine (a type of cytokine) whose level in the blood showed the biggest change — CCL11, or eotaxin. When this was injected into young mice, they indeed showed a decrease in neurogenesis, and this was reversed once an antibody for the chemokine was injected. Blood levels of CCL11 were found to increase with age in both mice and humans.

The chemokine was a surprise, because to date the only known role of CCL11 is that of attracting immune cells involved in allergy and asthma. It is thought that most likely it doesn’t have a direct effect on neurogenesis, but has its effect through, perhaps, triggering immune cells to produce inflammation.

Exercise is known to at least partially reverse loss of neurogenesis. Exercise has also been shown to produce chemicals that prevent inflammation. Following research showing that exercise after brain injury can help the brain repair itself, another mouse study has found that mice who exercised regularly produced interleukin-6 (a cytokine involved in immune response) in the hippocampus. When the mice were then exposed to a chemical that destroys the hippocampus, the interleukin-6 dampened the harmful inflammatory response, and prevented the loss of function that is usually observed.

One of the actions of interleukin-6 that brings about a reduction in inflammation is to inhibit tumor necrosis factor. Interestingly, I previously reported on a finding that inhibiting tumor necrosis factor in mice decreased cognitive decline that often follows surgery.

This suggests not only that exercise helps protect the brain from the damage caused by inflammation, but also that it might help protect against other damage, such as that caused by environmental toxins, injury, or post-surgical cognitive decline. The curry spice cucurmin, and green tea, are also thought to inhibit tumor necrosis factor.

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More ways exercise can help seniors fight memory loss

September, 2011

A recent study finds that cognitive decline is greater in older adults who have a high salt intake —but only if they’re not physically active. Another finds that older rats who exercise are protected from memory loss caused by bacterial infection.

A three-year study following 1,262 healthy older Canadians (aged 67-84) has found that, among those who exercised little, those who had high-salt diets showed significantly greater cognitive decline. On the bright side, sedentary older adults who had low-salt consumption did not show cognitive decline over the three years. And those who had higher levels of physical activity did not show any association between salt and cognition.

Low sodium intake is associated with reduced blood pressure and risk of heart disease, adding even more weight to the mantra: what’s good for the heart is good for the brain.

The analysis controlled for age, sex, education, waist circumference, diabetes, and dietary intakes. Salt intake was based on a food frequency questionnaire. Low sodium intake was defined as not exceeding 2,263 mg/day; mid sodium intake 3,090 mg/day; and high sodium intake 3,091 and greater mg/day. A third of the participants fell into each group. Physical activity was also measured by a self-reported questionnaire (Physical Activity Scale for the Elderly). Cognitive function was measured by the Modified MMSE.

And adding to the evidence that exercise is good for you (not that we really need any more!), a rat study has found that aging rats that ran just over half a kilometer each week were protected against long-term memory loss that can happen suddenly following bacterial infection.

Previous research found that older rats experienced memory loss following E. coli infection, but young adult rats did not. In the older animals, microglia (the brain’s immune cells) were more sensitive to infection, releasing greater quantities of inflammatory molecules called cytokines in the hippocampus. This exaggerated response brought about impairments in synaptic plasticity (the neural changes that underlie learning) and reductions in BDNF.

In this study, the rats were given unlimited access to running wheels. Although the old rats only ran an average of 0.43 miles per week (50 times less distance than the young rats), they performed better on a memory test than rats who only had access to a locked exercise wheel. Moreover, the runners performed as well on the memory test as rats that were not exposed to E. coli.

The researchers are now planning to examine the role that stress hormones may play in sensitizing microglia, and whether physical exercise slows these hormones in older rats.

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Brain prosthetic restores learning capability in rats

September, 2011

Effective patterns of neural activity replayed via an artificial device inserted in the hippocampus restores lost learning capability and even improves learning in normal rats.

In the experiment, rats learned which lever to press to receive water, where the correct lever depended on which lever they had pressed previously (the levers were retractable; there was a variable delay between the first and second presentation of the levers). Microelectrodes in the rats’ brains provided data that enabled researchers to work out the firing patterns of neurons in CA1 that resulted from particular firing patterns in CA3 (previous research had established that long-term memory involves CA3 outputs being received in CA1).

