Eating lots of fish, the ultimate brain food, was recently associated with reduced risk of stroke.

A study conducted by Jyrki Virtanen and his crew at the University of Kuopio in Finland found that people who ate more fish tended to have fewer strokes. Virtanen looked at a population of 2,313 participants over the age of 65 who had their brains scanned (via MRI) twice, with a 5-year lapse between scans. After analyzing answers the participants gave to diet-related questionnaires the researchers found that:

• Those eating fish 3 or more times a week had fewer sub-clinical infarcts or “mini-strokes” than those eating fish less than once a month.
• Consuming more fish was associated with more intact brain white matter.
• Fried fish is not so healthy, and seemed to negate the above benefits.

As seen in other research studying healthy brain food, omega-3 fatty acids, which are present in most fish oils, seem to be a key contributor to lowering the risk of stroke.

Reference: Virtanen, J. K., Siscovick, D. S., Longstreth, W. T., Kuller, L. H., & Mozaffarian, D. (2008). Fish consumption and risk of subclinical brain abnormalities on MRI in older adults. Neurology, 71(6), 439-446.

A study of brain function in mice reveals that a stimulating environment improves the memory of their offspring. If this improvement also occurs in humans, a mother’s youthful experiences may help shape her childrens’ ability to learn. Here’s the press release, with the paper reference below the fold:

Newswise — A study reveals that the severity of learning disorders may
depend not only on the child’s environment but also – remarkably – on
the mother’s environment when she was young. The study in
memory-deficient mice, published in the February 4 issue of The
Journal of Neuroscience, was led by Larry Feig, PhD, professor of
biochemistry at Tufts University School of Medicine and member of the
biochemistry and neuroscience programs at the Sackler School of
Graduate Biomedical Sciences at Tufts University.

The researchers studied the brain function of pre-adolescent mice with
a genetically-created defect in memory. When these young mice were
enriched by exposure to a stimulating environment – including novel
objects, opportunities for social interaction and voluntary exercise –
for two weeks, the memory defect was reversed. The work showed that
this enhancement was remarkably long-lasting because it was passed on
to the offspring even though the offspring had the same genetic
mutation and were never exposed to an enriched environment.

Previous research has shown that environmental exposures during
pregnancy can affect offspring. “A striking feature of this study is
that enrichment took place during pre-adolescence, months before the
mice were even fertile, yet the effect reached into the next
generation,” said Feig.

“The offsprings’ improved memory was not the result of better
nurturing by mothers who were enriched when they were young. When the
offspring were raised by non-enriched foster mothers, the offspring
maintained the beneficial effect,” said co-author Junko Arai, PhD,
postdoctoral associate in Feig’s laboratory.

“The effect lasted until adolescence, when it waned, suggesting that
this process is designed specifically to aid the young brain,”
continued Shaomin Li, PhD, MD, co-author, former postdoctoral
associate in Feig’s laboratory, now at Brigham and Women’s Hospital.

“This example of ‘inheritance of acquired characters,’ was first
proposed by Lamarck in the early 1800s. However, it is incompatible
with classical Mendelian genetics, which states that we inherit
qualities from our parents through specific DNA sequences they
inherited from their parents. We now refer to this type of inheritance
as epigenetics, which involves environmentally-induced changes in the
structure of DNA and the chromosomes in which DNA resides that are
passed on to offspring,” said Feig.

Previous research by Feig and his team showed that a relatively brief
exposure to an enriched environment in both normal and
memory-deficient mice unlocks an otherwise latent biochemical control
mechanism that enhances a cellular process in nerve cells called
long-term potentiation (LTP), which is known to be involved in
learning and memory. This enhancement was detected in pre-adolescent
mice but not in adult mice, reflecting the brain’s higher plasticity
in the young.

Feig concluded that the transgenerational inheritance of the effect of
an enriched environment may be a mechanism that has evolved to protect
one’s offspring from deleterious effects of sensory deprivation, which
may be particularly potent in the young and exacerbated in the
learning disabled.

Junko Arai and Shaomin Li, first authors, contributed equally to the
paper. Dean M. Hartley, PhD, of Rush University Medical Center is also
an author.

