The role of consolidation in memory

"Consolidation" is a term that is bandied about a lot in recent memory research. Here's my take on what it means.

Becoming a memory

Initially, information is thought to be encoded as patterns of neural activity — cells "talking" to each other. Later, the information is coded in more persistent molecular or structural formats (e.g., the formation of new synapses). It has been assumed that once this occurs, the memory is "fixed" — a permanent, unchanging, representation.

With new techniques, it has indeed become possible to observe these changes (you can see videos here). Researchers found that the changes to a cell that occurred in response to an initial stimulation lasted some three to five minutes and disappeared within five to 10 minutes. If the cell was stimulated four times over the course of an hour, however, the synapse would actually split and new synapses would form, producing a (presumably) permanent change.

Memory consolidation theory

The hypothesis that new memories consolidate slowly over time was proposed 100 years ago, and continues to guide memory research. In modern consolidation theory, it is assumed that new memories are initially 'labile' and sensitive to disruption before undergoing a series of processes (e.g., glutamate release, protein synthesis, neural growth and rearrangement) that render the memory representations progressively more stable. It is these processes that are generally referred to as “consolidation”.

Recently, however, the idea has been gaining support that stable representations can revert to a labile state on reactivation.

Memory as reconstruction

In a way, this is not surprising. We already have ample evidence that retrieval is a dynamic process during which new information merges with and modifies the existing representation — memory is now seen as reconstructive, rather than a simple replaying of stored information

Reconsolidation of memories

Researchers who have found evidence that supposedly stable representations have become labile again after reactivation, have called the process “reconsolidation”, and suggest that consolidation, rather than being a one-time event, occurs repeatedly every time the representation is activated.

This raises the question: does reconsolidation involve replacing the previously stable representation, or the establishment of a new representation, that coexists with the old?

Whether reconsolidation is the creating of a new representation, or the modifying of an old, is this something other than the reconstruction of memories as they are retrieved? In other words, is this recent research telling us something about consolidation (part of the encoding process), or something about reconstruction (part of the retrieval process)?

Hippocampus involved in memory consolidation

The principal player in memory consolidation research, in terms of brain regions, is the hippocampus. The hippocampus is involved in the recognition of place and the consolidation of contextual memories, and is part of a region called the medial temporal lobe (MTL), that also includes the perirhinal, parahippocampal,and entorhinal cortices. Lesions in the medial temporal lobe typically produce amnesia characterized by the disproportionate loss of recently acquired memories. This has been interpreted as evidence for a memory consolidation process.

Some research suggests that the hippocampus may participate only in consolidation processes lasting a few years. The entorhinal cortex, on the other hand, gives evidence of temporally graded changes extending up to 20 years, suggesting that it is this region that participates in memory consolidation over decades. The entorhinal cortex is damaged in the early stages of Alzheimer’s disease.

There is, however, some evidence that the hippocampus can be involved in older memories — perhaps when they are particularly vivid.

A recent idea that has been floated suggests that the entorhinal cortex, through which all information passes on its way to the hippocampus, handles “incremental learning” — learning that requires repeated experiences. “Episodic learning” — memories that are stored after only one occurrence — might be mainly stored in the hippocampus.

This may help explain the persistence of some vivid memories in the hippocampus. Memories of emotionally arousing events tend to be more vivid and to persist longer than do memories of neutral or trivial events, and are, moreover, more likely to require only a single experience.

Whether or not the hippocampus may retain some older memories, the evidence that some memories might be held in the hippocampus for several years, only to move on, as it were, to another region, is another challenge to a simple consolidation theory.

Memory more complex than we thought

So where does all this leave us? What is consolidation? Do memories reach a fixed state?

My own feeling is that, no, memories don't reach this fabled "cast in stone" state. Memories are subject to change every time they are activated (such activation doesn't have to bring the memory to your conscious awareness). But consolidation traditionally (and logically) refers to encoding processes. It is reasonable, and useful, to distinguish between:

  • the initial encoding, the "working memory" state, when new information is held precariously in shifting patterns of neural activity,
  • the later encoding processes, when the information is consolidated into a more permanent form with the growth of new connections between nerve cells,
  • the (possibly much) later retrieval processes, when the information is retrieved in, most probably, a new context, and is activated anew

I think that "reconsolidation" is a retrieval process rather than part of the encoding processes, but of course, if you admit retrieval as involving a return to the active state and a modification of the original representation in line with new associations, then the differences between retrieval and encoding become less evident.

