The brain’s ability to learn and form memories of day-to-day facts and events depends on the hippocampus, a structure deep within the brain. But is the hippocampus still maintaining the memory of, say, the commencement address at your college graduation 20 years ago? The latest evidence suggests that as memories age, the hippocampus’s participation wanes.

In a 2006 study, neuroscientist Larry R. Squire of the University of California, San Diego, and the Veterans Affairs San Diego Healthcare System studied patients who had hippocampal damage. These indi­viduals did not remember details of newsworthy events that occurred in the five to 10 years prior to their injuries, but they did recall older events.

Building on those results, Squire turned to healthy brains. His team questioned 15 people in their 50s and 60s about events in the news over the past 30 years while scanning the participants’ brains with functional MRI. To single out brain activity related to the date of the event, the researchers separately evaluated activity tied to learning and remem­bering the test questions. They also accounted for the richness of participants’ recollections of events, to make sure the degree to which someone was able to recall an event did not influence the data.

Squire’s team reported in January that activity in the hippocampus steadily declined as subjects remembered events that were up to 12 years old. With more remote memories, the structure’s activity leveled off. In contrast, areas in the frontal, temporal and parietal lobes displayed increasing activity for recalled events from those dozen years, then reached a plateau during older remembrances.

The biology behind how the brain makes and keeps memories is not fully understood, Squire notes, but it appears that, initially, a memory resides in the hippocampus and in areas the structure connects to in the neocortex, the outer part of the cerebral cortex. “A time comes when the cortical regions important to a memory are connected [to one another] heavily enough to form a stable representation,” Squire says. “Then the hippocampus isn’t needed to hold the whole thing together.”

Original article here

Myfitbrain brain games

Interrupting sleep seriously disrupts memory-making, new research suggests. But taking a nap may boost a sophisticated kind of memory that helps a person see the big picture and get creative.

‘Not only do we need to remember to sleep, but most certainly we sleep to remember,’ Dr William Fishbein, a cognitive neuroscientist at the City University of New York, told a recent meeting of the Society for Neuroscience.”….

“Dr Fishbein suspected a more active role for the slow-wave sleep that can emerge even in a short power nap. Maybe the brain keeps working during that time to solve problems and come up with new ideas. So he and graduate student Hiuyan Lau devised a simple test: documenting relational memory, where the brain puts together separately learnt facts in new ways.

First, they taught 20 English-speaking college students lists of Chinese words spelled with two characters, such as sister, mother, maid. Then half the students took a nap, being monitored to be sure they did not move from slow-wave sleep into the REM stage.

Upon awakening, they took a multiple-choice test of Chinese words they had never seen before. They did much better at automatically learning that the first of the two-pair characters in the words they had memorised earlier always meant the same thing – female, for example.

‘The nap group has essentially teased out what’s going on,’ Dr Fishbein concludes. These students took a 90-minute nap, quite a luxury for most adults. But even a 12-minute nap can boost some forms of memory, adds Dr Robert Stickgold of Harvard Medical School.

Conversely, Wisconsin researchers briefly interrupted night-time slow-wave sleep by playing a beep – just loudly enough to disturb sleep but not awaken – and found those people could not remember a task they had learnt the day before as well as those whose slow-wave sleep was not disrupted.

Myfitbrain brain games

ScienceDaily (Aug. 27, 2009) — Researchers at MIT’s Picower Institute for Learning and Memory have found that rats use a mental instant replay of their actions to help them decide what to do next, shedding new light on how animals and humans learn and remember.

“By understanding how thoughts and memories are structured, we can gain insight into how they might be disrupted in diseases and disorders of memory and thought such as Alzheimer’s and schizophrenia,” said study author Matthew A. Wilson, the Sherman Fairchild Professor of Neuroscience at the Picower Institute. “This understanding may lead to new methods of diagnosis and treatment.”

Wilson’s laboratory explores how rats form and recall memories by recording — with an unprecedented level of accuracy — the activity of single neurons in the hippocampus while the animal is performing tasks, pausing between actions and sleeping. The hippocampus is the seahorse-shaped brain region researchers believe to be critical for learning and memory.

Wilson’s previous work has shown that after the animals run a maze, their brains “replay” during sleep the sequence of events they experienced while awake. Researchers believe this process is key to sleep-reinforced memory consolidation in both animals and humans.