The work was supported by the National Cancer Institute of the
National Institutes of Health because these findings were derived as
an offshoot of the Feig lab’s long-term experience working on Ras
proteins that are involved in cancer. Fundamental principles of how
Ras proteins function gained by studying its role in cancer expedited
subsequent studies on Ras function in the brain. This work highlights
how major breakthroughs can arise by allowing researches to follow new
leads that cross disciplines. The work was also supported by the Tufts
Center for Neuroscience Research.

Arai J, Li S, Hartley DM, and Feig LA. The Journal of Neuroscience.
2009. (February 4); 29(5): 1496-1502. “Transgenerational Rescue of a
Genetic Defect in Long-Term Potentiation and Memory Formation by
Juvenile Enrichment.” Published online February 3, 2009, doi:
10.1523/JNEUROSCI.5057-08.2009

About Tufts University School of Medicine
Tufts University School of Medicine and the Sackler School of Graduate
Biomedical Sciences at Tufts University are international leaders in
innovative medical education and advanced research. The School of
Medicine and the Sackler School are renowned for excellence in
education in general medicine, special combined degree programs in
business, health management, public health, bioengineering, and
international relations, as well as basic and clinical research at the
cellular and molecular level. Ranked among the top in the nation, the
School of Medicine is affiliated with six major teaching hospitals and
more than 30 health care facilities. The Sackler School undertakes
research that is consistently rated among the highest in the nation
for its impact on the advancement of medical science.

Data collected by Agnes Flöel and her crew at the University of Munster in Germany seems to give yet another reason to resist that second helping of chocolate cake.

The research compared short-term memory performance of overweight individuals who reduced their caloric intake by 30% over 3 months with individuals who maintained their regular diet over the same 3 months.

Results:

• After 3 months, those on the decreased calorie diet improved by 20% on short-term memory tests of word recall.
• Participants who did not change their caloric intake showed no improvements.

The study coincides with multiple other studies demonstrating improved brain plasticity in animals fed calorie restricted diets. Some possible mechanisms at work include:

• The modified action of neurotransmitters
• The stimulation of neurogenesis (production of neurons)
• Increases in cell metabolism

However, in the above study, there may be other factors at work. As all the participants were overweight to begin with, the improvements could simply be due to an increase in overall health (IE blood flow, increased oxygen etc). Studies “starving” healthy individuals seem to be called for in order to eliminate this possibility.

References:
Caloric restriction improves memory in elderly humans. (2009, January 26). . Retrieved January 27, 2009, from http://www.pnas.org/content/early/2009/01/26/0808587106.

Fontán-Lozano, A., Sáez-Cassanelli, J. L., Inda, M. C., de los Santos-Arteaga, M., Sierra-Domínguez, S. A., López-Lluch, G., et al. (2007). Caloric restriction increases learning consolidation and facilitates synaptic plasticity through mechanisms dependent on NR2B subunits of the NMDA receptor. The Journal of Neuroscience: The Official Journal of the Society for Neuroscience, 27(38), 10185-95. doi: 10.1523/JNEUROSCI.2757-07.2007.

Stranahan, A., & Mattson, M. (2008). Impact of Energy Intake and Expenditure on Neuronal Plasticity. Neuromolecular Medicine.

Ever wonder about the workings of your nervous system?  As mentioned in our previous post on cognition, the nervous system is responsible for integrating and processing information about your surroundings while directing action towards the achievement of goals; whether this be eating a tuna sandwich, serenading a lover or getting out of the way of a speeding bus. Physically, it is made up of your brain, spinal cord and peripheral nerves.

Let’s look at the structural components of this biological orchestra.

Neurons and Glia
The basic functional units of the nervous system include neurons (cells who’s primary job is to communicate) and glia (cells which support neurons and their communication).

The average brain has about 100 billion neurons and about 9 times as many glia.

Neurons (with the help of glia) connect and coordinate senses such as sight, hearing, smell, touch and taste with the activity of your muscles and organs. They are either taking information in for integration, communicating with other neurons for information processing, or sending information out to generate action.

Glial cells (of which there are multiple types) do a variety of tasks to support the functioning of neurons, including removing waste, providing nutritional and structural support and facilitating connections. Some glia have also been shown to communicate with neurons, as well as each other, in order to help coordinate neuronal activity.

Synapses and Neurotransmitters
Synapses are the actual locations at which neurons communicate with each other, and a typical neuron has about 10,000 of them.

