Out of shape? Your memory may suffer

Here’s another reason to drop that doughnut and hit the treadmill: A new study suggests aerobic fitness affects long-term memory.

Michigan State University researchers tested 75 college students during a two-day period and found those who were less fit had a harder time retaining information.

“The findings show that lower-fit individuals lose more memory across time,” said Kimberly Fenn, study co-author and assistant professor of psychology.

The study, which appears online in the research journal Cognitive, Affective & Behavioral Neuroscience, is one of the first to investigate young, supposedly healthy adults. Previous research on fitness and memory has focused largely on children, whose brains are still developing, and the elderly, whose memories are declining.

Participants studied related word pairs such as “camp” and “trail.” The next day, they were tested on the word pairs to evaluate long-term memory retention. Long-term memory is anything remembered more than about 30 seconds ago.

Aerobic fitness was gauged by oxygen consumption derived from a treadmill test and factored with the participants’ weight, percent body fat, age and sex.

The findings speak to the increasingly sedentary lifestyles found in the United States and other Western cultures. A surprising number of the college students in the study were significantly out of shape and did much worse at retaining information than those who were extremely fit, Fenn said.

Her co-authors included kinesiology researchers Matthew Pontifex and Karin Pfeiffer.

Coming soon: a brain implant to restore memory

In the next few months, highly secretive US military researchers say they will unveil new advances toward developing a brain implant that could one day restore a wounded soldier’s memory.

The Defense Advanced Research Projects Agency (DARPA) is forging ahead with a four-year plan to build a sophisticated memory stimulator, as part of President Barack Obama’s $100 million initiative to better understand the human brain.

The science has never been done before, and raises ethical questions about whether the human mind should be manipulated in the name of staving off war injuries or managing the aging brain.

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Diet Can Predict Cognitive Decline

The importance of long-chain polyunsaturated fatty acids (PUFAs) to brain health has been demonstrated in multiple studies. To assess whether lower dietary intake of alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexanoic acid (DHA) were risk factors for cognitive decline, Tammy Scott, PhD, a scientist at the Jean Mayer USDA Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University recently conducted a longitudinal, observational study using the Boston Puerto Rican Health Study cohort. Alice Lichtenstein, DSc, also from the USDA HNRCA at Tufts University, and Katherine Tucker, PhD, the cohort director from the University of Massachusetts-Lowell, were co-authors of the study, which has been published as an abstract.

“The participants were put through an intensive series of cognitive tests such as memory tests using a list of words, an attention test to repeat lists of numbers forward and backward, and a test of organization and planning involving copying complex figures,” said Dr. Scott. To determine the participants’ intake of PUFAs they were given a questionnaire. The results were determined after comparing baseline test numbers with a 2 year follow up.

The researchers found that the intake of omega-3 PUFAs in the study sample of 895 participants was low. The 2010 U.S. Dietary Guidelines recommended an intake of 8 or more ounces of seafood per week (less for young children) to ensure an adequate intake of the very long chain omega-3 fatty acids (EPA and DHA). This translates to about 1,750 mg of EPA and DHA per week, which averages to 250 mg per day. Scott’s group reported that only 27% of the participants in their study met or exceeded that recommendation. The major source of EPA and DHA in their diets appeared to be from canned tuna. Based on the scientists’ findings, being in the lowest four quintiles of EPA and DHA intake was predictive of cognitive decline over 2 years.

What is the takeaway from this research? There is growing evidence that very long chain omega-3 fatty acids are beneficial for maintaining cognitive health, and many Americans do not have an adequate intake of these nutrients. “While more research is needed to determine whether intake of fatty fish such as salmon, tuna and trout can help prevent against cognitive decline, our preliminary data support previous research showing that intake of these types of fish have health benefits,” Scott said.

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Fight Memory Loss with a Smile (or Chuckle)

Too much stress can take its toll on the body, mood, and mind. As we age it can contribute to a number of health problems, including high blood pressure, diabetes, and heart disease. Recent research has shown that the stress hormone cortisol damages certain neurons in the brain and can negatively affect memory and learning ability in the elderly. Researchers at Loma Linda University have delved deeper into cortisol’s relationship to memory and whether humor and laughter—a well-known stress reliever—can help lessen the damage that cortisol can cause. Their findings were presented on Sunday, April 27, at the Experimental Biology meeting.

Gurinder Singh Bains et al. showed a 20-minute laugh-inducing funny video to a group of healthy elderly individuals and a group of elderly people with diabetes. The groups where then asked to complete a memory assessment that measured their learning, recall, and sight recognition. Their performance was compared to a control group of elderly people who also completed the memory assessment, but were not shown a funny video. Cortisol concentrations for both groups were also recorded at the beginning and end of the experiment.

The research team found a significant decrease in cortisol concentrations among both groups who watched the video. Video-watchers also showed greater improvement in all areas of the memory assessment when compared to controls, with the diabetic group seeing the most dramatic benefit in cortisol level changes and the healthy elderly seeing the most significant changes in memory test scores.

From the authors: “Our research findings offer potential clinical and rehabilitative benefits that can be applied to wellness programs for the elderly,” Dr. Bains said. “The cognitive components—learning ability and delayed recall—become more challenging as we age and are essential to older adults for an improved quality of life: mind, body, and spirit. Although older adults have age-related memory deficits, complimentary, enjoyable, and beneficial humor therapies need to be implemented for these individuals.”

