Posts tagged memory
Articles and news from the latest research reports.
Immune response affects sleep and memory
Fighting off illness- rather than the illness itself- causes sleep deprivation and affects memory, a new study has found.
University of Leicester biologist Dr Eamonn Mallon said a common perception is that if you are sick, you sleep more.
But the study, carried out in flies, found that sickness induced insomnia is quite common.
The research has been published in the journal PeerJ.
Dr Mallon said: “Think about when you are sick. Your sleep is disturbed and you’re generally not feeling at your sharpest. Previously work has been carried out showing that being infected leads to exactly these behaviours in fruit flies.
“In this paper we show that it can be the immune system itself that can cause these problems. By turning on the immune system in flies artificially (with no infection present) we reduced how long they slept and how well they performed in a memory test.
“This is an interesting result as these connections between the brain and the immune system have come to the fore recently in medicine. It seems to be because the two systems speak the same chemical language and often cross-talk. Having a model of this in the fly, one of the main systems used in genetic research will be a boost to the field.
“The key message of this study is that the immune response, sleep and memory seem to be intimately linked. Medicine is beginning to study these links between the brain and the immune system in humans. Having an easy to use insect model would be very helpful.”
(Source: www2.le.ac.uk)
Poor cardiovascular health linked to memory, learning deficits
The risk of developing cognitive impairment, especially learning and memory problems, is significantly greater for people with poor cardiovascular health than people with intermediate or ideal cardiovascular health, according to a study in the Journal of the American Heart Association.
Cardiovascular health plays a critical role in brain health, with several cardiovascular risk factors also playing a role in higher risk for cognitive decline.
Researchers found that people with the lowest cardiovascular health scores were more likely have impairment on learning, memory and verbal fluency tests than their counterparts with intermediate or better risk profiles.
The study involved 17,761 people aged 45 and older at the outset who had normal cognitive function and no history of stroke. Mental function was evaluated four years later.
Researchers used data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study to determine cardiovascular health status based on The American Heart Association Life’s Simple 7™ score. The REGARDS study population is 55 percent women, 42 percent blacks, 58 percent whites and 56 percent are residents of the “stroke belt” states of Alabama, Arkansas, Georgia, Louisiana, Mississippi, North Carolina, South Carolina and Tennessee.
The Life’s Simple 7™ initiative is a new system to measure the benefits of modifiable health behaviors and risk factors in cardiovascular health, such as smoking, diet, physical activity, body mass index, blood pressure, total cholesterol, and fasting glucose. It classifies each of the seven factors of heart health as either poor, intermediate or ideal.
After accounting for differences in age, sex, race and education, researchers identified cognitive impairment in:
- 4.6 percent of people with the worst cardiovascular health scores;
- 2.7 percent of those with intermediate health profiles; and
- 2.6 percent of those in the best cardiovascular health category.
“Even when ideal cardiovascular health is not achieved intermediate levels of cardiovascular health are preferable to low levels for better cognitive function,” said lead investigator Evan L. Thacker, Ph.D., an assistant professor and chronic disease epidemiologist at Brigham Young University Department of Health Science, in Provo, Utah.
“This is an encouraging message because intermediate cardiovascular health is a more realistic target for many individuals than ideal cardiovascular health.”
The differences were seen regardless of race, gender, pre-existing cardiovascular conditions, or geographic region, although higher cardiovascular health scores were more common in men, people with higher education, higher income, and among people without any cardiovascular disease.
Cognitive function assessments involved tests to measure verbal learning, memory and fluency. Verbal learning was determined using a three-trial, ten-item word list, while verbal memory was assessed by free recall of the ten-item list after a brief delay filled with non-cognitive questions. Verbal fluency was determined by asking each participant to name as many animals as possible in 60 seconds.
Although mechanisms that might explain the findings remain unclear, Thacker said that undetected subclinical strokes could not be ruled out.
That Sounds Familiar, But Why?
When it comes to familiarity, a slew of memories including seemingly unrelated ones can come flooding into the brain, according to mathematical theories called global similarity models.