When you add to this the possibility that memories might "move" from one area of the brain to another after a certain period of time (although it is likely that the triggering factor is not time per se), then you cast into disarray the whole concept of memories becoming stable.

Perhaps our best approach is to see memory as a series of processes, and consolidation as an agreed-upon (and possibly arbitrary) subset of those processes.


  • Frankland, P.W., O'Brien, C., Ohno, M., Kirkwood, A. & Silva, A.J. 2001. -CaMKII-dependent plasticity in the cortex is required for permanent memory. Nature, 411, 309-313.
  • Gluck, M.A., Meeter, M. & Myers, C.E. 2003. Computational models of the hippocampal region: linking incremental learning and episodic memory. Trends in Cognitive Sciences, 7 (6), 269-276.
  • Haist, F., Gore, J.B. & Mao, H. 2001. Consolidation of human memory over decades revealed by functional magnetic resonance imaging. Nature neuroscience, 4 (11), 1139-1145.
  • Kang, H., Sun, L.D., Atkins, C.M., Soderling, T.R., Wilson, M.A. & Tonegawa, S. (2001). An Important Role of Neural Activity-Dependent CaMKIV Signaling in the Consolidation of Long-Term Memory. Cell, 106, 771-783.
  • Lopez, J.C. 2000. Shaky memories in indelible ink. Nature Reviews Neuroscience, 1, 6-7.
  • Miller, R.R. & Matzel, L.D. 2000. Memory involves far more than 'consolidation'. Nature Reviews Neuroscience, 1, 214-216.
  • Slotnick, S.D., Moo, L.R., Kraut, M.A., Lesser, R.P. & Hart, J. Jr. 2002. Interactions between thalamic and cortical rhythms during semantic memory recall in human. Proc. Natl. Acad. Sci. U.S.A., 99, 6440-6443.
  • Spinney, L. 2002. Memory debate focuses on hippocampal role. BioMedNet News, 18 March 2002.
  • Wirth, S., Yanike, M., Frank, L.M., Smith, A.C., Brown, E.N. & Suzuki, W.A. 2003. Single Neurons in the Monkey Hippocampus and Learning of New Associations. Science, 300, 1578-1581.
  • Zeineh, M.M., Engel, S.A., Thompson, P.M. & Bookheimer, S.Y. 2003. Dynamics of the Hippocampus During Encoding and Retrieval of Face-Name Pairs, Science, 299, 577-580.

For more, see the research reports


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Improve learning with co-occurring novelty

  • An animal study shows that following learning with a novel experience makes the learning stronger.
  • A human study shows that giving information positive associations improves your memory for future experiences with similar information.

We know that the neurotransmitter dopamine is involved in making strong memories. Now a mouse study helps us get more specific — and suggests how we can help ourselves learn.

The study, involving 120 mice, found that mice tasked with remembering where food had been hidden did better if they had been given a novel experience (exploring an unfamiliar floor surface) 30 minutes after being trained to remember the food location.

This memory improvement also occurred when the novel experience was replaced by the selective activation of dopamine-carrying neurons in the locus coeruleus that go to the hippocampus. The locus coeruleus is located in the brain stem and involved in several functions that affect emotion, anxiety levels, sleep patterns, and memory. The dopamine-carrying neurons in the locus coeruleus appear to be especially sensitive to environmental novelty.

In other words, if we’re given attention-grabbing experiences that trigger these LC neurons carrying dopamine to the hippocampus at around the time of learning, our memories will be stronger.

Now we already know that emotion helps memory, but what this new study tells us is that, as witness to the mice simply being given a new environment to explore, these dopamine-triggering experiences don’t have to be dramatic. It’s suggested that it could be as simple as playing a new video game during a quick break while studying for an exam, or playing tennis right after trying to memorize a big speech.

Remember that we’re designed to respond to novelty, to pay it more attention — and, it seems, that attention is extended to more mundane events that occur closely in time.

Emotionally positive situations boost memory for similar future events

In a similar vein, a human study has found that the benefits of reward extend forward in time.