Normal neural communication between these two subregions of the hippocampus was then chemically inhibited. While the rats still remembered the general rule, and still remembered that pressing the levers would gain them water, they could only remember which lever they had pressed for 5-10 seconds.

An artificial hippocampal system that could reproduce effective firing patterns (established in earlier training) was then implanted in the rats’ brains and long-term memory function was restored. Furthermore, when the ‘memory prosthetic’ was implanted in animals whose hippocampus was functioning normally, their memory improved.

The findings open up amazing possibilities for ameliorating brain damage. There is of course the greatly limiting factor that effective memory traces (spatiotemporal firing patterns) need to be recorded for each activity. This will be particularly problematic for individuals with significant damage. Perhaps one day we will all ‘record’ ourselves as a matter of course, in the same way that we might put by blood or genetic material ‘in case’! Still, it’s an exciting development.

The next step will be to repeat these results in monkeys.

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Running faster changes brain rhythms associated with learning

September, 2011

A mouse study finds that gamma waves in the hippocampus, critically involved in learning, grow stronger as mice run faster.

I’ve always felt that better thinking was associated with my brain working ‘in a higher gear’ — literally working at a faster rhythm. So I was particularly intrigued by the findings of a recent mouse study that found that brainwaves associated with learning became stronger as the mice ran faster.

In the study, 12 male mice were implanted with microelectrodes that monitored gamma waves in the hippocampus, then trained to run back and forth on a linear track for a food reward. Gamma waves are thought to help synchronize neural activity in various cognitive functions, including attention, learning, temporal binding, and awareness.

We know that the hippocampus has specialized ‘place cells’ that record where we are and help us navigate. But to navigate the world, to create a map of where things are, we need to also know how fast we are moving. Having the same cells encode both speed and position could be problematic, so researchers set out to find how speed was being encoded. To their surprise and excitement, they found that the strength of the gamma rhythm grew substantially as the mice ran faster.

The results also confirmed recent claims that the gamma rhythm, which oscillates between 30 and 120 times a second, can be divided into slow and fast signals (20-45 Hz vs 45-120 Hz for mice, consistent with the 30-55 Hz vs 45-120 Hz bands found in rats) that originate from separate parts of the brain. The slow gamma waves in the CA1 region of the hippocampus were synchronized with slow gamma waves in CA3, while the fast gamma in CA1 were synchronized with fast gamma waves in the entorhinal cortex.

The two signals became increasingly separated with increasing speed, because the two bands were differentially affected by speed. While the slow waves increased linearly, the fast waves increased logarithmically. This differential effect could have to do with mechanisms in the source regions (CA3 and the medial entorhinal cortex, respectively), or to mechanisms in the different regions in CA1 where the inputs terminate (the waves coming from CA3 and the entorhinal cortex enter CA1 in different places).

In the hippocampus, gamma waves are known to interact with theta waves. Further analysis of the data revealed that the effects of speed on gamma rhythm only occurred within a narrow range of theta phases — but this ‘preferred’ theta phase also changed with running speed, more so for the slow gamma waves than the fast gamma waves (which is not inconsistent with the fact that slow gamma waves are more affected by running speed than fast gamma waves). Thus, while slow and fast gamma rhythms preferred similar phases of theta at low speeds, the two rhythms became increasingly phase-separated with increasing running speed.

What’s all this mean? Previous research has shown that if inputs from CA3 and the entorhinal cortex enter CA1 at the same time, the kind of long-term changes at the synapses that bring about learning are stronger and more likely in CA1. So at low speeds, synchronous inputs from CA3 and the entorhinal cortex at similar theta phases make them more effective at activating CA1 and inducing learning. But the faster you move, the more quickly you need to process information. The stronger gamma waves may help you do that. Moreover, the theta phase separation of slow and fast gamma that increases with running speed means that activity in CA3 (slow gamma source) increasingly anticipates activity in the medial entorhinal cortex (fast gamma source).

What does this mean at the practical level? Well at this point it can only be speculation that moving / exercising can affect learning and attention, but I personally am taking this on board. Most of us think better when we walk. This suggests that if you’re having trouble focusing and don’t have time for that, maybe walking down the hall or even jogging on the spot will help bring your brain cells into order!

Pushing speculation even further, I note that meditation by expert meditators has been associated with changes in gamma and theta rhythms. And in an intriguing comparison of the effect of spoken versus sung presentation on learning and remembering word lists, the group that sang showed greater coherence in both gamma and theta rhythms (in the frontal lobes, admittedly, but they weren’t looking elsewhere).

