Habits - a TED talk

Gene find could lead to drug for chronic back pain

A gene responsible for chronic pain has been identified, with scientists saying this could lead to drugs for treating long-lasting back pain.

Writing in the journal Science, University of Cambridge researchers removed the HCN2 gene from pain-sensitive nerves in mice. Deleting the gene stopped any chronic pain but did not affect acute pain. About one in seven people in the UK suffer from chronic pain, which can also include arthritis and headaches.

The researchers say their findings open up the possibility that new drugs could be developed to block the protein produced by the HCN2 gene, which regulates chronic pain.

The HCN2 gene, which is expressed in pain-sensitive nerve endings, has been known for several years, but its role in regulating pain was not understood.

For the study, the researchers removed the HCN2 gene from pain-sensitive nerves. They then carried out studies using electrical stimuli on these nerves in cell cultures to determine how they were altered by the removal of HCN2.

Individuals suffering from neuropathic pain often have little or no respite because of the lack of effective medications”

Prof Peter McNaughtonUniversity of Cambridge

They then studied genetically modified mice in which the HCN2 gene had been deleted.

By measuring the speed that the mice withdrew from different types of painful stimuli, the scientists were able to conclude that deleting the HCN2 gene abolished neuropathic pain.

However, they found that deleting HCN2 did not affect normal acute pain - which occurs suddenly, for example when biting one's tongue.

'No respite'

Chronic pain comes in two main varieties. Inflammatory pain occurs when a persistent injury, such as a burn or arthritis, results in very sensitive nerve endings which increase the sensation of pain.

Neuropathic pain occurs when nerves are damaged, causing ongoing pain. This type of chronic pain, which is often lifelong, is surprisingly common and is poorly treated by current drugs, the study says.

It is often seen in patients with diabetes and shingles, and in the aftermath of cancer chemotherapy. It is also common in lower back pain and other chronic painful conditions.

Professor Peter McNaughton, lead author of the study and head of the department of pharmacology at the University of Cambridge, said there was now hope for these people.

"Individuals suffering from neuropathic pain often have little or no respite because of the lack of effective medications. Our research lays the groundwork for the development of new drugs to treat chronic pain by blocking HCN2."

He added: "Many genes play a critical role in pain sensation, but in most cases interfering with them simply abolishes all pain, or even all sensation.

"What is exciting about the work on the HCN2 gene is that removing it - or blocking it pharmacologically - eliminates neuropathic pain without affecting normal acute pain. This finding could be very valuable clinically because normal pain sensation is essential for avoiding accidental damage."

Dr Brian Hammond, chairman of charity BackCare, said the findings of the study were good news.

"Any effective treatment which relieves the suffering of chronic pain is to be welcomed. Treatment which helps reduce pain but still leaves the body's warning mechanisms intact is a major breakthrough."

The study was funded by the Biotechnology and Biological Sciences Research Council (BBSRC), and the European Union.

The Brain and High :evels of Iron and Copper

High Iron Or Copper Levels Block Brain-cell DNA RepairDiscovery could shed light on Alzheimer’s, Parkinson’s and other neurodegenerative disorders


No one knows the cause of most cases of Alzheimer’s, Parkinson’s and other neurodegenerative disorders. But researchers have found that certain factors are consistently associated with these debilitating conditions. One is DNA damage by reactive oxygen species, highly destructive molecules usually formed as a byproduct of cellular respiration. Another is the presence of excessive levels of copper and iron in regions of the brain associated with the particular disorder.

University of Texas Medical Branch at Galveston researchers have discovered how these two pieces of the neurodegenerative disease puzzle fit together, a connection they describe in a review article in the current Journal of Alzheimer’s Disease. A high level of copper or iron, they say, can function as a “double whammy” in the brain by both helping generate large numbers of the DNA-attacking reactive oxygen species and interfering with the machinery of DNA repair that prevents the deleterious consequences of genome damage.

“It’s been suggested that an imbalance of DNA damage and repair produces a buildup of unrepaired genetic damage that can initiate neurodegenerative pathology,” said postdoctoral fellow Muralidhar Hegde, lead author of the paper. “We don’t yet know enough about all the biochemical mechanisms involved, but we have found multiple toxic mechanisms linking elevated iron and copper levels in the brain and extensive DNA damage — pathological features associated with most neurodegenerative disorders.”
Humans ordinarily have small amounts of iron and copper in their bodies — in fact, the elements are essential to health. But some people’s tissues contain much larger quantities of iron or copper, which overwhelm the proteins that normally bind the metals and sequester them for safe storage. The result: so-called “free” iron or copper ions, circulating in the blood and able to initiate chemical reactions that produce reactive oxygen species.

“Reactive oxygen species cause the majority of the brain cell DNA damage that we see in Alzheimer’s and Parkinson’s disease, as well as most other neurodegenerative disorders,” Hegde said. “It’s bad enough if this damage occurs on one strand of the DNA double helix, but if both strands are damaged at locations close to each other you could have a double-strand break, which would be fatal to the cell.”

Normally, special DNA repair enzymes would quickly mend the injury, restoring the genome’s integrity. But experiments conducted by Hegde and his colleagues showed that iron and copper significantly interfere with the activity of two DNA repair enzymes, known as NEIL1 and NEIL2.

“Our results show that by inhibiting NEIL1 and NEIL2, iron and copper play an important role in the accumulation of DNA damage in neurodegenerative diseases,” Hegde said.
The researchers got a surprise when they tested substances that bond to iron and copper and could protect NEIL1 from the metals. One of the strongest protective agents was the common South Asian spice curcumin, which also has been shown to have other beneficial health effects.

“The results from curcumin were quite beautiful, actually,” Hegde said. “It was very effective in maintaining NEIL activity in cells exposed to both copper and iron.” Other authors of the Journal of Alzheimer’s Disease paper include research associate Pavana Hegde; K.S. Rao, director of the Institute for Scientific Research and High Technology Services in Panama; and UTMB Professor Sankar Mitra. The United States Public Health Service and the American Parkinson’s Disease Association supported this research.

ABOUT UTMB Health

Established in 1891, Texas’ first academic health center comprises four health sciences schools, three institutes for advanced study, a research enterprise that includes one of only two national laboratories dedicated to the safe study of infectious threats to human health, and a health system offering a full range of primary and specialized medical services throughout Galveston County and the Texas Gulf Coast region. UTMB Health is a component of the University of Texas System and a member of the Texas Medical Center.
Contact: Jim Kelly

Source: University of Texas Medical Branch at Galveston

Could H. Pylori bacteria cause Parkinson's disease?