In the study, volunteers were shown images from two categories (objects and animals), and were financially rewarded for one of these categories. As expected, they remembered images associated with a reward better. In a second session, however, they were shown new images of animals and objects without any reward. Participants still remembered the previously positively-associated category better.

Now, this doesn’t seem in any way surprising, but the interesting thing is that this benefit wasn’t seen immediately, but only after 24 hours — that is, after participants had slept and consolidated the learning.

Previous research has shown similar results when semantically related information has been paired with negative, that is, aversive stimuli.



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Sleep helps you remember new names

  • A small study has found that a night's sleep helps you better remember new names.

Sleep, as I have said on many occasions, helps your brain consolidate new memories. I have reported before on a number of studies showing how sleep helps the learning of various types of new information. Most of those studies have looked at procedural learning (learning new skills), or verbal learning. A new study adds to these by looking at face-name associations.

The small study, involving 14 young adults, found that that they were significantly better at remembering faces and names if they were given an opportunity to have a full night's sleep hours after seeing those faces and names for the first time.

Participants were shown 20 photos of faces with corresponding names and asked to memorize them. After a twelve-hour period, they were then shown the photos again with either a correct or incorrect name. They were also asked to rate their confidence in their answer. Each participant completed the test twice — once with an interval of sleep in between and once with a period of regular, waking day activities in between.

After a night's sleep, participants correctly matched 12% more of the faces and names, and were much more confident of their answers.

Of course, this is not a huge difference, given the small number of face-name pairs, and the sample is small. I would have also liked to see further testing 12 hours later, so that we could compare the effects of a day followed by a night, versus a night followed by a day (this would have required more stimuli and more participants, of course).

So, not madly exciting, but taken in context of other research, it adds to the growing evidence that sleep helps you consolidate new learning of all kinds.



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Older news items (pre-2010) brought over from the old website

Reactivating single memory does not affect associated memories

Recent studies have indicated that consolidated memories can in fact be manipulated when reactivated. This process, often referred to as reconsolidation, has been proposed as a possible way of treating traumatic memories. But one concern is that reactivating and disrupting a single memory may also affect other associated memories. A new rat study has found that only those memories directly reactivated are vulnerable, not those associated to them.

Debiec, J., Doyère, V., Nader, K. & LeDoux, J.E. 2006. Directly reactivated, but not indirectly reactivated, memories undergo reconsolidation in the amygdala. Proceedings of the National Academy of Sciences, 103 (9), 3428-3433.

Protein found to inhibit conversion to long-term memory

In a study using genetically engineered mice, researchers have found that mice without a protein called GCN2 acquire new information that doesn’t fade as easily as it does in normal mice. After weak training on the Morris water maze, their spatial memory was enhanced, but it was impaired after more intense training. The researchers concluded that GCN2 may prevent new information from being stored in long-term memory, suggesting the conversion of new information into long-term memory requires both the activation of molecules that facilitate memory storage, and the silencing of proteins such as GCN2 that inhibit memory storage.

Wingfield, A., Tun, P.A. & McCoy, S.L. 2005. Hearing Loss in Older Adulthood: What It Is and How It Interacts With Cognitive Performance. Current Directions in Psychological Science, 14(3), 144-148.

New theory challenges current view of how brain stores long-term memory

The current view of long-term memory storage is that, at the molecular level, new proteins are manufactured (a process known as translation), and these newly synthesized proteins subsequently stabilize the changes underlying the memory. Thus, every new memory results in a permanent representation in the brain. A new theory of memory storage suggests instead that there is no permanent representation. Rather, memories are copied across many different brain networks. The advantage is that it is a highly flexible system, enabling rapid retrieval even of infrequent elements.
The theory suggests that the brain stores long-term memory by rapidly changing the shape of proteins already present at those synapses activated by learning. The theory explains a number of phenomena that are not properly answered by the existing theory. The theory doesn’t disagree with the view that it is the synapse that is modified in response to learning; the disagreement concerns how that synaptic modification occurs. Current theory says it is brought about by recently synthesized proteins; the new theory suggests that learning leads to a post-synthesis (post-translational) synaptic protein modification that results in changes to the shape, activity and/or location of existing synaptic proteins. It is suggested that long-term memory storage relies on a positive-feedback rehearsal system that continually updates or fine-tunes post-translational modification of previously modified synaptic proteins, thus allowing for the continual modifications of memories.