So, while we’re a long way from pinning any of this down, it may be that all of these — movement, meditation, music — can be useful in synchronizing your brain rhythms in a way that helps attention and learning. This exciting discovery will hopefully be the start of an exploration of these possibilities.

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Preventing interference between topics or skills

September, 2011

Learning two tasks or subjects one after another typically leads to poorer remembering of the first. A new study indicates the cause and suggests a remedy.

Trying to learn two different things one after another is challenging. Almost always some of the information from the first topic or task gets lost. Why does this happen? A new study suggests the problem occurs when the two information-sets interact, and demonstrates that disrupting that interaction prevents interference. (The study is a little complicated, but bear with me, or skip to the bottom for my conclusions.)

In the study, young adults learned two memory tasks back-to-back: a list of words, and a finger-tapping motor skills task. Immediately afterwards, they received either sham stimulation or real transcranial magnetic stimulation to the dorsolateral prefrontal cortex or the primary motor cortex. Twelve hours later the same day, they were re-tested.

As expected from previous research, word recall (being the first-learned task) declined in the control condition (sham stimulation), and this decline correlated with initial skill in the motor task. That is, the better they were at the second task, the more they forgot from the first task. This same pattern occurred among those whose motor cortex had been stimulated. However, there was no significant decrease in word recall for those who had received TMS to the dorsolateral prefrontal cortex.

Learning of the motor skill didn't differ between the three groups, indicating that this effect wasn't due to a disruption of the second task. Rather, it seems that the two tasks were interacting, and TMS to the DLPFC disrupted that interaction. This hypothesis was supported when the motor learning task was replaced by a motor performance task, which shouldn’t interfere with the word-learning task (the motor performance task was almost identical to the motor learning task except that it didn’t have a repeating sequence that could be learned). In this situation, TMS to the DLPFC produced a decrease in word recall (as it did in the other conditions, and as it would after a word-learning task without any other task following).

In the second set of experiments, the order of the motor and word tasks was reversed. Similar results occurred, with this time stimulation to the motor cortex being the effective intervention. In this case, there was a significant increase in motor skill on re-testing — which is what normally happens when a motor skill is learned on its own, without interference from another task (see my blog post on Mempowered for more on this). The word-learning task was then replaced with a vowel-counting task, which produced a non-significant trend toward a decrease in motor skill learning when TMS was applied to the motor cortex.

The effect of TMS depends on the activity in the region at the time of application. In this case, TMS was applied to the primary motor cortex and the DLPFC in the right hemisphere, because the right hemisphere is thought to be involved in integrating different types of information. The timing of the stimulation was critical: not during learning, and long before testing. The timing was designed to maximize any effects on interference between the two tasks.

The effect in this case mimics that of sleep — sleeping between tasks reduces interference between them. It’s suggested that both TMS and sleep reduce interference by reducing the communication between the prefrontal cortex and the mediotemporal lobe (of which the hippocampus is a part).

Here’s the problem: we're consolidating one set of memories while encoding another. So, we can do both at the same time, but as with any multitasking, one task is going to be done better than the other. Unsurprisingly, encoding appears to have priority over consolidation.

So something needs to regulate the activity of these two concurrent processes. Maybe something looks for commonalities between two actions occurring at the same time — this is, after all, what we’re programmed to do: we link things that occur together in space and time. So why shouldn’t that occur at this level too? Something’s just happened, and now something else is happening, and chances are they’re connected. So something in our brain works on that.

If the two events/sets of information are connected, that’s a good thing. If they’re not, we get interference, and loss of data.

So when we apply TMS to the prefrontal cortex, that integrating processor is perhaps disrupted.

The situation may be a little different where the motor task is followed by the word-list, because motor skill consolidation (during wakefulness at least) may not depend on the hippocampus (although declarative encoding does). However, the primary motor cortex may act as a bridge between motor skills and declarative memories (think of how we gesture when we explain something), and so it may this region that provides a place where the two types of information can interact (and thus interfere with each other).

In other words, the important thing appears to be whether consolidation of the first task occurs in a region where the two sets of information can interact. If it does, and assuming you don’t want the two information-sets to interact, then you want to disrupt that interaction.