Neurons communicate at synapses through the use of neurotransmitters. Neurotransmitters are chemicals sent between neurons as well as the muscles and organs they work with. They attach to receptors on receiving cells, translating into one of three basic types of messages:

•    Excitatory- Encouraging connected neurons and other related cells to “pass it on” or activate; perhaps prompting you to swat at that fly after being buzzed by the umpteenth time or dilate your pupils when the lights go out.

•    Inhibitory- Suggesting that the receiving cell not continue passing on the signal or take action. This could be involved in the shutting down of appetite in response to the non-acquired taste of anchovies or the ability to ignore the radio in your car while figuring out how to get un-lost.

• Adaptive- Instructing a neuron to change something in its structure or the way it functions. This is the basis of plasticity where neurons may reduce or increase the number of connections, move them around and or adjust their sensitivity; all of which are part of the learning process.

Neural Networks

Neurons which collaborate on a specific physiological function, such as hearing high pitches, moving your pinky or remembering to take the trash out, are considered to be part of a shared neural network. Typically these functionally related neurons will use only one or two of the over 100 different types of neurotransmitters available. Neurotransmitters, however, can and often are associated with several types of neural networks.

Serotonin is an example of a neurotransmitter involved with the regulation of multiple systems including mood, appetite, temperature, pain sensation and sleep.

Dopamine is the neurotransmitter of choice for neural networks dealing with reward, such as the feeling you get after winning an egg toss or eating a delicious meal. It is however also used by circuits involving memory and attention.

Complexity
As much as we do know about how our nervous systems work, there is still much more to be discovered. One of the many areas where little is known involves how different neural networks, responsible for such diverse tasks as detecting movement, recognizing objects and generating action, can communicate between themselves. The mechanisms involved in coordinating the information from different specialized neural systems into a seamless experience of say, catching a ball, is still a mystery.  This is referred to as the binding problem, and although there are plenty of theories, there are no clear answers as of yet.

As you can see, the interactions between our neurons, neurotransmitters and constantly shifting surroundings are complex…..especially when they are trying to grasp the complexity of interactions between neurons, neurotransmitters and constantly shifting surroundings;)

A recent research review to be published in the journal Progress in Neuropsychopharmacology & Biological Psychiatry shows a link between cigarette smoking and adverse changes in the function and physiology of the brain. Summarizing the findings of dozens of experiments, the review indicates that:

• Strokes are more prevalent in smokers than non-smokers.
• Gray matter (made up of brain cells) shrinks in long-term smokers.
• Smoking is associated with less integrity in the white matter connecting brain hemispheres.
• Puffing tobacco can be bad for neurotransmitters.

There are a few factors clouding the picture however. These include the fact that alcohol consumption often accompanies cigarette smoking and has also been shown to have detrimental effects on the brain.

In addition there is the question of which comes first: brain abnormalities or smoking habits. It is possible that preexisting brain abnormalities increase the likelihood of smoking and addiction.  The author suggested more research in order to answer these questions, as well as to determine if these symptoms are reversible after quitting.

References:

Domino, E. (2008). Tobacco Smoking and MRI/MRS Brain Abnormalities Compared to Nonsmokers. Progress in Neuro-Psychopharmacology and Biological Psychiatry, In press.

We’re on a roll! Following the debut of Name Tag last month, we are now ready to release Top Chimp, a brain game that sharpens visual attention and trains working memory. We think it’s more fun than a barrel of…well, monkeys, but would love to have your feedback before the game becomes part of the regular set of brain exercises. Please find the game here http://games.lumosity.com/top_chimp.html and send any suggestions to games@lumosity.com.

Path Finder is based on the classic test of executive function, Trail Making, Part B. You can also try a larger version of Path Finder in the Warm Ups section of Lumosity. The average time to complete this version is 34 seconds (the typical time to complete the smaller version above is shorter).

Coffee is not just a popular beverage–it’s a drug, an addicting habit that many of us partake every morning to begin our day. Considering that most major cities have coffee shops in virtually every street corner, it is not easy to avoid coffee. And maybe you shouldn’t try to.

Recent studies indicate that coffee may somewhat delay the onset of dementia. One study found that women over the age of 65 who had mild cognitive impairment (MCI), but who also drank at least 3 cups per day, were at reduced risk of progressing to Alzheimer’s disease. Their slowed mental deterioration may be attributed to the caffeine, which could protect neurons that are involved in forming memories.