The bacteria responsible for stomach ulcers have been linked to Parkinson's disease, according to researchers in the US.Mice infected with Helicobacter pylori went onto develop Parkinson's like symptoms.
The study, presented at a meeting of the American Society for Microbiology, argues that infection could play "a significant role".

The charity Parkinson's UK said the results should be treated with caution. Parkinson's disease affects the brain and results in slow movements and a tremor. Middle-aged mice, the equivalent of being between 55 and 65 in humans, were infected. Six months later they showed symptoms related to Parkinson's, such as reduced movement and decreased levels of a chemical, dopamine, in the brain. These changes were not noticed in younger mice.

Toxic

Dr Traci Testerman, from the Louisiana State University Health Sciences Center, said: "Our findings suggest that H. pylori infection could play a significant role in the development of Parkinson's disease in humans."The results were far more dramatic in aged mice than in young mice, demonstrating that normal ageing increases susceptibility to Parkinsonian changes in mice, as is seen in humans."The researchers believe the bacteria are producing chemicals which are toxic to the brain.

They said H. pylori was able to "steal" cholesterol from the body and process it by adding a sugar group.
The bacteria responsible for stomach ulcers may have a role in Parkinson's say researchers. Dr Testerman said this new chemical was almost identical to one found in seeds from the cycad plant, which had been shown to trigger a Parkinson's-like disease among people in Guam.: "H. pylori eradication in late stage Parkinson's disease is unlikely to result in significant improvement.

"Certain neurons are killed before symptoms begin, and more are killed as the disease progresses. Those neurons will not grow back." Dr Kieran Breen, director of research at Parkinson's UK, said: "We believe Parkinson's is most likely caused by a combination of environmental factors together with an individual's genetic susceptibility to developing the condition. He said there was some evidence that bacteria can prevent the main drug to treat Parkinson's, levodopa, being absorbed, but there was no strong evidence that people who have H. pylori in their gut are actually more likely to develop Parkinson's.He added: "The current study is interesting and suggests that the bacteria may release a toxin that could kill nerve cells.

"However, the results should be treated with caution. The research was carried out in mice that were infected with relatively high doses of the bacterium or its extract. "While they developed movement problems, we don't know whether this was actually due to the death of nerve cells. Further research needs to be carried out".

Broken Hearts lead to early risk of death

Earlier this year, Paul Boyle, a geography professor at the University of St. Andrew’s, published a longitudinal study of a large sample of the Scottish population — roughly 58,000 men and 58,000 women — that strived to determine the existence of a widowhood effect. Boyle’s team analyzed data about the couples dating back to the early 1990s.


“We did find a significant effect … about a 40 per cent higher risk of death following widowhood than you would otherwise expect,” Boyle says. While the risk was most evident in the six months following the death of one’s spouse, Boyle says a higher mortality risk for the surviving spouse was evident for a decade after the loss of their partner.

A body of earlier research supports Boyle’s intriguing findings. One study published in 2006 in the New England Journal of Medicine found that, among elderly people, the hospitalization of a spouse was associated with an increased risk of death for the other partner.Another study published a year later, conducted by University of Glasgow researchers, tracked 4,000 couples and found surviving spouses were at least 30 per cent more likely to die of any cause in the first six months following the death of their partner, versus those who hadn’t lost a spouse. Dr. Joshua Shadd, palliative care specialist, London, Ont., says married couples share many of the same environmental influences on their health Lauren Pelley/Western

It wasn’t until after his death that Ed Charette 's family learned he had been suffering from multiple myeloma — a hard-to-treat cancer of the plasma cells, a type of blood cell. He’d only been in the hospital 10 days before he died, and doctors hadn’t yet diagnosed his condition.“Up until then, he hadn’t complained of anything, really,” Deloughery recalls. “He was very sad, really saddened by her passing. [We] could see that his life was not the same for him. He was quieter. He was determined to carry on but the same spirit wasn’t there, that energy, that will.”

So why is widowhood such a noticeable factor in the death of a surviving spouse? One potential reason is simple: spouses are just so much alike.“Married couples share many of the same environmental influences on their health,” explains Dr. Joshua Shadd, a London, Ontario-based palliative care researcher. “Couples have, generally speaking, a similar dietary history, history of exposure to toxins and carcinogens, similar history of stressers, psycho-social support [and] similar socio-economic level.”But Boyle says his study took these environmental factors into account and the widowhood effect still remained.
“This is a very clear example of a social effect — the fact that you lose your partner — [that has] an impact on your own life expectancy,” Boyle says.
Shadd says some grieving spouses may simply have some emotional or psychological control over when they choose to die. “I certainly believe that emotions and psyche have an influence on people’s living and dying process,” he adds.

A true broken heart

The mere shock of losing a loved one can also take a toll on the human body — and can even lead to an actual broken heart. "Broken heart syndrome’ is a documented medical phenomenon brought on by sudden physical or emotional stress, such as the death of a partner.While the condition is rarely fatal, it mimics a heart attack and results in severe heart muscle weakness.Cardiologist Ilan Wittstein, an assistant professor at the Johns Hopkins University School of Medicine and its Heart Institute, led a 2005 study on the condition.
Middle-aged and elderly women are most likely to develop broken heart syndrome — or stress cardiomyopathy —according to Wittstein’s research.“[It’s] a sudden deterioration in the squeezing ability of the heart,” he says.

The pain of losing a partner is both physiological and psychological, if this research is any indication.
Boyle says his study on the widowhood effect also highlights important difficulties faced by widowed spouses.
“Widows are a vulnerable group,” he explains. “We need to pay attention to people who’ve been left behind and lost their partner.”Since the increased mortality risk continues for ten years, Boyle says the data suggests long-term care strategies for widows and widowers are necessary.Reflecting on the loss of her parents, Ed and Muriel, within a few weeks of each other, Deloughery understands how hard it must be for a surviving spouse to carry on after losing their lifelong partner.“You’re so joined — you finish each other’s thoughts, you know their likes, their dislikes — everything,” she says. “It’s somebody who totally gets you. You lose that part.”
And Deloughery knows from her own experience, too. At 57, she’s now a widow herself, having lost her husband of 27 years, Tom, last autumn.“So I can only imagine what 67 years was like,” she says.

Sodium channels evolved before Animal's nervous systems

Sodium Channels Evolved Before Animals’ Nervous Systems, Research ShowsAn essential component of animal nervous systems—sodium channels—evolved prior to the evolution of those systems, researchers from The University of Texas at Austin have discovered.“The first nervous systems appeared in jellyfish-like animals six hundred million years ago or so,” says Harold Zakon, professor of neurobiology, “and it was thought that sodium channels evolved around that time. We have now discovered that sodium channels were around well before nervous systems evolved.”