After conducting an fMRI study on memory and categorization, researchers including a Texas Tech University psychologist have shown for the first time that these mathematical models seem to correctly explain processing in the medial temporal lobes, a region of the brain associated with long-term memory that is disrupted by memory disorders like Alzheimer’s disease.
The findings were published in The Journal of Neuroscience.
Tyler Davis, assistant director of Texas Tech’s Neuroimaging Institute and an assistant professor of psychology, specializes in neurobiological approaches to learning and memory. He was part of a team that delved into global similarity models.
“Since at least the 1980s, scientists researching memory have believed that when a person finds someone’s face or a new experience familiar, that person is not simply retrieving a memory of only this previous experience, but memories of many other related and unrelated experiences as well,” Davis said. “Formal mathematical theories of memory called global similarity models suggest that when we judge familiarity, we match an experience, such as a face or a trip to a restaurant, to all of the memories that we have stored in our brains. Our recent work using fMRI suggests these models are correct.”
People may believe when they see someone’s familiar face or take a trip to a familiar restaurant, they only activate the most similar or recent memories for comparison. However, Davis said this is not the case. According to global similarity models, the feeling of familiarity for the taste of brisket at a particular restaurant draws on a spectrum of memories that a person has stored in his or her brain.
Eating the brisket can activate memories not only of a previous trip to that restaurant, but also of the décor, eating brisket at a similar restaurant, what that person’s home-cooked brisket tastes like and even seemingly tangential memories such as a recent trip to another city.
“In terms of global similarity theories and our new findings, the important thing is when you are judging familiarity, your brain doesn’t just retrieve the most relevant memories but many other memories as well,” Davis said. “This seems counter-intuitive to how memory feels. We often feel like we are just retrieving that previous trip to that one particular restaurant when we are asked whether we’d been there before, but there is a lot of behavioral evidence that we activate many other memories as well when we judge familiarity.”
This does not mean that every memory we have stored contributes to familiarity in the same way. The more similar a previous memory is to the current experience, the more it will contribute to judgments of familiarity.
In terms of the brisket example, Davis said, previous trips to the restaurant are going to impact the familiarity more than dissimilar memories, such as the recent trip out of town. However, similarity from these other less-related experiences can have a measurable effect in judgments of familiarity.
In his recent research, Davis and others used fMRI to examine how memory similarity related to behavioral measures of familiarity, in terms of activation patterns in the medial temporal lobes.
“We found that peoples’ memory for the items in our experiments was related to their activation patterns in the medial temporal lobes in a manner that was anticipated by mathematical global similarity models,” Davis said. “The more similar the activation pattern for an item was to all of the other activation patterns, the more strongly people remembered it. This is consistent with global similarity models, which suggest that the items that are most similar to all other items stored in memory will be most familiar.”
The findings suggest that global similarity models may have a neurobiological basis, he said. This is evidence that similarity, in terms of neural processing, may impact memory. People may find things familiar not just because they are identical to things we’ve previously experienced, but because they are similar to a number of things we’ve previously experienced.
(Source: today.ttu.edu)
Study shows anaesthesia may harm memory
General anaesthesia before the age of one may impair memory later in childhood, and the effects may possibly be lifelong, a study said Monday.
This was the conclusion of scientists who compared the recollection skills of two groups of children — some who had undergone anaesthesia in infancy and others who had not.
The children, aged six to 11 and divided into two groups of 28 each, were tested over a period of 10 months for their ability to recollect specific drawings and details therein.
The children who had been anaesthetised as babies had about 28 per cent less recollection on average than their peers, and scored 20 per cent lower in tests that assessed how much detail they could remember about the drawings.
"The children did not differ in tests measuring intelligence or behaviour, but those who had received anaesthesia had significantly lower recollection scores," said a media summary provided by the journal Neuropsychopharmacology, which published the results.
Sleep After Learning Strengthens Connections Between Brain Cells and Enhances Memory
In study published today in Science, researchers at NYU Langone Medical Center show for the first time that sleep after learning encourages the growth of dendritic spines, the tiny protrusions from brain cells that connect to other brain cells and facilitate the passage of information across synapses, the junctions at which brain cells meet. Moreover, the activity of brain cells during deep sleep, or slow-wave sleep, after learning is critical for such growth.