Routtenberg, A. & Rekart, J.L. 2005. Post-translational protein modification as the substrate for long-lasting memory. Trends in Neurosciences, 28 (1), 12-19.

Brain circuit crucial for memory consolidation identified

A rat study has identified a circuit in the brain that appears crucial in converting short-term memories into long-term memories. The circuit is the temporoammonic (TA) projection, which directly links the CA1 region of the hippocampus and the neocortex.

Remondes, M. &Schuman, E.M. 2004. Role for a cortical input to hippocampal area CA1 in the consolidation of a long-term memory.Nature, 431, 699 - 703.

Confirmation that a memory code is held in many different regions

Mapping of brain activity patterns has cast new light on how our memories integrate sights, smells, tastes, and sounds. Previous research has shown that the visual and auditory brain regions are activated during memories of pictures and sounds. A new imaging study investigated taste and smell. Volunteers were presented with random combinations of an odor and the image of an object and asked to imagine a link or story that associated the two. They were then presented with a series of both previously seen images and new images and asked to recall whether they were viewing new or old images. It was found that the region involved in processing smells, the piriform cortex, was activated when participants saw objects previously associated with odors. On questioning, participants said they recalled the story linking image and smell, but had not tried to summon up the smell itself. These findings confirm models of memory recall in which the sensory-specific components of a memory are preserved in the sensory-related brain regions, and the hippocampus draws on those components to reconstruct a sensory-rich memory (as opposed to the complete memory being stored in one place). This allows memories to be recalled from one sensory cue.

Gottfried, J.A., Smith, A.P.R., Rugg, M.D. & Dolan, R.J. 2004. Remembrance of Odors Past: Human Olfactory Cortex in Cross-Modal Recognition Memory. Neuron, 42 (4), 687-695.

Memories are harder to forget than recently thought

Previous rodent studies have shown that the process of encoding a memory can be blocked by the use of a protein synthesis inhibitor called anisomycin ( Experiments with anisomycin helped lead to the acceptance of a theory in which a learned behavior is consolidated into a stored form and that then enters a 'labile' - or adaptable - state when it is recalled. According to these previous studies, the act of putting a labile memory back into storage involves a reconsolidation process identical to the one used to store the memory initially. Indeed, experiments showed that anisomycin could make a mouse forget a memory if it were given anisomycin directly after remembering an event. In a new study, however, researchers have showed that disruption of a "re-remembered" memory was not permanent. Mice demonstrated that they could remember the original learned behavior 21 days later. This research thus casts doubt on the concept of “reconsolidation”, or at least demonstrates that we still have much to learn about this process.

Lattal, K.M. & Abel, T. 2004. Behavioral impairments caused by injections of the protein synthesis inhibitor anisomycin after contextual retrieval reverse with time. PNAS, 101, 4667-4672

Another step in understanding how memories are formed

The electrical activity of individual neurons in the brains of two adult rhesus monkeys was monitored while the monkeys played a memory-based video game in which an image pops up on the computer screen with four targets—white dots—superimposed on it. The monkeys’ task was to learn which target on which image was associated with a reward (a drop of their favorite fruit juice). Dramatic changes in the activity of some hippocampal neurons, which the scientists called "changing cells", paralleled their learning, indicating that these neurons are involved in the initial formation of new associative memories. In some of the cells, activity continued after the animal had learned the association, suggesting that these cells may participate in the eventual storage of the associations in long-term memory.

Wirth, S., Yanike, M., Frank, L.M., Smith, A.C., Brown, E.N. & Suzuki, W.A. 2003. Single Neurons in the Monkey Hippocampus and Learning of New Associations. Science, 300, 1578-1581.

More details about how memories are formed in the hippocampus

We know how important the hippocampus is in forming memories, but now, using newly developed imaging techniques, researchers have managed to observe how activity patterns within specific substructures of the hippocampus change during learning. The study identified areas within the hippocampus (the cornu ammonis and the dentate gyrus) as highly active during encoding of face-name pairs. This activity decreased as the associations were learned. A different area of the hippocampus (the subiculum) was active primarily during the retrieval of the face-name associations. Activity in the subiculum also decreased as retrieval became more practiced.