Zakon and his coauthors, Professor David Hillis and graduate student Benjamin Liebeskind, published their findings this week in PNAS. Nervous systems and their component neuron cells were a key  innovation in the evolution of animals, allowing for communication across vast distances between cells in the body and leading to sensory perception, behavior and the evolution of complex animal brains.

Sodium channels are an integral part of a neuron’s complex machinery. The channels are like floodgates lodged throughout a neuron’s levee-like cellular membrane. When the channels open, sodium floods through the membrane into the neuron, and this generates nerve impulses. Zakon, Hillis and Liebeskind discovered the genes for such sodium channels hiding within an organism that isn’t even made of multiple cells, much less any neurons. The single-celled organism is a choanoflagellate, and it is distantly related to multi-cellular animals such as jellyfish and humans.

The researchers then constructed evolutionary trees, or phylogenies, showing the relationship of those genes in the single-celled choanoflagellate to multi-cellular animals, including jellyfish, sponges, flies and humans.Because the sodium channel genes were found in choanoflagellates, the scientists propose that the genes originated not only before the advent of the nervous system, but even before the evolution of multicellularity itself.

“These genes were then co-opted by the nervous systems evolving in multi-cellular animals,” says Hillis, the Alfred W. Roark Centennial Professor in Natural Sciences. “This study shows how complex traits, such as the nervous system, can evolve gradually, often from parts that evolved for other purposes.” “Evolutionarily novel organs do not spring up from nowhere,” adds Zakon, “but from pre-existing genes that were likely doing something else previously.” Liebeskind, a graduate student in the university’s ecology, evolution and behavior program, is directing his next research efforts toward understanding what the sodium channels do in choanoflagellates.

Notes about this neuroscience research article
Contacts: Harold Zakon, Ben Liebeskind, David Hillis – University of Texas at Austin
Source: University of Texas at Austin press release

Human Taste Cells Regenerate in a Dish

Success opens doors extending from health to new taste molecules

Following years of futile attempts, new research from the Monell Center demonstrates that living human taste cells can be maintained in culture for at least seven months. The findings provide scientists with a valuable tool to learn about the human sense of taste and how it functions in health and disease.This advance ultimately will assist efforts to prevent and treat taste loss or impairment due to infection, radiation, chemotherapy and chemical exposures.“People who undergo chemotherapy or radiation therapy for oral cancer often lose their sense of taste, leading to decreased interest in food, weight loss, and malnutrition,” said lead author M. Hakan Ozdener, M.D., Ph.D., M.P.H., a cellular biologist at Monell. “The success of this technique should provide hope for these people, as it finally provides us with a way to test drugs to promote recovery.”Taste cells are found in papillae, the little bumps on our tongues. These cells contain the receptors that interact with chemicals in foods to allow us to sense sweet, salty, sour, bitter, and umami. They also are among the few cells in the body with the special capacity to regenerate, with new taste cells maturing from progenitor ‘stem’ cells every 10-14 days.

For many years it was believed that taste cells needed to be attached to nerves in order to both function properly and regenerate. For this reason, scientists thought that it was not possible to isolate and grow these cells in culture, which limited the scope of studies to understand how human taste cells function.
“It had become engrained in the collective consciousness that it wouldn’t work,” said Monell cellular biologist Nancy E. Rawson, Ph.D To dispel the long-held belief, the Monell scientists first demonstrated in 2006 that taste cells from rats could successfully be maintained in culture. In the current study, published online in the journal Chemical Senses, they then applied that methodology to a more clinically relevant population – humans.

Taking tiny samples of tongue tissue from human volunteers, the researchers first adapted existing techniques to demonstrate that the human taste cells indeed can regenerate in culture.They went on to show that the new taste cells were functional, maintaining key molecular and physiological properties characteristic of the parent cells. For example, the new cells also were activated by sweet and bitter taste molecules.“By producing new taste cells outside the body, our results demonstrate that direct stimulation from nerves is not necessary to generate functional taste cells from precursors,” said Ozdener.

The establishment of a feasible long-term taste cell culture model opens a range of opportunities to increase understanding of the sense of taste.“Results from these cells are more likely to translate to the clinic than those obtained from other species or from systems not derived from taste tissue,” said Rawson.The cells also can be used to screen and identify molecules that activate the taste receptors; one such example might be a salt replacer or enhancer.

“The model will help scientists identify new approaches to design and establish cell culture models for other human cells that previously had resisted viable culture conditions,” said Ozdener

Notes about this neuroscience research article
Also contributing to the study were Joseph Brand, Fritz Lischka, John Teeter, and Paul Breslin of Monell and Andrew Spielman of the New York University School of Medicine. Dr. Rawson is currently employed by AFB International. Dr. Lischka is currently at the Uniformed Services University of the Health Sciences. Dr. Breslin is also faculty at Rutgers University School of Environmental and Biological Sciences. The research was funded by the National Institute on Deafness and Other Communication Disorders, the National Science Foundation, and Givaudan Inc.

Contact: Leslie Stein

Source: Monell Chemical Senses Center press release

Light switches in the brain

Brain Food

Simply put, your brain likes to eat. And it likes powerful fuel: quality fats, antioxidants, and small, steady amounts of the best carbs.


On a deadline? Need to rally? Avoid the soda, vending machine snacks and tempting Starbucks pastries and go for these powerful brain boosters instead. The path to a bigger, better brain is loaded with Omega-3 fats, antioxidants, and fiber. Give your brain a kick start: eat the following foods on a daily or weekly basis for results you will notice.

20 foods that will supercharge your brain:
1. Avocado
Start each day with a mix of high-quality protein and beneficial fats to build the foundation for an energized day. Avocado with scrambled eggs provides both, and the monounsaturated fat helps blood circulate better, which is essential for optimal brain function. Worst alternative: a trans-fat-filled, sugar-laden cream cheese Danish.
Green it: you don’t need to buy an organic avocado – conventional is fine. But make sure your supplementary protein is free range, cage free, or organic.

2. Blueberries
These delicious berries are one of the best foods for you, period, but they’re very good for your brain as well. Since they’re high in fiber and low on the glycemic index, they are safe for diabetics and they do not spike blood sugar. Blueberries are possibly the best brain food on earth: they have been linked to reduced risk for Alzheimer’s, shown to improve learning ability and motor skills in rats, and they are one of the most powerful anti-stress foods you can eat. Avoid: dried, sweetened blueberries.

Green it: buy local and organic, and be mindful of seasonality. When blueberries are out of season, opt for cranberries, grapes, goji berries, blackberries or cherries to get your brain boost.