The findings, in mice, provide important physical evidence in support of the hypothesis that sleep helps consolidate and strengthen new memories, and show for the first time how learning and sleep cause physical changes in the motor cortex, a brain region responsible for voluntary movements.
“We’ve known for a long time that sleep plays an important role in learning and memory. If you don’t sleep well you won’t learn well,” says senior investigator Wen-Biao Gan, PhD, professor of neuroscience and physiology and a member of the Skirball Institute of Biomolecular Medicine at NYU Langone Medical Center. “But what’s the underlying physical mechanism responsible for this phenomenon? Here we’ve shown how sleep helps neurons form very specific connections on dendritic branches that may facilitate long-term memory. We also show how different types of learning form synapses on different branches of the same neurons, suggesting that learning causes very specific structural changes in the brain.”
On the cellular level, sleep is anything but restful: Brain cells that spark as we digest new information during waking hours replay during deep sleep, also known as slow-wave sleep, when brain waves slow down and rapid-eye movement, as well as dreaming, stops. Scientists have long believed that this nocturnal replay helps us form and recall new memories, yet the structural changes underpinning this process have remained poorly understood.
To shed light on this process, Dr. Gan and colleagues employed mice genetically engineered to express a fluorescent protein in neurons. Using a special laser-scanning microscope that illuminates the glowing fluorescent proteins in the motor cortex, the scientists were then able to track and image the growth of dendritic spines along individual branches of dendrites before and after mice learned to balance on a spin rod. Over time mice learned how to balance on the rod as it gradually spun faster. “It’s like learning to ride a bike,” says Dr. Gan. “Once you learn it, you never forget.”
After documenting that mice, in fact, sprout new spines along dendritic branches, within six hours after training on the spinning rod, the researchers set out to understand how sleep would impact this physical growth. They trained two sets of mice: one trained on the spinning rod for an hour and then slept for 7 hours; the second trained for the same period of time on the rod but stayed awake for 7 hours. The scientists found that the sleep-deprived mice experienced significantly less dendritic spine growth than the well-rested mice. Furthermore, they found that the type of task learned determined which dendritic branches spines would grow.
Running forward on the spinning rod, for instance, produced spine growth on different dendritic branches than running backward on the rod, suggesting that learning specific tasks causes specific structural changes in the brain.
“Now we know that when we learn something new, a neuron will grow new connections on a specific branch,” says Dr. Gan. “Imagine a tree that grows leaves (spines) on one branch but not another branch. When we learn something new, it’s like we’re sprouting leaves on a specific branch.”
Finally, the scientists showed that brain cells in the motor cortex that activate when mice learn a task reactivate during slow-wave deep sleep. Disrupting this process, they found, prevents dendritic spine growth. Their findings offer an important insight into the functional role of neuronal replay—the process by which the sleeping brain rehearses tasks learned during the day—observed in the motor cortex.
“Our data suggest that neuronal reactivation during sleep is quite important for growing specific connections within the motor cortex,” Dr. Gan adds.
(Image: Shutterstock)
How to Erase a Memory – And Restore It
Researchers at the University of California, San Diego School of Medicine have erased and reactivated memories in rats, profoundly altering the animals’ reaction to past events.
The study, published in the June 1 advanced online issue of the journal Nature, is the first to show the ability to selectively remove a memory and predictably reactivate it by stimulating nerves in the brain at frequencies that are known to weaken and strengthen the connections between nerve cells, called synapses.
“We can form a memory, erase that memory and we can reactivate it, at will, by applying a stimulus that selectively strengthens or weakens synaptic connections,” said Roberto Malinow, MD, PhD, professor of neurosciences and senior author of the study.
Scientists optically stimulated a group of nerves in a rat’s brain that had been genetically modified to make them sensitive to light, and simultaneously delivered an electrical shock to the animal’s foot. The rats soon learned to associate the optical nerve stimulation with pain and displayed fear behaviors when these nerves were stimulated.
Analyses showed chemical changes within the optically stimulated nerve synapses, indicative of synaptic strengthening.
