Data from 28,485 older Canadians (45+) found that those with chronic insomnia performed significantly worse on cognitive tests than those who had symptoms of insomnia without any noticable impact on their daytime functioning and those with normal sleep quality. The main type of memory affected was declarative memory (memory of concepts, events and facts).
Following rat studies, a study involving 36 healthy young adults has found that 10 minutes of light exercise (such as tai chi, yoga, or walking) significantly improved highly detailed memory processing and resulted in increased activity in the hippocampus.
A study involving epilepsy patients who had electrodes implanted into their brain has revealed that memory consolidation during sleep doesn’t simply involve reactivation of the new memories.
A laboratory study has found that sleeping after watching a trauma event reduced emotional distress and memories related to traumatic events. The laboratory study involved 65 women being shown a neutral and a traumatic video. Typically, recurring memories of certain images haunted the test subjects for a few days (these were recorded in detail in a diary). Some participants slept in the lab for a night after the video, while the other group remained awake.
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.
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.
Also see Sleep's role in memory
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.
http://www.eurekalert.org/pub_releases/2006-02/nyu-nrs021306.php
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.
http://www.eurekalert.org/pub_releases/2005-08/uom-mrp082905.php
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.
http://www.eurekalert.org/pub_releases/2005-01/nu-ntc011405.php
http://www.sciencedirect.com/science/journal/01662236
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.
http://www.eurekalert.org/pub_releases/2004-10/hhmi-bcm100604.php
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.
http://www.eurekalert.org/pub_releases/2004-05/cp-hoh052104.php
http://www.eurekalert.org/pub_releases/2004-05/ucl-ros052404.php
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 ( http://www.eurekalert.org/pub_releases/2000-08/NYU-Nnfl-1508100.htm). 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
http://www.eurekalert.org/pub_releases/2004-03/uop-mah031504.php
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.
http://www.eurekalert.org/pub_releases/2003-06/nyu-fir060503.php
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.
http://www.eurekalert.org/pub_releases/2003-01/uoc--som012303.php
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.
http://www.eurekalert.org/pub_releases/2002-05/uoaf-mi050902.php
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.
http://ucsdnews.ucsd.edu/newsrel/science/mccell.htm
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.
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.
http://www.nature.com/neurolink/v4/n11/abs/nn739.html
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.
http://www.eurekalert.org/pub_releases/2001-09/hhmi-rfe092001.php
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.
http://www.eurekalert.org/pub_releases/2001-05/UNKN-BrfU-1505101.php
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.
http://www.eurekalert.org/pub_releases/2000-12/UoR-Simt-2612100.php
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.
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.
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.