3. Wild Salmon

Omega-3 fatty acids are essential for your brain. These beneficial fats are linked to improved cognition and alertness, reduced risk of degenerative mental disease (such as dementia), improved memory, improved mood, and reduced depression, anxiety and hyperactivity. Wild salmon is a premium source, but we’ll highlight a few other sources on this list for vegetarians and people who just don’t like salmon. Avoid farmed (read: sea lice infested) salmon.

Green it: the California salmon stock is threatened, so choose wild Alaskan salmon only, and eat small portions no more than twice a week.

4. Nuts
Nuts contain protein, high amounts of fiber, and they are rich in beneficial fats. For getting an immediate energy boost that won’t turn into a spike later, you can’t do better than nuts. The complex carbs will perk you up while the fat and protein will sustain you. Nuts also contain plenty of vitamin E, which is essential to cognitive function. You don’t have to eat raw, plain, unsalted nuts, but do avoid the ones with a lot of sweetening or seasoning blends. Filberts, hazelnuts, cashews, and walnuts are great choices, with almonds being the king of nuts.

For those avoiding carbs, macadamia nuts are much higher in fat than most nuts. By the way, peanuts just aren’t ideal. Aside from the fact that many people are allergic, peanuts have less healthy fat than many other types of nuts…maybe that’s because peanuts are not actually a nut! They’re still much better than a candy bar, however.

Green it: try to choose organic, raw nuts, and if you can’t get those, at least avoid the tins of heavily-seasoned, preservative-laden nuts that may have taken many food miles to get to your mouth.

5. Seeds

Try sunflower seeds, sesame seeds, flax seed, and tahini (a tangy, nutty sesame butter that tastes great in replacement of mayo and salad dressing). Seeds contain a lot of protein, beneficial fat, and vitamin E, as well as stress-fighting antioxidants and important brain-boosting minerals like magnesium.

Green it: Again, just look for organic and try to avoid the highly-seasoned, processed options. In general, things like fruits, vegetables, seeds and nuts are pretty low-impact, environmentally speaking, in comparison to meats and cheeses.

6. Coffee

Thine eyes do not deceive (even if you are in the midst of a sugar crash). Coffee is good for your brain. Did you know coffee actually contains fiber? That’s going to help your cardiovascular system. Coffee also exerts some noted benefit to your brain in addition to providing you with a detectable energy boost.
The trick is not to have more than a few cups. But you can safely enjoy 2-4 cups daily – we are talking about supercharging here. Just please don’t go ruining a good thing by loading it up with sugar! Espresso beans are actually a phenomenally healthy snack, by the way.

Green it: brew yourself some fair-trade organic coffee to benefit both the planet and the workers who grow your beans. Use a thermos instead of a throwaway cup.

7. Oatmeal

Nature’s scrub brush is one of the best foods for cardiovascular health, which translates to brain health. Additionally, oatmeal is packed with fiber, a reasonable amount of protein, and even a small amount of Omega-3′s. It’s a good grain that will sustain you throughout the morning so you aren’t prone to irritability or an energy crash.
Green it: the healthiest oatmeal is the real, steel-cut deal. Steer clear of those little microwavable packets that are loaded with sugar. All that packaging isn’t very green.

8. Beans
One more for carb-lovers. (The brain uses about 20% of your carbohydrate intake and it likes a consistent supply.) Beans are truly an amazing food that is sadly overlooked. They’re humble, but very smart. Not only are they loaded with fiber, vitamins, minerals and protein, they’re ridiculously cheap. An entire bag of beans usually costs only a few dollars and will provide many meals. Beans provide a steady, slow release of glucose to your brain – which means energy all day without the sugar crash. Don’t go eating a whole platter of frijoles, though – just 1/4 of a cup is fine.

Green it: look for heirloom beans that are raised sustainably, like those from Rancho Gordo.

9. Pomegranate
Opt for the fruit over the juice so you get more fiber. Pomegranates contain blueberry-like levels of antioxidants, which are essential for a healthy brain. Your brain is the first organ to feel the effects of stress, so anything you can do to offset stress is a smart choice.

Green it: pomegranates are seasonal and not generally local for most of us, so enjoy sparingly and rely on other berries like acai, grapes and cherries when you can’t get this fruit.

10. Brown Rice

Brown rice is a low-glycemic complex carbohydrate that is excellent for people sensitive to gluten who still want to maintain cardiovascular health. The better your circulation, the sharper your brain.
Green it: don’t buy the excessively-packaged “boil in a bag” rice packets. Just make up a big batch of brown rice in a rice cooker on Sunday so you have it on hand for easy lunches all week.

11. Tea

You have to brew tea fresh or you won’t get the benefits of all those catechines (antioxidants) that boost your brain. Because tea has caffeine, don’t have more than 2-3 cups daily.
Green it: buy organic, fair trade loose leaf or packets to support sustainable business practices.

12. Chocolate

Things are looking increasingly better for chocolate. It’s got brain-boosting compounds, it’s loaded with antioxidants, and it has just the right amount of caffeine. Chocolate sends your serotonin through the roof, so you’ll feel happy in short order. Dark chocolate is also rich in fiber. (Remember, fiber = healthy cardiovascular system = healthy brain.)

Green it: go for super dark, fair-trade, pure organic chocolate, not the sugary, processed milk chocolate candy bars.

13. Oysters

Oysters are rich in selenium, magnesium, protein and several other nutrients vital to brain health. In one study researchers found that men who ate oysters reported significantly improved cognition and mood! Not all shellfish are good for you but oysters are a sure bet.

Green it: oysters are actually one of the most eco-friendly seafood options, so eat up!

14. Olive Oil

Though we know the brain does need a small, steady supply of glucose, don’t overlook fat. Studies have consistently shown that a low-fat diet is not the health boon we hoped it would be (remember the 90s low-fat craze?). In fact, avoiding fat can increase foggy thinking, mood swings, and insomnia. A diet rich in healthy fats is essential to clear thinking, good memory, and a balanced mood. Your brain is made of fat, after all. ne study of men found that those who relied on the processed vegetable fats found in salad dressings, snacks and prepared foods had 75% higher rates of mental degradation (dementia, memory loss) than men who ate healthy fats. Most processed foods and fast foods use corn oil, palm oil, soybean oil and other Omega-6 fats. You don’t want Omega 6 fats. Even saturated fat is safer than Omega 6′s.

Choose healthy fats such as those present in olive oil, nut butters, nuts and seeds, flax, oily fish, and avocados. Avoid processed fats found in pastries, chips, candy bars, snacks, junk food, fried foods and prepared foods. Eating the wrong fat can literally alter your brain’s communication pathways.

Green it: look for organic, local, or farmers’ market options when it comes to your food. You should also explore herbal remedies for mood swings and brain health.