The latest study shows that these sequences also occur when the animals are awake and may help them decide what to do next.

Not-so-instant replay

When a rat moves through a maze, certain neurons called “place cells,” which respond to the animal’s physical environment, fire in patterns and sequences unique to different locations. By looking at the patterns of firing cells, researchers can tell which part of the maze the animal is running.

While the rat is awake but standing still in the maze, its neurons fire in the same pattern of activity that occurred while it was running. The mental replay of sequences of the animals’ experience occurs in both forward and reverse time order.

“This may be the rat equivalent of ‘thinking,’” Wilson said. “This thinking process looks very much like the reactivation of memory that we see during non-REM dream states, consisting of bursts of time-compressed memory sequences lasting a fraction of a second.

“So, thinking and dreaming may share the same memory reactivation mechanisms,” he said.

Memory’s building blocks

“This study brings together concepts related to thought, memory and dreams that all potentially arise from a unified mechanism rooted in the hippocampus,” said co-author Fabian Kloosterman, senior postdoctoral associate.

The team’s results show that long experiences, which in reality could have taken tens of seconds or minutes, are replayed in only a fraction of a second. To do this, the brain links together smaller pieces to construct the memory of the long experience.

The researchers speculated that this strategy could help different areas of the brain share information — and deal with multiple memories that may share content — in a flexible and efficient way. “These results suggest that extended replay is composed of chains of shorter subsequences, which may reflect a strategy for the storage and flexible expression of memories of prolonged experience,” Wilson said.

Moreover, by comparing the content of the replay with the rat’s physical location on the track and his actual behavior immediately before and after the replay event the researchers could tell the rat was not just thinking about his most recent experience but also about other options, such as: “What if I turned around and went back the way I came?” or “How would I get here if my starting point is at a distant location?”

This suggests that the same brain mechanisms come into play to remember the past and consider future actions, reinforcing recent work by neuroscientists outside of MIT who determined that in humans, cognitive processes related to episodic recall and evaluation of future events overlap to a high degree.

Memory formation and future planning are among the cognitive functions ravaged by diseases such as Alzheimer’s disease, schizophrenia and psychosis.

“A better understanding of how we use memories, not only to learn from past experiences but also to explore our future options, can give us insights into how the system fails under these disease conditions,” Kloosterman said.

The MIT researchers plan to further explore the link between awake replay and cognition in animals engaged in more cognitively demanding tasks such as those involving multiple choices, where the rat has to make a decision (”do I go left or right?”) based on a prior learned rule.

In addition to Wilson, the study was led jointly by Kloosterman and MIT brain and cognitive sciences graduate student Thomas J. Davidson.

This research was supported by National Institutes of Health (NIH).

Original article here.

Researchers at MIT’s Picower Institute for Learning and Memory conducted learning and memory tasks using transgenic mice that were induced to lose a significant number of brain cells. Following Alzheimer’s-like brain atrophy, the mice acted as though they did not remember tasks they had previously learned.  But after taking HDAC inhibitors, the mice regained their long-term memories and ability to learn new tasks. In addition, mice genetically engineered to produce no HDAC2 at all exhibited enhanced memory formation.

The fact that long-term memories can be recovered by elevated histone acetylation supports the idea that apparent memory “loss” is really a reflection of inaccessible memories, Tsai said. “These findings are in line with a phenomenon known as ‘fluctuating memories,’ in which demented patients experience temporary periods of apparent clarity,” she said.

A team led by researchers at MIT’s Picower Institute for Learning and Memory has now pinpointed the exact gene responsible for a 2007 breakthrough in which mice with symptoms of Alzheimer’s disease regained long-term memories and the ability to learn. In the latest development, reported in the May 7 issue of Nature, Li-Huei Tsai, Picower Professor of Neuroscience, and colleagues found that drugs that work on the gene HDAC2 reverse the effects of Alzheimer’s and boost cognitive function in mice.

Original article here

Eating fatty food appears to take an almost immediate toll on both short-term memory and exercise performance, according to new research on rats and people.

It’s already known that long-term consumption of a high-fat diet is associated with weight gain, heart disease and declines in cognitive function. But the new research shows how indulging in fatty foods over the course of a few days can affect the brain and body long before the extra pounds show up.