Zeineh, M.M., Engel, S.A., Thompson, P.M. & Bookheimer, S.Y. 2003. Dynamics of the Hippocampus During Encoding and Retrieval of Face-Name Pairs, Science, 299, 577-580.

Memories may be hard to find when thalamus fails to synchronize rhythms

Memory codes - the representation of an object or experience in memory - are patterns of connected neurons. The neurons that are linked are not necessarily in the same region of the brain. Exciting new research has measured the electrical rhythms that parts of the brain use to communicate with each other and found that the thalamus regulates these rhythms. "Memory appears to be a constructive process in combining the features of the items to be remembered rather than simply remembering each object as a whole form. The thalamus seems to direct or modulate the brain's activity so that the regions needed for memory are connected." The authors suggest that tips of the tongue experiences (when only part of a memory is recalled) may occur when the rhythms don't synchronize with the regions properly.

Slotnick, S.D., Moo, L.R., Kraut, M.A., Lesser, R.P. & Hart, J. Jr. 2002. Interactions between thalamic and cortical rhythms during semantic memory recall in human. Proc. Natl. Acad. Sci. U.S.A., 99, 6440-6443.

Pictures show how nerve cells form connections to store memories

Scientists at the University of California, San Diego have produced dramatic images of brain cells forming temporary and permanent connections in response to various stimuli, illustrating for the first time the structural changes between neurons in the brain that, many scientists have long believed, take place when we store short-term and long-term memories.

Colicos, M.A., Collins, B.E., Sailor, M.J. & Goda, Y. 2001. Remodeling of Synaptic Actin Induced by Photoconductive Stimulation. Cell, 107 (5), 605-616.

The neural bases of effective encoding

Failure to remember experiences often occurs not because the memory is hard to retrieve, but because it was not properly encoded in the first place. Imaging studies are beginning to give us a better idea of the neurocognitive processes that lead to more effective encoding.

Wagner, A.D. & Davachi, L. 2001. Cognitive neuroscience: Forgetting of things past. Current Biology, 11, R964-R967.

Imaging study confirms role of medial temporal lobe in memory consolidation

Lesions in the medial temporal lobe (MTL) typically produce amnesia characterized by the disproportionate loss of recently acquired memories. Such memory loss has been interpreted as evidence for a memory consolidation process guided by the MTL. A recent imaging study confirms this view by showing temporally graded changes in MTL activity in healthy older adults taking a famous faces remote memory test. Evidence for such temporally graded change in the hippocampal formation was mixed, suggesting it may participate only in consolidation processes lasting a few years. The entorhinal cortex (also part of the MTL) was associated with temporally graded changes extending up to 20 years, suggesting that it is the entorhinal cortex, rather than the hippocampal formation, that participates in memory consolidation over decades. The entorhinal cortex is damaged in the early stages of Alzheimer’s disease.

Haist, F., Gore, J.B. & Mao, H. 2001. Consolidation of human memory over decades revealed by functional magnetic resonance imaging. Nature neuroscience, 4 (11), 1139-1145.

Crucial enzyme for consolidating long-term memories

Susumu Tonegawa and colleagues at the Massachusetts Institute of Technology and the Vollum Institute have released the first of a series of studies illuminating how short-term memories are turned into long-term ones via consolidation, how different types of learning occurs in unexpected ways, and how memory recall occurs. In this first study, the researchers eliminated the function of a single enzyme in a restricted memory-related region in the brains of mice, and thus showed that the enzyme is important in consolidating long-term memories. While this enzyme (calcium-calmodulin dependent kinase (CaMKIV)), has been implicated in the process of establishing long-term memories, previous research has been inconclusive because the techniques used to knock out the enzyme were so global. A series of behavioral experiments led the researchers to conclude that the CaMKIV pathway was primarily involved in memory consolidation and retention. However, memory consolidation was not completely extinguished, suggesting that there may be parallel signaling pathways involved in consolidation, or that there may have been incomplete knockout of CaMKIV activity.