15. Tuna

In addition to being another rich source of Omega-3′s, tuna, particularly yellowfin, has the highest level of vitamin B6 of any food. Studies have shown that B6 is directly linked to memory, cognition and long term brain health. Generally, the B vitamins are among the most important for balancing your mood. B6 in particular influences dopamine receptors (dopamine is one of your “feel good” hormones along with serotonin).
My personal cocktail: SAMe (nature’s happiness molecule) and a mega-dose of B-complex keeps me humming even when I’ve got a mountain of work to do. Which, like you, is all the time.

Green it: only eat tuna from sustainable fisheries, and if you’re looking for a B6 source that is vegetarian, opt for a banana, which contains a third of your day’s requirement (tuna offers nearly 60%).

16. Garlic
Garlic – the fresher the better – is one of the most potent nutritional weapons in your arsenal. Eat it as much as your significant other can stand. Not only is it fabulous for reducing bad cholesterol and strengthening your cardiovascular system, it exerts a protective antioxidant effect on the brain.
Avoid: I know it makes life easier, but don’t even think about buying the chopped or peeled garlic. Nutritional benefits = zero.

Green it: just choose organic, and go for local if you can get it.


17. Eggs

Eggs contain protein and fat to provide energy to your brain for hours, and the selenium in organic eggs is proven to help your mood. You really needn’t worry about the overblown cholesterol fears. (I have quite a bit to say on this topic but I’ll restrain myself for once.)
Green it: choose organic, free range, vegetarian fed eggs.

18. Green Leafy Vegetables
Spinach, kale, chard, romaine, arugula, lolla rossa – whatever green you like, eat it daily. Green, leafy vegetables are high in iron (slightly less “green” iron sources include beef, pork and lamb). Americans tend to be deficient in iron, which is too bad, because the deficiency is linked to restless leg syndrome, fatigue, poor mood, foggy thinking, and other cognition issues.Green it: choose organic, and shop at your farmers’ market or order from a local CSA. Leave out the red meat a few days a week and rely on a big, well-seasoned green stir fry or salad.

19. Tomatoes

Go figure, but tomatoes don’t usually make the brain-boosting food lists. (Thank goodness I found the one that did so I’m not the only one.) Tomatoes contain lycopene, an antioxidant that is particularly good for your brain – it even helps prevent dementia. You have to cook tomatoes to get the lycopene – take that, raw foodies! Just kidding. But this does mean that ketchup is good for your brain. Although because of the sugar in it, you should look to other sources for most of your lycopene intake, such as fresh tomato sauce.

Green it: try to eat tomatoes that are local and get your lycopene in vitamin form when tomatoes aren’t in season. You’ll know when that is – the tomatoes will be pale, tasteless, and pithy.

20. Cacao nibs
That’s right, I’m putting chocolate on this list twice. My boyfriend knows I need it. I eat chocolate or cacao nibs daily and I think you might want to consider it, too. Cacao nibs are among the top five most powerful brain foods, right next to wild salmon and blueberries. My girlfriends and I like to mix cacao nibs with frozen blueberries and a generous splash of organic heavy cream while we watch really bad television on Sunday nights.
Green it: as long as it’s fair trade and organic, it’s green.

Things that drain your brain:

Alcohol kills your brain cells outright! Alcohol also interferes with dopamine production. Moderate amounts of alcohol, particularly resveratrol-rich red wine, can help improve your health, but anything beyond a glass or two of wine daily is a recipe for reduced brain function and energy loss.

Corn Syrup and Sugar lead to health problems like diabetes and obesity, and they’re terrible for your brain. Don’t eat sugar except on special occasions or as an infrequent treat. If you can’t cut back that much, try to limit yourself to just two bites of whatever tempts you daily.

Nicotine constricts blood flow to the brain, so while it may “soothe” jittery nerves, smoking will actally reduce your brain function severely – and the effects are cumulative.

A high carbohydrate lunch will make you sleepy and sluggish. Opt for a light meal with some quality protein, such as a salad with grilled chicken breast or vegetables and hummus or wild American shrimp and avocado.



Vita Search Public Library of Science
PubMed

– with additional reporting by Sarah Irani

Making memories as we age

As Time Goes by, It Gets Tougher to ‘Just Remember This’It’s something we just accept: the fact that the older we get, the more difficulty we seem to have remembering things.


Yassa and his team used MRI scans to observe the brains of 40 healthy young college students and older adults, ages 60 to 80, while these participants viewed pictures of everyday objects such as pineapples, test tubes and tractors and classified each — by pressing a button — as either “indoor” or “outdoor.” (The team used three kinds of MRI scans in the study: structural MRI scans, which detect structural abnormalities; functional MRI scans, which document how hard various regions of the brain work during tasks; and diffusion MRIs, which monitor how well different regions of the brain communicate by tracking the movement of water molecules along pathways.)

Some of the pictures were similar but not identical, and others were markedly different. The team used functional MRI to watch the hippocampus when participants saw items that were exactly the same or slightly different to ascertain how this region of the brain classified that item: as familiar or not.

n the same space each and every day, it’s a challenge eight hours later to recall whether we left the SUV in the second or fifth row. Or, we can be introduced to new colleagues at a meeting and will have forgotten their names before the handshake is over. We shrug and nervously reassure ourselves that our brains’ “hard drives” are just too full to handle the barrage of new information that comes in daily.


According to a John Hopkins neuroscientist, however, the real trouble is that our aging brains are unable to process this information as “new” because the brain pathways leading to the hippocampus — the area of the brain that stores memories — become degraded over time. As a result, our brains cannot accurately “file” new information (like where we left the car that particular morning), and confusion results.
“Our research uses brain imaging techniques that investigate both the brain’s functional and structural integrity to demonstrate that age is associated with a reduction in the hippocampus’s ability to do its job, and this is related to the reduced input it is getting from the rest of the brain,” said Michael Yassa, assistant professor of psychological and brain sciences in Johns Hopkins’ Krieger School of Arts and Sciences. “As we get older, we are much more susceptible to ‘interference’ from older memories than we are when we are younger.”

In other words, when faced with an experience similar to what it has encountered before, such as parking the car, our brain tends to recall old information it already has stored instead of filing new information and being able to retrieve that. The result? You can’t find your car immediately and find yourself wandering the parking lot.
“Maybe this is also why we tend to reminisce so much more as we get older: because it is easier to recall old memories than make new ones,” Yassa speculated.The study appears in the May 9 Early Online edition of the Proceedings of the National Academy of Sciences and is available at www.pnas.org/content/early/2011/05/05/1101567108.