Study co-author and long-time psychoneuroimmunology humor researcher, Dr. Lee Berk, added, “It’s simple, the less stress you have the better your memory. Humor reduces detrimental stress hormones like cortisol that decrease memory hippocampal neurons, lowers your blood pressure, and increases blood flow and your mood state. The act of laughter—or simply enjoying some humor—increases the release of endorphins and dopamine in the brain, which provides a sense of pleasure and reward. These positive and beneficial neurochemical changes, in turn, make the immune system function better. There are even changes in brain wave activity towards what’s called the “gamma wave band frequency”, which also amp up memory and recall. So, indeed, laughter is turning out to be not only a good medicine, but also a memory enhancer adding to our quality of life.”

Oops! Researchers find neural signature for mistake correction

Culminating an 8 year search, scientists at the RIKEN-MIT Center for Neural Circuit Genetics captured an elusive brain signal underlying memory transfer and, in doing so, pinpointed the first neural circuit for “oops”—the precise moment when one becomes consciously aware of a self-made mistake and takes corrective action.

Loss of Memory in Alzheimer’s Mice Models Reversed through Gene Therapy

Alzheimer’s disease is the first cause of dementia and affects some 400,000 people in Spain alone. However, no effective cure has yet been found. One of the reasons for this is the lack of knowledge on the cellular mechanisms which cause alterations in nerve transmissions and the loss of memory in the initial stages of the disease.

Researchers from the Institute of Neuroscience at the Universitat Autònoma de Barcelona have discovered the cellular mechanism involved in memory consolidation and were able to develop a gene therapy which reverses the loss of memory in mice models with initial stages of Alzheimer’s disease. The therapy consists in injecting into the hippocampus - a region of the brain essential to memory processing - a gene which causes the production of a protein blocked in patients with Alzheimer’s, the “Crtc1” (CREB regulated transcription coactivator-1). The protein restored through gene therapy gives way to the signals needed to activate the genes involved in long-term memory consolidation.

To identify this protein, researchers compared gene expression in the hippocampus of healthy control mice with that of transgenic mice which had developed the disease. Through DNA microchips, they identified the genes (“transcriptome”) and the proteins (“proteome”) which expressed themselves in each of the mice in different phases of the disease. Researchers observed that the set of genes involved in memory consolidation coincided with the genes regulating Crtc1, a protein which also controls genes related to the metabolism of glucose and to cancer. The alteration of this group of genes could cause memory loss in the initial stages of Alzheimer’s disease.

In persons with the disease, the formation of amyloid plaque aggregates, a process known to cause the onset of Alzheimer’s disease, prevents the Crtc1 protein from functioning correctly. “When the Crtc1 protein is altered, the genes responsible for the synapsis or connections between neurons in the hippocampus cannot be activated and the individual cannot perform memory tasks correctly”, explains Carlos Saura, researcher of the UAB Institute of Neuroscience and head of the research. According to Saura, “this study opens up new perspectives on therapeutic prevention and treatment of Alzheimer’s disease, given that we have demonstrated that a gene therapy which activates the Crtc1 protein is effective in preventing the loss of memory in lab mice”.

The research, published today as a featured article in The Journal of Neuroscience, the official journal of the US Society of Neuroscience, paves the way for a new therapeutic approach to the disease. One of the main challenges in finding a treatment for the disease in the future is the research and development of pharmacological therapies capable of activating the Crtc1 protein, with the aim of preventing, slowing down or reverting cognitive alterations in patients.

Scientists Identify Critical New Protein Complex Involved in Learning and Memory

Scientists from the Florida campus of The Scripps Research Institute (TSRI) have identified a protein complex that plays a critical but previously unknown role in learning and memory formation.

The study, which showed a novel role for a protein known as RGS7, was published April 22, 2014 in the journal eLife, a publisher supported by the Howard Hughes Medical Institute, the Max Planck Society and the Wellcome Trust.

“This is a critical building block that regulates a fundamental process—memory,” said Kirill Martemyanov, a TSRI associate professor who led the study. “Now that we know about this important new player, it offers a unique therapeutic window if we can find a way to enhance its function.”

The team looked at RGS7 in the hippocampus, a small part of the brain that helps turn short-term memory in long-term memory.

The scientists found the RGS7 protein works in concert with another protein, R7BP, to regulate a key signaling cascade that is increasingly seen as a critical to cognitive development. The cascade involves the neurotransmitter GABA, which binds to the GABA_b receptor and opens inhibitory channels known as GIRKs in the cell membrane. This process ultimately makes it more difficult for a nerve cell to fire.

This process turned out to be critical to normal functioning, as the research showed mice lacking RGS7 exhibited deficits in learning and memory.

Martemyanov believes the findings could ultimately have broad therapeutic application. “GIRK channels are implicated in a range of neuropsychiatric conditions, including drug addiction and Down’s syndrome, that result from a disproportionate increase in neuronal inhibition as a result of greater mobilization of these channels,” he said. ^“Now that we know the identity of the critical modulator of GIRK channels we can try to find a way to increase its power with the hopes of reducing the inhibitory overdrive, and that might potentially alleviate some of the  disruptions seen in Down’s syndrome. It is possible that similar strategies might apply for dealing with addiction, where adaptations in the GABAb-GIRK pathway play a significant role.”

Targeting the RGS7 protein could allow for better therapeutic outcomes with fewer side effects because it allows for fine tuning of the signaling, according to Olga Ostrovskaya, the first author of the study and a member of Martemyanov’s lab, who sees many ways to follow up on the findings.

“We’re looking into how RGS7 is involved in neural circuitry and functions tied to the striatum, another part of the brain responsible for procedural memory, mood disorders, motivation and addiction,” Ostrovskaya said. “We may uncover the RGS7 regulation of other signaling complexes that may be very different from those in hippocampus.”