Kang, H., Sun, L.D., Atkins, C.M., Soderling, T.R., Wilson, M.A. & Tonegawa, S. (2001). An Important Role of Neural Activity-Dependent CaMKIV Signaling in the Consolidation of Long-Term Memory. Cell, 106, 771-783.

Protein that allows information to be converted from short-term into lifelong memories identified

Scientists from UCLA and Johns Hopkins University have taken the first step in discovering how the brain, at the molecular and cellular level, converts short-term memories into permanent ones."Memories last different amounts of time," Frankland said. "You might remember a phone number for just a few minutes, for example, while certain childhood events will be remembered for a lifetime. Our study reveals the role of a protein that must be present in the cortex for information to be converted from short-term into lifelong memories."

Frankland, P.W., O'Brien, C., Ohno, M., Kirkwood, A. & Silva, A.J. 2001. α-CaMKII-dependent plasticity in the cortex is required for permanent memory. Nature, 411, 309-313.

Specific molecule that helps brain reorganize in the face of new experiences targeted

For the first time scientists have been able to pinpoint a specific molecule that assists the brain to reorganize in the face of new experiences. Neuroscientists at the University of Rochester Medical Center found that genetically engineered mice that were challenged with new tasks improved their learning abilities. The team then boosted the amount of the molecule, nerve growth factor (NGF), in their brains, and found that the mice learned to run unfamiliar mazes more quickly than their unmodified counterparts.

The study was published in the Proceedings of the National Academy of Science.

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Reactivate if you want to remember

We know sleep helps consolidate memories. Now a new study sheds light on how your sleeping brain decides what’s worth keeping. The study found that when the information that makes up a memory has a high value—associated with, for example, making more money—the memory is more likely to be rehearsed and consolidated during sleep.



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Cognitive decline in old age related to poorer sleep

February, 2013

A new study confirms the role slow-wave sleep plays in consolidating memories, and reveals that one reason for older adults’ memory problems may be the quality of their sleep.

Recent research has suggested that sleep problems might be a risk factor in developing Alzheimer’s, and in mild cognitive impairment. A new study adds to this gathering evidence by connecting reduced slow-wave sleep in older adults to brain atrophy and poorer learning.

The study involved 18 healthy young adults (mostly in their 20s) and 15 healthy older adults (mostly in their 70s). Participants learned 120 word- nonsense word pairs and were tested for recognition before going to bed. Their brain activity was recorded while they slept. Brain activity was also measured in the morning, when they were tested again on the word pairs.

As has been found previously, older adults showed markedly less slow-wave activity (both over the whole brain and specifically in the prefrontal cortex) than the younger adults. Again, as in previous studies, the biggest difference between young and older adults in terms of gray matter volume was found in the medial prefrontal cortex (mPFC). Moreover, significant differences were also found in the insula and posterior cingulate cortex. These regions, like the mPFC, have also been associated with the generation of slow waves.

When mPFC volume was taken into account, age no longer significantly predicted the extent of the decline in slow-wave activity — in other words, the decline in slow-wave activity appears to be due to the brain atrophy in the medial prefrontal cortex. Atrophy in other regions of the brain (precuneus, hippocampus, temporal lobe) was not associated with the decline in slow-wave activity when age was considered.

Older adults did significantly worse on the delayed recognition test than young adults. Performance on the immediate test did not predict performance on the delayed test. Moreover, the highest performers on the immediate test among the older adults performed at the same level as the lowest young adult performers — nevertheless, these older adults did worse the following day.

Slow-wave activity during sleep was significantly associated with performance on the next day’s test. Moreover, when slow-wave activity was taken into account, neither age nor mPFC atrophy significantly predicted test performance.

In other words, age relates to shrinkage of the prefrontal cortex, this shrinkage relates to a decline in slow-wave activity during sleep, and this decline in slow-wave sleep relates to poorer cognitive performance.

The findings confirm the importance of slow-wave brainwaves for memory consolidation.

All of this suggests that poorer sleep quality contributes significantly to age-related cognitive decline, and that efforts should be made to improve quality of sleep rather than just assuming lighter, more disturbed sleep is ‘natural’ in old age!



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Reviewing alcohol's effects on normal sleep

February, 2013

A review on the immediate effects of alcohol on sleep has found that alcohol shortens the time it takes to fall asleep, increases deep sleep, and reduces REM sleep.