To determine the effect of a fatty diet on memory and muscle performance, researchers studied 32 rats that were fed low-fat rat chow and trained for two months to complete a challenging maze. The maze included eight different paths that ended with a treat of sweetened condensed milk. The goal was for the rat to find each treat without doubling back into a corridor where it had already been. The maze was wiped down with alcohol, so the rat had to rely on memory rather than sense of smell.

All of the rats studied had mastered the maze, finding at least six or seven of the eight treats before making a mistake. Some rats even found all eight on the first try.

Then half the rats were switched to high-fat rat chow (comprised of 55 percent fat), while the remaining rats stayed on their regular chow (which had 7.5 percent fat). After four days, the rats eating the fatty chow began to falter on the maze test — all of them did worse than when they were on their regular chow. On average, the rats on the fatty diet found only five treats before making a mistake. The rats who stayed with their regular food continued the same high level of performance on the maze, finding six or more treats before making a mistake.

Read rest of article here.

Getting your daily caffeine hit may help keep your memory sharp.

A new study shows caffeine reversed memory loss in mice bred to develop Alzheimer’s disease and reduced the level of beta-amyloid protein in the blood and brain. Plaques containing beta-amyloid protein are found in the brains of people with Alzheimer’s disease.

“The new findings provide evidence that caffeine could be a viable ‘treatment’ for established Alzheimer’s disease, and not simply a protective strategy,” researcher Gary Arendash, PhD, a neuroscientist at the University of South Florida, says in a news release. “That’s important because caffeine is a safe drug for most people, it easily enters the brain, and it appears to directly affect the disease process.”

Caffeine Reduces Memory Loss

In the study, mice bred to develop symptoms of Alzheimer’s disease were given 500 milligrams of caffeine (equivalent to five cups of regular coffee) in their daily drinking water once they started developing memory problems at age 18 to 19 months, about age 70 in human years.

After two months, the mice that drank the caffeinated water performed much better on tests of their memory and thinking skills — to the level of normal mice of the same age. Those given plain water continued to do poorly on these tests. The study also showed that the brains of the caffeinated mice experienced a nearly 50% reduction in the level of beta-amyloid.

The researchers also looked at long-term caffeine treatment in normal mice. With 10 months of caffeine treatment, there was no improvement in memory and thinking skills.

Based on these findings, published in the Journal of Alzheimer’s Disease, Arendash and colleagues say they plan to start human trials to see whether caffeine can benefit people with early signs of Alzheimer’s disease.

Why is it that once you learn something incorrectly (say, 7 X 9 = 65), it seems you never can correct your recall?
—J. Kruger, Cherry Hill, N.J.

Cognitive psychologist Gordon H. Bower of Stanford University answers:

Identifying, correcting and averting our memory errors are part of a cognitive process called memory monitoring. Incorrect associations can be tough to change, but we can use techniques to retrain our brain.

When strong habits impede our ability to acquire a desired new habit or association, we experience a common phenomenon known as proactive interference. Wrong associations appear in common spelling errors such as “wierd” for “weird” and “neice” for “niece.” Persistent mistaken connections also can cause embarrassing errors, such as calling a man’s second wife by the name of his first. Interference is stronger the more previous wives you’ve had to deal with, and it is more difficult to overcome the stronger the habits are.

Accurate memory monitoring requires a well-functioning prefrontal cortex (PFC). Young children, who have an immature PFC, and stroke patients with extensive PFC damage make more errors as a result of memory-monitoring failures. They are more likely to confuse the source of information they recall, and they are more susceptible to accepting as true an event they only imagined.

You can overcome proactive interference by consistent (even silent) correction, especially when you space rehearsals over time. But it takes some conscious practice. We have to identify (or be told) when we have just made an error so that we can correct it immediately. Our inability to do so is typically the cause of the error’s persistence.

Building on the correct information can help you learn new associations to it: add something to change how you retrieve the item from your memory. You might replace your question “Name of John’s wife?” with “Name of John’s second wife?”; or use an elaboration that contains the accurate information, such as “We are weird” or “My niece is nice”; or convert 7 X 9 into 7 X (10 – 1) = 70 – 7 = 63. As you practice the elaborated association, the simpler direct association (7 X 9 = 63) eventually replaces the earlier one, which weakens without rehearsals. Labeling and rehearsing the wrong association (for example, saying to yourself, “7 X 9 is not 63”), however, are distinctly counterproductive.

See original article here.