So imbibing some coffee might indeed be a good thing, as long as you don’t mind the palpitations or coffee jitters (see our previous post on coffee). If further research supports these findings, perhaps we should thank our local Starbucks or Coffee Bean for keeping us wide awake and sharp through the years.

Imagine being home on a moonless night when the power unexpectedly goes out. You are shrouded by silent darkness, instantly blind to your surroundings. Yet despite this sensory deprivation, you can navigate somewhat effortlessly around the futon, through the doorway of the kitchen, and across to the middle drawer where your lighter is stored, avoiding walls, furniture, and other familiar obstacles along the way. How, without vision or echolocation, did you remember where everything was in relation you and to everything else?

The brain’s “spatial memory,” as this ability is called, relies on the operation of neural “maps.” Critical to these maps are specialized neurons known as “place cells,” which are located in the hippocampal formation. These cells show place-specific firing patters; that is, a given place cell will become highly activated only when an animal is at a specific location within a particular environment. Theoretically, networks of place cells, each activated in a distinct but partially overlapping spatial region, form maps of every environment encountered. If an environment is experienced repeatedly, the map will be committed to long-term memory; the brain can then deduce its animal’s location by
interpreting the activation of place cells along the relatively stable map.

Importantly, place cell activation patterns are based on spatial clues. In the introductory example, you could navigate in darkness only because you knew your relative position at the time of the power outage. If, however, you were to close your eyes and twirl around on your toes, and open your eyes immediately after the outage began, your internal map (and thus you), would be spatially bewildered. Yet if you were to grope and fumble until you found the futon, your map would reorient, allowing you to immediately intuit the rest of your spatial world.

What about when two environments have similar spatial cues? For example, imagine two parallel streets in San Francisco, each lined by eminent Victorians, peppered with sushi restaurants, cafes, and liquor stores, a Muni rail cutting a rugged metallic swath down the middle of each street. The spatial cues of these two environments would activate a somewhat overlapping pattern of place cells, yet the subtle differences on each street (an Indian-Pakistani restaurant on the north side of one, a pirate store on
the south side of the other) would allow you to recognize the differences and navigate each uniquely. How does your brain recognize such relatively small differences to construct the distinct maps the environments deserve?

Researchers at the University of Bristol and MIT published a report in the early online edition of Science on June 7 that explored this question. The group focused on the role of a particular region of the hippocampal formation, the dentate gyrus, and found it to be crucial for distinguishing between similar locations. The dentate gyrus does not contain place cells, but it does serve as an interface between the hippocampus (where the place cells are located) and the rest of the brain (which would provide the sensory information, the spatial cues). Thus, it may provide the neural input necessary for “map” construction.

The group removed the NMDA receptor, a protein crucial for synaptic plasticity (the process by which the connection between two neurons adapts to become stronger or weaker, thus enabling learning and memory), specifically from the dentate gyrus. Although these mice perform normally in several learning and memory tasks, they had trouble discriminating between similar yet distinct environments. At the neuronal level, their place cells showed decreased spatial specificity, becoming activated in a significantly broader range.

This type of deficit is similar to what has been previously observed in aged animals; these results may thus help explain the disorientation experienced by some older people, who often struggle to adapt to new spatial locations. Perhaps a major component of their impairment is an age-related dysfunction in the dentate gyrus, which makes it difficult to encode subtle differences and form unique place cell maps for similar yet distinct places. Such individuals would also lose their bearings as a result of changes to familiar environments; e.g., a few years ago I moved some of my grandmother’s icons around on her computer’s desktop, and she was completely bewildered until I dragged
them all back to their original, recognizable locations.

Reference:
McHugh TJ et al. “Dentate gyrus NMDA receptors mediate rapid pattern separation in the hippocampal network” Science. [Published online June 7 2007, DOI: 10.1126/science.1140263]

Video games have been used with some success for pain management in children. This works primarily by providing a captivating distraction from the discomfort. In cancer patients, playing video games can mitigate the nausea that comes with chemotherapy. Even after treatment, patients that played video games had a  lower systolic blood pressure and required fewer analgesics. [Note that Stanford researchers are currently evaluating the possibility that cognitive deficits due to chemotherapy can be reversed with Lumosity exercises. Visit the chemobrain research page to learn more.]

Though sometimes criticized for inciting violence and displacing more worthwhile activities, if gaming is approached in moderation and with a modicum of maturity it is safe for most people.