Because sleep is so important for memory and learning (and gathering evidence suggests sleep problems may play a significant role in age-related cognitive impairment), I thought I’d make quick note of a recent review bringing together all research on the immediate effects of alcohol on the sleep of healthy individuals.

The review found that alcohol in any amount reduces the time it takes to fall asleep, while greater amounts produce increasing amounts of deep sleep in the first half of the night. However, sleep is more disrupted in the second half. While increased deep sleep is generally good, there are two down sides here: first, it’s paired with sleep disruption in the second half of the night; second, those predisposed to problems such as sleepwalking or sleep apnea may be more vulnerable to them. (A comment from the researchers that makes me wonder if the relationship between deep sleep and slow-wave activity is more complicated than I realized.)

Additionally, at high doses of alcohol, REM sleep is significantly reduced in the first half, and overall. This may impair attention, memory, and motor skills. Moreover, at all doses, the first REM period is significantly delayed, producing less restful sleep.

The researchers conclude that, while alcohol may give the illusion of improving sleep, it is not in fact doing so.


[3269] Ebrahim IO, Shapiro CM, Williams AJ, Fenwick PB. Alcohol and Sleep I: Effects on Normal Sleep. Alcoholism: Clinical and Experimental Research [Internet]. 2013 :n/a - n/a. Available from:




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Why learning gets harder as we get older

February, 2013

A mouse study shows that weakening unwanted or out-of-date connections is as important as making new connections, and that neurological changes as we age reduces our ability to weaken old connections.

A new study adds more support to the idea that the increasing difficulty in learning new information and skills that most of us experience as we age is not down to any difficulty in acquiring new information, but rests on the interference from all the old information.

Memory is about strengthening some connections and weakening others. A vital player in this process of synaptic plasticity is the NMDA receptor in the hippocampus. This glutamate receptor has two subunits (NR2A and NR2B), whose ratio changes as the brain develops. Children have higher ratios of NR2B, which lengthens the time neurons talk to each other, enabling them to make stronger connections, thus optimizing learning. After puberty, the ratio shifts, so there is more NR2A.

Of course, there are many other changes in the aging brain, so it’s been difficult to disentangle the effects of this changing ratio from other changes. This new study genetically modified mice to have more NR2A and less NR2B (reflecting the ratio typical of older humans), thus avoiding the other confounds.

To the researchers’ surprise, the mice were found to be still good at making strong connections (‘long-term potentiation’ - LTP), but instead had an impaired ability to weaken existing connections (‘long-term depression’ - LTD). This produces too much noise (bear in mind that each neuron averages 3,000 potential points of contact (i.e., synapses), and you will see the importance of turning down the noise!).

Interestingly, LTD responses were only abolished within a particular frequency range (3-5 Hz), and didn’t affect 1Hz-induced LTD (or 100Hz-induced LTP). Moreover, while the mice showed impaired long-term learning, their short-term memory was unaffected. The researchers suggest that these particular LTD responses are critical for ‘post-learning information sculpting’, which they suggest is a step (hitherto unknown) in the consolidation process. This step, they postulate, involves modifying the new information to fit in with existing networks of knowledge.

Previous work by these researchers has found that mice genetically modified to have an excess of NR2B became ‘super-learners’. Until now, the emphasis in learning and memory has always been on long-term potentiation, and the role (if any) of long-term depression has been much less clear. These results point to the importance of both these processes in sculpting learning and memory.

The findings also seem to fit in with the idea that a major cause of age-related cognitive decline is the failure to inhibit unwanted information, and confirm the importance of keeping your mind actively engaged and learning, because this ratio is also affected by experience.



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Dopamine decline underlies episodic memory decline in old age

December, 2012

Findings supporting dopamine’s role in long-term episodic memory point to a decline in dopamine levels as part of the reason for cognitive decline in old age, and perhaps in Alzheimer’s.

The neurotransmitter dopamine is found throughout the brain and has been implicated in a number of cognitive processes, including memory. It is well-known, of course, that Parkinson's disease is characterized by low levels of dopamine, and is treated by raising dopamine levels.