“Pictures had to be very distinct from each other for an older person’s hippocampus to correctly classify them as new. The more similar the pictures were, the more the older person’s hippocampus struggled to do this. A young person’s hippocampus, on the other hand, treated all of these similar pictures as new,” Yassa explained.Later, the participants viewed a series of completely new pictures (all different) and again were asked to classify them as either “indoor” or “outdoor.” A few minutes later, the researchers presented the participants with the new set of pictures and asked whether each item was “old,” “new” or “similar.”


“The ‘similar’ response was the critical response for us, because it let us know that participants could distinguish between similar items and knew that they’re not identical to the ones they’d seen before,” Yassa said. “We found that older adults tended to have fewer ‘similar’ responses and more ‘old’ responses instead, indicating that they could not distinguish between similar items.”

Yassa said that this inability among older adults to recognize information as “similar” to something they had seen recently is linked to what is known as the “perforant pathway,” which directs input from the rest of the brain into the hippocampus. The more degraded the pathway, the less likely the hippocampus is to store similar memories as distinct from old memories.

“We are now closer to understanding some of the mechanisms that underlie memory loss with increasing age,” Yassa said. “These results have possible practical ramifications in the treatment of Alzheimer’s disease, because the hippocampus is one of the places that deteriorate very early in the course of that disease.”  The team’s next step would be to conduct clinical trials in early Alzheimer’s disease patients using the mechanisms that they have isolated as a way to measure the efficacy of therapeutic medications.

“Basically, we will now be able to investigate the effect of a drug on hippocampal function and pathway integrity,” he said. “If the drug slows down pathway degradation and hippocampal dysfunction, it’s possible that it could delay the onset of Alzheimer’s by five to 10 years, which may be enough for a large proportion of older adults to not get the disease at all. This would be a huge breakthrough in the field.”

Notes about this neuroscience research article
The study was funded by the National Institute on Aging.

Contact: Lisa De Nike – John Hopkins University

Source: Johns Hopkins University press release

Image Source: Neuroscience News Image

USC creates functioning synapse from carbon nanotubes

Engineering researchers at the University of Southern California have made a significant breakthrough in the use of nanotechnologies for the construction of a synthetic brain. They have built a carbon nanotube synapse circuit whose behavior in tests reproduces the function of a neuron, the building block of the brain.

The team, which was led by Professor Alice Parker and Professor Chongwu Zhou in the USC Viterbi School of Engineering Ming Hsieh Department of Electrical Engineering, used an interdisciplinary approach combining circuit design with nanotechnology to address the complex problem of capturing brain function. In a paper published in the proceedings of the IEEE/NIH 2011 Life Science Systems and Applications Workshop in April 2011, the Viterbi team detailed how they were able to use carbon nanotubes to create a synapse.

Carbon nanotubes are molecular carbon structures that are extremely small, with a diameter a million times smaller than a pencil point. These nanotubes can be used in electronic circuits, acting as metallic conductors or semiconductors.“This is a necessary first step in the process,” said Parker, who began the looking at the possibility of developing a synthetic brain in 2006. “We wanted to answer the question: Can you build a circuit that would act like a neuron? The next step is even more complex. How can we build structures out of these circuits that mimic the function of the brain, which has 100 billion neurons and 10,000 synapses per neuron?”
Parker emphasized that the actual development of a synthetic brain, or even a functional brain area is decades away, and she said the next hurdle for the research centers on reproducing brain plasticity in the circuits.The human brain continually produces new neurons, makes new connections and adapts throughout life, and creating this process through analog circuits will be a monumental task, according to Parker.

She believes the ongoing research of understanding the process of human intelligence could have long-term implications for everything from developing prosthetic nanotechnology that would heal traumatic brain injuries to developing intelligent, safe cars that would protect drivers in bold new ways.For Jonathan Joshi, a USC Viterbi Ph.D. student who is a co-author of the paper, the interdisciplinary approach to the problem was key to the initial progress. Joshi said that working with Zhou and his group of nanotechnology researchers provided the ideal dynamic of circuit technology and nanotechnology.
“The interdisciplinary approach is the only approach that will lead to a solution. We need more than one type of engineer working on this solution,” said Joshi. “We should constantly be in search of new technologies to solve this problem.”

Notes about this neuroscience research article
Contact: Eric Mankin – USC
Source: University of Southern California Press Release
Image Source: Image adapted from USC Viterbi School of Engineering

How aging bilingual brains cope

How the Bilingual Brain Copes with AgingAs brain power decreases, older adults find new ways to compute language Older bilingual adults compensate for age-related declines in brainpower by developing new strategies to process language, according to a recent study published in the journal Aging, Neuropsychology, and Cognition.

Concordia University researchers studied two groups of fluently bilingual adults – aged from 19 to 35 and from 60 to 81 years old – and found significant age-related differences in the manner their brains interpreted written language. “We wanted to know whether older adults relied on context to process interlingual homographs (IH) – words that are spelled the same in both languages but have a different meaning,” says lead author Shanna Kousaie, a PhD candidate at Concordia University’s Department of Psychology and Centre for Research in Human Development (CRDH).

Does “coin” mean “money” or “corner”?

As part of the study, subjects were asked to read hundreds of trios of words. The first word in the triplet was in either English or French, indicating the language of the IH, putting it in context for readers. The second was an IH – a word such as “coin,” which means “money” in English but “corner” in French. The third word was one that might or might not help the person understand the meaning of the IH more quickly.Subjects’ neurophysiological responses to these words were recorded using an electroencephalograph, an instrument that records the brain’s electrical activity.

Kousaie and co-author Natalie Phillips, a professor in Concordia’s Department of Psychology and member of the CRDH, found that the older adults processed these letter strings differently, using context to a greater extent to determine meaning.These findings were based on the relative speed of responses for younger and older bilingual research participants and on the differences in their EEG recordings as they “processed” the word triplets. Both measures indicated younger participants relied less on the first (contextual) word when processing the trios of words in the test.

“As we get older, our working memory capacity and ability to quickly process words declines,” says Phillips. “As a result, older adults become a little more strategic with capacity. It’s important to stress these are normal and mild age-related changes. Participants didn’t have any cognitive deficit. Rather, they were making the best use of mental resources by using context to help them process language.”

More than half the world is bilingual

These findings shed light on how bilingual adults process language. Although some 50 per cent of the world’s population is bilingual, much language research has so far focused only on single language speakers.
Understanding the effects of bilingualism on the brain may be of more than academic interest. Evidence is mounting that bilingual people have a cognitive advantage over monolingual individuals because their brains are accustomed to “manipulating” two languages.

“Our study suggests that bilingual adults, as they age, are able to find strategies to compensate for changes in language comprehension,” says Phillips.

Notes about this brain research article
Partners in research: This work was supported by the Canadian Institutes of Health Research and the Natural Sciences and Engineering Research Council of Canada.