In the next stage of the experiment, the research team demonstrated the ability to weaken this circuitry by stimulating the same nerves with a memory-erasing, low-frequency train of optical pulses. These rats subsequently no longer responded to the original nerve stimulation with fear, suggesting the pain-association memory had been erased.
In what may be the study’s most startlingly discovery, scientists found they could re-activate the lost memory by re-stimulating the same nerves with a memory-forming, high-frequency train of optical pulses. These re-conditioned rats once again responded to the original stimulation with fear, even though they had not had their feet re-shocked.
“We can cause an animal to have fear and then not have fear and then to have fear again by stimulating the nerves at frequencies that strengthen or weaken the synapses,” said Sadegh Nabavi, a postdoctoral researcher in the Malinow lab and the study’s lead author.
In terms of potential clinical applications, Malinow, who holds the Shiley Endowed Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal, noted that the beta amyloid peptide that accumulates in the brains of people with Alzheimer’s disease weakens synaptic connections in much the same way that low-frequency stimulation erased memories in the rats. “Since our work shows we can reverse the processes that weaken synapses, we could potentially counteract some of the beta amyloid’s effects in Alzheimer’s patients,” he said.
Memory Problems After Chemo Linked to Brain Changes
Breast cancer survivors who had chemotherapy show changes in brain activity during multitasking chores, according to a new Belgian study.
These findings may partly explain the phenomenon dubbed “chemo brain.” For years, people who’ve had chemotherapy have reported changes in thinking and memory, especially when doing more than one thing at once.
"Before you can fix a problem, you need to know what the problem is. And this study demonstrates what the problem may be. It’s a really good first step to understanding the what. Now we need to understand the why and how to fix it," said Dr. Courtney Vito, a breast surgeon and assistant clinical professor of surgical oncology at the City of Hope Comprehensive Cancer Center in Duarte, Calif. Vito was not involved in the current study, but reviewed the study’s findings.
In her experience, Vito said, women tend to be affected more by chemo brain than are men after chemotherapy. However, she said, ”women tend to multitask more, so this might explain part of it.”
The new study was published online May 27 in the Journal of Clinical Oncology.
Cynical? You May Be Hurting Your Brain Health
People with high levels of cynical distrust may be more likely to develop dementia, according to a study published in the May 28, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology.
Cynical distrust, which is defined as the belief that others are mainly motivated by selfish concerns, has been associated with other health problems, such as heart disease. This is the first study to look at the relationship between cynicism and dementia.
“These results add to the evidence that people’s view on life and personality may have an impact on their health,” said study author Anna-Maija Tolppanen, PhD, of the University of Eastern Finland in Kuopio. “Understanding how a personality trait like cynicism affects risk for dementia might provide us with important insights on how to reduce risks for dementia.”
For the study, 1,449 people with an average age of 71 were given tests for dementia and a questionnaire to measure their level of cynicism. The questionnaire has been shown to be reliable, and people’s scores tend to remain stable over periods of several years. People are asked how much they agree with statements such as “I think most people would lie to get ahead,” “It is safer to trust nobody” and “Most people will use somewhat unfair reasons to gain profit or an advantage rather than lose it.” Based on their scores, participants were grouped in low, moderate and high levels of cynical distrust.
A total of 622 people completed two tests for dementia, with the last one an average of eight years after the study started. During that time, 46 people were diagnosed with dementia. Once researchers adjusted for other factors that could affect dementia risk, such as high blood pressure, high cholesterol and smoking, people with high levels of cynical distrust were three times more likely to develop dementia than people with low levels of cynicism. Of the 164 people with high levels of cynicism, 14 people developed dementia, compared to nine of the 212 people with low levels of cynicism.
The study also looked at whether people with high levels of cynicism were more likely to die sooner than people with low levels of cynicism. A total of 1,146 people were included in this part of the analysis, and 361 people died during the average of 10 years of follow-up. High cynicism was initially associated with earlier death, but after researchers accounted for factors such as socioeconomic status, behaviors such as smoking and health status, there was no longer any link between cynicism and earlier death.
(Image: Shutterstock)
Drug used to treat multiple sclerosis may have beneficial effects on memory
Virginia Commonwealth University School of Medicine researchers have uncovered a new mechanism of action of fingolimod, a drug widely used to treat multiple sclerosis: elimination of adverse or traumatic memories.