A new study of older adults has now demonstrated the effect of dopamine on episodic memory. In the study, participants (aged 65-75) were shown black and white photos of indoor scenes and landscapes. The subsequent recognition test presented them with these photos mixed in with new ones, and required them to note which photos they had seen before. Half of the participants were first given Levodopa (‘L-dopa’), and half a placebo.

Recognition tests were given two and six hours after being shown the photos. There was no difference between the groups at the two-hour test, but at the six-hour test, those given L-dopa recognized up to 20% more photos than controls.

The failure to find a difference at the two-hour test was expected, if dopamine’s role is to help strengthen the memory code for long-term storage, which occurs after 4-6 hours.

Individual differences indicated that the ratio between the amount of Levodopa taken and body weight is key for an optimally effective dose.

The findings therefore suggest that at least part of the reason for the decline in episodic memory typically seen in older adults is caused by declining levels of dopamine.

Given that episodic memory is one of the first and greatest types of memory hit by Alzheimer’s, this finding also has implications for Alzheimer’s treatment.

Caffeine improves recognition of positive words

Another recent study also demonstrates, rather more obliquely, the benefits of dopamine. In this study, 200 mg of caffeine (equivalent to 2-3 cups of coffee), taken 30 minutes earlier by healthy young adults, was found to improve recognition of positive words, but had no effect on the processing of emotionally neutral or negative words. Positive words are consistently processed faster and more accurately than negative and neutral words.

Because caffeine is linked to an increase in dopamine transmission (an indirect effect, stemming from caffeine’s inhibitory effect on adenosine receptors), the researchers suggest that this effect of caffeine on positive words demonstrates that the processing advantage enjoyed by positive words is driven by the involvement of the dopaminergic system.



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Rest briefly after learning

October, 2012

A small study with older adults provides support for the idea that learning is helped if you follow it with a few minutes ‘wakeful rest’.

Back in 2010, I briefly reported on a study suggesting that a few minutes of ‘quiet time’ could help you consolidate new information. A new study provides more support for this idea.

In the first experiment, 14 older adults (aged 61-81) were told a short story, with instructions to remember as many details as possible. Immediately afterward, they were asked to describe what happened in the story. Ten minutes then elapsed, during which they either rested quietly (with eyes closed in a darkened room), or played a spot-the-difference game on the computer (comparing pairs of pictures). This task was chosen because it was non-verbal and sufficiently different from the story task to not directly compete for cognitive resources.

This first learning phase was followed by five minutes of playing the spot-the-difference game (for all participants) and then a second learning phase, in which the process was repeated with a second story, and participants experienced the other activity during the delay period (e.g., rest if they had previously played the game).

Some 30 minutes after the first story presentation (15 minutes after the second), participants were unexpectedly asked to once again recall as many details as they could from the stories. A further recall test was also given one week later.

Recall on the first delayed test (at the end of both learning phases) was significantly better for stories that had been followed by wakeful resting rather than a game. While recall declined at the same rate for both story conditions, the benefits of wakeful resting were maintained at the test one week later.

In a second experiment, the researchers looked at whether these benefits would still occur if there was no repetition (i.e., no delayed recall test at the time, only at a week). Nineteen older adults (61-87) participated.

As expected, in the absence of the short-delay retrieval test, recall at a week was slightly diminished. Nevertheless, recall for stories that had been followed by rest was still significantly better than recall for stories followed by the game.

It’s worth noting that, in a post-session interview, only 3 participants (of the 33 total) reported thinking about the story during the period of wakeful rest. One participant fell asleep. Twelve participants reported thinking about the stories at least once during the week, but there was no difference between these participants’ scores and those who didn’t think about them.

These findings support the idea that a quiet period of reflection after new learning helps the memories be consolidated. While the absence of interfering information may underlie this, the researchers did select the game specifically to interfere as little as possible with the story task. Moreover, the use of the same task as a ‘filler’ between the two learning phases was also designed to equalize any interference it might engender.

The weight of the evidence, therefore, is that ten minutes of wakeful resting aided memory by providing the mental space in which to consolidate the memory. Moreover, the fact that so few participants actively thought about the stories during that rest indicates that such consolidation is automatic and doesn’t require deliberate rehearsal.

The study did, of course, only involve older adults. I hope we will see a larger study with a wider participant pool.



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