Applying TMS is not, of course, a practical strategy for most of us! But the findings do suggest an approach to reducing interference. Sleep is one way, and even brief 20-minute naps have been shown to help learning. An intriguing speculation (I just throw this out) is that meditation might act similarly (rather like a sorbet between courses, clearing the palate).

Failing a way to disrupt the interaction, you might take this as a warning that it’s best to give your brain time to consolidate one lot of information before embarking on an unrelated set — even if it's in what appears to be a completely unrelated domain. This is particularly so as we get older, because consolidation appears to take longer as we age. For children, on the other hand, this is not such a worry. (See my blog post on Mempowered for more on this.)

Reference: 

[2338] Cohen, D. A., & Robertson E. M.
(2011).  Preventing interference between different memory tasks.
Nat Neurosci. 14(8), 953 - 955.

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Theta brainwaves improve remembering

September, 2011

New research suggests that successful retrieval depends not only on retrieval cues, but also on your preceding brain state.

What governs whether or not you’ll retrieve a memory? I’ve talked about the importance of retrieval cues, of the match between the cue and the memory code you’re trying to retrieve, of the strength of the connections leading to the code. But these all have to do with the memory code.

Theta brainwaves, in the hippocampus especially, have been shown to be particularly important in memory function. It has been suggested that theta waves before an item is presented for processing lead to better encoding. Now a new study reveals that, when volunteers had to memorize words with a related context, they were better at later remembering the context of the word if high theta waves were evident in their brains immediately before being prompted to remember the item.

In the study, 17 students made pleasantness or animacy judgments about a series of words. Shortly afterwards, they were presented with both new and studied words, and asked to indicate whether the word was old or new, and if old, whether the word had been encountered in the context of “pleasant” or “alive”. Each trial began with a 1000 ms presentation of a simple mark for the student to focus on. Theta activity during this fixation period correlated with successful retrieval of the episodic memory relating to that item, and larger theta waves were associated with better source memory accuracy (memory for the context).

Theta activity has not been found to be particularly associated with greater attention (the reverse, if anything). It seems more likely that theta activity reflects a state of mind that is oriented toward evaluating retrieval cues (“retrieval mode”), or that it reflects reinstatement of the contextual state employed during study.

The researchers are currently investigating whether you can deliberately put your brain into a better state for memory recall.

Reference: 

[2333] Addante, R. J., Watrous A. J., Yonelinas A. P., Ekstrom A. D., & Ranganath C.
(2011).  Prestimulus theta activity predicts correct source memory retrieval.
Proceedings of the National Academy of Sciences. 108(26), 10702 - 10707.

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Adolescent binge drinking can damage spatial working memory

August, 2011
  • This study finds that adolescent females are particularly vulnerable to the effects of binge drinking, and points to specific changes in brain activation patterns seen in binge drinkers.

Binge drinking occurs most frequently among young people, and there has been concern that consequences will be especially severe if the brain is still developing, as it is in adolescence. Because of the fact that it is only some parts of the brain — most crucially the prefrontal cortex and the hippocampus — that are still developing, it makes sense that only some functions will be affected.

I recently reported on a finding that binge drinking university students, performed more poorly on tests of verbal memory, but not on a test of visual memory. A new study looks at another function: spatial working memory. This task involves the hippocampus, and animal research has indicated that this region may be especially vulnerable to binge drinking. Spatial working memory is involved in such activities as driving, figural reasoning, sports, and navigation.

The study involved 95 adolescents (aged 16-19) from San Diego-area public schools: 40 binge drinking (27 males, 13 females) and 55 control (31 males, 24 females). Brain scans while performing a spatial working memory task revealed that there were significant gender differences in brain activation patterns for those who engaged in binge drinking. Specifically, in eight regions spanning the frontal cortex, anterior cingulate, temporal cortex, and cerebellum, female binge drinkers showed less activation than female controls, while male bingers exhibited greater activation than male controls. For female binge drinkers, less activation was associated with poorer sustained attention and working memory performances, while for male binge drinkers, greater activation was linked to better spatial performance.

The differences between male binge drinkers and controls were smaller than that seen in the female groups, suggesting that female teens may be particularly vulnerable. This is not the first study to find a gender difference in the brains’ response to excess alcohol. In this case it may have to do, at least partly, with differences in maturity — female brains mature earlier than males’.

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