Related links:

Cited research: http://www.informaworld.com/smpp/content~content=a927919047~db=all~jumptype=rss

Concordia Department of Psychology: http://psychology.concordia.ca/

Centre for Research in Human Development: http://crdh.concordia.ca/


Contact: Sylvain-Jacques Desjardins – Senior advisor, external communications at Concordia University
Source: Concordia News press release
Image Source: Neuroscience News Image

Brain cells from skin cells to study Schizophrenia safely

Schizophrenia SafelyA team of scientists at Penn State University, the Salk Institute for Biological Studies, and other institutions have developed a method for recreating a schizophrenic patient’s own brain cells, which then can be studied safely and effectively in a Petri dish. The method brings researchers a step closer to understanding the biological underpinnings of schizophrenia. The method also is expected to be used to study other mysterious diseases such as autism and bipolar disorder, and the researchers hope that it will open the door to personalized medicine — customized treatments for individual sufferers of a disease based on genetic and cellular information. The study will be published in a future edition of the journal Nature and will be posted on the journal’s advance online website on 13 April 2011.


Gong Chen, an associate professor of biology at Penn State and one of the study’s authors, explained that the team first took samples of skin cells from schizophrenic patients. Then, using molecular-biology techniques, they reprogrammed these original skin cells to become unspecialized or undifferentiated stem cells called induced pluripotent stem cells (iPSCs). “A pluripotent stem cell is a kind of blank slate,” Chen explained. “During development, such stem cells differentiate into many diverse, specialized cell types, such as a muscle cell, a brain cell, or a blood cell.”

After generating iPSCs from skin cells, the authors cultured them to become brain cells, or neurons. They then compared the neurons derived from schizophrenic patients to the neurons created from the iPSCs of healthy individuals. They found that the neurons generated from schizophrenic patients were, in fact, distinct: compared with healthy neurons, they made fewer connections with each other. Kristen Brennand, a Salk researcher and one of the study’s authors, then administered a number of frequently prescribed antipsychotic medications to test the drugs’ ability to improve how neurons communicate with neighboring cells. “Now, for the very first time, we have a model system that allows us to study how antipsychotic drugs work in live, genetically identical neurons from patients with known clinical outcomes, and we can start correlating pharmacological effects with symptoms,” Brennand said.

Chen, who contributed to the study by using electrophysiology techniques to test the function of the iPSC-derived neurons, described the new method as “patient specific,” offering a step toward personalized medicine for sufferers of schizophrenia and potentially other diseases. “What’s so exciting about this approach is that we can examine patient-derived neurons that are perhaps equivalent to a particular patient’s own neural cells,” Chen said. “Obviously, we don’t want to remove someone’s brain cells to experiment on, so recreating the patient’s brain cells in a Petri dish is the next best thing for research purposes. Using this method, we can figure out how a particular drug will affect that particular patient’s brain cells, without needing the patient to try the drug, and potentially, to suffer the side effects. The patient can be his or her own guinea pig for the design of his or her own treatment, without having to be experimented on directly.”

Lead author Fred Gage, a professor at Salk’s Laboratory of Genetics and holder of the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Diseases, explained that schizophrenia exemplifies many of the research challenges posed by complex psychiatric disorders. “This model not only affords us the opportunity to look at live neurons from schizophrenia patients and healthy individuals to understand more about the disease mechanism, but also it allows us to screen for drugs that may be effective in reversing it,” Gage said.

Schizophrenia, which is defined by a combination of paranoid delusions, auditory hallucinations, and diminished cognitive function, afflicts one percent of the population worldwide, corresponding to nearly three million people in the United States alone. Genetic evidence indicates that many different combinations of genetic lesions — some of them affecting the susceptibility to environmental influences — may lead to a variety of signs and symptoms collectively labeled schizophrenia.

“Nobody knows how much the environment contributes to the disease,” said Brennand. “By growing neurons in a dish, we can take the environment out of the equation and start focusing on the underlying biological problems.” In another part of the study, Brennand used a modified rabies virus, developed by Salk professors Edward Callaway and John Young, to highlight the connections between neurons. The viral tracer made it apparent that the schizophrenic neurons connected less frequently with each other and had fewer projections growing out from their cell bodies. In addition, gene-expression profiles identified almost 600 genes whose activity was misregulated in these neurons; 25 percent of those genes had been implicated in schizophrenia before.

Gage added that, for many years, mental illness has been thought of as a strictly social or environmental disease. “Many people believed that if affected individuals just worked through their problems, they could overcome them,” he said. “But we are showing real biological dysfunctions in neurons that are independent of the environment.”

Notes about this neuroscience research article

In addition to Gage, Brennand, and Chen, other researchers who contributed to the study include Anthony Simone, Jessica Jou, Chelsea Gelboin-Burkhart, Ngoc Tran, Sarah Sangar, Yan Li, Yanglin Mu and Diana Yu in the Gage Laboratory; Shane McCarthy at the Cold Spring Harbor Laboratory in New York; and Jonathan Sebat at the University of California at San Diego.

The work was funded, in part, by the California Institute for Regenerative Medicine, the Lookout Foundation, the Mathers Foundation, and the Helmsley Foundation.
Katrina Voss & Gina Kirchweger

Contacts:

Gong Chen: Penn State
Fred Gage: gage@salk.edu
Barbara Kennedy (PIO): Penn State
Image Source: Gong Chen laboratory, Penn State University
Aigh-resolution images associated with this research are online at http://www.science.psu.edu/news-and-events/2011-news/Chen4-2011

Scientists at Penn State University, the Salk Institute for Biological Studies, and other institutions have developed a method for recreating a schizophrenic patient's own neurons in the laboratory. The research is expected to help in understanding the biological underpinnings of schizophrenia and also to lead to treatments customized for individual patients. With the new method, some of the patient's own DNA-containing skin cells are collected and transformed with molecular-biology techniques first into stem cells and then into neurons. In this microscopic image, nuclei originated from human cells are stained red and stem-cell-derived newborn neurons are stained green.

Doctors diagnose stroke with iPhone app

University of Calgary researchers have developed an iPhone application that allows doctors to diagnose a stroke in a patient thousands of kilometres away.The application will be particularly helpful to doctors in rural areas who need the expertise of a specialist, such as a neurologist or radiologist, who is working in an urban setting, say researchers.