The findings shed light on how the drug works on the molecular level – something that has not been well understood until now.
Fingolimod, or FTY720, which is the first orally available drug for treatment of multiple sclerosis, works by suppressing the immune system. Fingolimod is a prodrug that is phosphorylated in the body to its active form, FTY720-phosphate.
In a study published by the Nature Neuroscience journal on May 25 as an Advanced Online Publication, researchers used a mouse model to show that fingolimod accumulates in the brain and inhibits histone deacetylases, which are enzymes important to regulate gene expression. The team observed an increased expression of a limited number of genes important for certain memory processes. Fingolimod acted similarly to the natural signaling lipid, sphingosine-1-phosphate, which it closely resembles.
“Our work suggests that some of the beneficial effects of FTY720/fingolimod that are not well understood might be mediated by this new activity that we have discovered,” said first author Sarah Spiegel, Ph.D., an internationally renowned researcher and professor and chair of the Department of Biochemistry and Molecular Biology in the VCU School of Medicine.
“It will be important in the future to determine whether this prodrug can reduce loss of cognitive functions and can erase adverse memories,” she said.
Spiegel added that other histone deacetylase inhibitors have long been used for treatment of psychiatric and neurological disorders, yet the mechanism of their effectiveness is not fully understood.
“FTY720/fingolimod may be a useful adjuvant therapy to help stop aversive memories such as in post-traumatic stress disorder and other anxiety disorders,” Spiegel said.
“The work has not been extended to show effectiveness in humans at this time. We are still working to fully understand the molecular underpinnings of the drug and its link to memory,” she said.
The work is based on previous findings by Spiegel’s group that were published in Science in 2009. They had reported that sphingosine-1-phosphate formed in the nucleus of cells is a natural inhibitor of histone deacetylases and a regulator of gene expression.
(Source: spectrum.vcu.edu)
‘Sticky synapses’ can impair new memories by holding on to old ones
A team of UBC neuroscientists has found that synapses that are too strong or ‘sticky’ can actually hinder our capacity to learn new things.
University of British Columbia researchers have discovered that so-called “sticky synapses” in the brain can impair new learning by excessively hard-wiring old memories and inhibiting our ability to adapt to our changing environment.
Memories are formed by strong synaptic connections between nerve cells. Now a team of UBC neuroscientists has found that synapses that are too strong or “sticky” can actually hinder our capacity to learn new things by affecting cognitive flexibility, the ability to modify our behaviours to adjust to circumstances that are similar, but not identical, to previous experiences.
“We tend to think that strong retention of memories is always a good thing,” says Fergil Mills, UBC PhD candidate and the study’s first author. “But our study shows that cognitive flexibility involves actively weakening old memory traces. In certain situations, you have to be able to ‘forget’ to learn.”
The study, published today in the Proceedings of the National Academy of Sciences, shows that mice with excessive beta-catenin – a protein that is part of the “molecular glue” that holds synapses together – can learn a task just as well as normal mice, but lacked the mental dexterity to adapt if the task was altered.
“Increased levels of beta-catenin have previously been reported in disorders such as Alzheimer’s disease and Huntington’s disease, and, intriguingly, patients with these diseases have been shown to have deficits in cognitive flexibility similar to those we observed in this study,” says Shernaz Bamji, an associate professor in UBC’s Dept. of Cellular and Physiological Sciences.
“Now, we see that changes in beta-catenin levels can dramatically affect learning and memory, and may indeed play a role in the cognitive deficits associated with these diseases,” she adds. “This opens up many exciting new avenues for research into these diseases and potential therapeutic approaches.”
BACKGROUND
To test cognitive flexibility in mice, researchers conducted an experiment where the mice were placed in a pool of water and had to learn to find a submerged hidden platform. The mice with excessive beta-catenin could learn to find the platform just as well as normal mice. However, if the platform was moved to a different location in the pool, these mice kept swimming to the platform’s previous location. Even after many days of training, the ‘sticky synapses’ in their brains made them unable to effectively learn to find the new platform.