The specialist will be able to see diagnostic images from a CT scan on their phone, whether they are at a Calgary hospital or a hockey game.Ross Mitchell, a professor of radiology at U of C, holds an iPad showing a CT scan of the brain. "Now a physician anywhere can get a call on their iPhone and can immediately take a look at the images in the remote community," said Ross Mitchell, a professor of radiology at the university who helped develop the software. "They can do more than just look at them. They can cut into them, rotate it in 3D, they can do all kinds of advanced visualizations and analysis, which may be critical to make the diagnosis."
Every minute counts when diagnosing a stroke, he added.
A study published in the current issue of the Journal of Medical Internet Research found that doctors using the application were 94 to 100 per cent accurate in diagnosing acute stroke, compared to a traditional medical diagnostic work station.Health Canada approved the application last month so Canadian doctors can now legally use it as a primary diagnosis device.
The application, called ResolutionMD Mobile, works on iPhones, iPads and Android smartphones and tablets.CT scanners in rural communities would be attached to a server protected by the hospital's firewall. That means patient information would be kept safe, says Mitchell. Also the doctor with the iPhone doesn't have to wait for all the information to download, the server is doing the hard work and streams the images to the phone in real time.

Calgary Scientific Inc., the company that helped refine the software, has already licensed the application to over 50,000 hospitals around the world.

Can Traumatic Memories be Erased?

The study appears in the April 27 issue of the Journal of Neuroscience, a premier neuroscience journal.

Can Traumatic Memories Be Erased?Could veterans of war, rape victims and other people who have seen horrific crimes someday have the traumatic memories that haunt them weakened in their brains? In a new study, UCLA life scientists report a discovery that may make the reduction of such memories a reality.


“I think we will be able to alter memories someday to reduce the trauma from our brains,” said the study’s senior author, David Glanzman, a UCLA professor of integrative biology and physiology and of neurobiology.Glanzman, a cellular neuroscientist, and his colleagues report that they have eliminated, or at least substantially weakened, a long-term memory in both the marine snail known as Aplysia and neurons in a Petri dish. The researchers say they gaining important insights into the cell biology of long-term memory.

They discovered that the long-term memory for sensitization in the marine snail can be erased by inhibiting the activity of a specific protein kinase — a class of molecules that modifies proteins by chemically adding to them a phosphate (an inorganic chemical), which changes the proteins’ structure and activity. The protein kinase is called PKM (protein kinase M), a member of the class known as protein kinase C (PKC), which is associated with memory.

The research has important potential implications for the treatment of post-traumatic stress disorder, as well as drug addiction, in which memory plays an important role, and perhaps Alzheimer’s disease and other long-term memory disorders.“Almost all the processes that are involved in memory in the snail also have been shown to be involved in memory in the brains of mammals,” said Glanzman, who added that the human brain is far too complicated to study directly.

PKM is rare in that while most protein kinases have both a catalytic domain, which is the part of the molecule that does its work, and a regulatory domain, akin to an on–off switch that can be used by other signaling pathways to shut off the activity of the kinase, PKM has only the catalytic domain — not the regulatory domain.“This means that once PKM is formed, there is no way to shut it off,” said Glanzman, who is a member of UCLA’s Brain Research Institute. “Once it is activated, PKM’s continual activity maintains a memory until PKM degrades.”

Glanzman decided to study PKM in the marine snail, which has simple forms of learning and a simple nervous system, so that he could understand in precise detail how PKM’s activity maintains a long-term memory, a process that is not well understood. Glanzman and his colleagues — researchers Diancai Cai, lead author of the study; Kaycey Pearce; and Shanping Chen, all of whom work in his laboratory — studied a simple kind of memory called sensitization. If marine snails are attacked by a predator, the attack heightens their sensitivity to environmental stimuli — a “fundamental form of learning that is necessary for survival and is very robust in the marine snail,” Glanzman said.“The advantage of Aplysia,” he said, “is that we know the neurons that produce this reflex; we know where they are in the nervous system.”

The scientists removed the key neurons from the snail’s nervous system and put them in a Petri dish, thereby recreating in the dish the two-neuron “circuit” — a sensory neuron and a motor neuron — that produces the reflex.“The point is to reduce the problem so we can study on a fundamental biological level how PKM is maintaining long-term memory,” Glanzman said.They succeeded in erasing a long-term memory, both in the snail itself and in the circuit in the dish. They are the first scientists to show that long-term memory can be erased at a connection between just two neurons.“We found that if we inhibit PKM in the marine snail, we will erase the memory for long-term sensitization,” Glanzman said. “In addition, we can erase the long-term change at a single synapse that underlies long-term memory in the snail.”

The scientists administered electric shocks to the snails’ tails. Following this training, when the scientists gently touched a snail’s siphon (an organ in their mid-section used in respiration), the animal responded with a reflexive contraction that lasted about 50 seconds. A week later, when the scientists touched the siphon, the reflex still lasted 30 seconds or more, rather than just the second or two the reflex normally lasts without the shock training. This constituted a long-term memory.Then, once the marine snail had formed the long-term memory, the scientists injected an inhibitor of PKM into the snail and 24 hours later touched the siphon; the marine snail responded as though it had never received the tail shocks, with a very brief contraction. “The long-term memory is gone,” Glanzman said.

Life scientists agree that learning is due to changes in the synaptic connections, some of which strengthen and some of which weaken, in the brain. This new research opens the door to learning how the changes in synaptic connections are maintained and what role PKM plays in this memory maintenance. Glanzman and his colleagues are now conducting detailed analyses.

During the long-term memory, new synaptic connections grow between the sensory neuron and the motor neuron. If the scientists inhibit PKM, will those synaptic connections disappear? "We’re going to study that,” Glanzman said. “Now we can study the cell biology of how PKM maintains long-term memory. Once we know that, we may be able to alter long-term memories. This has implications for psychiatric disorders that are related to memory. Post-traumatic stress disorder is a hyper-induction of a long-term memory that won’t go away.”

Targeting specific memories

Is there a way to turn the traumatic memory down?“This is the first step toward figuring that out,” Glanzman said. “Even after we know this, we will still need a way to target the memory. We have captured the memory in the dish, but we also have to know where in the brain the memory is.”Does he think it will become possible to target and weaken specific traumatic memories?“I do,” Glanzman said. “Not in the immediate future, but I think we will be able to go into one’s brain, identify the location of the memory of a traumatic experience and try to dampen it down. We can do this in culture, and there is no essential difference between the synapse in culture and the synapse in your brain. We have captured the memory in the dish; now we have to figure out a way to target the memories in human brains. Once we know the neural circuit that contains the memory, then we need a selective way to inhibit the activity of PKM in that circuit.”

People have different brain circuits — collections of neurons and synapses that join neurons — for different memories, Glanzman believes. Scientists may seek to inhibit PKM in a particular circuit. The goal would be to find the brain circuit that is predominantly associated with a traumatic memory and target PKM in that circuit. If you boost rather than inhibit PKM activity, might that have a beneficial affect for patients with Alzheimer’s disease? Alzheimer’s disease appears to initially disrupt the synaptic basis of learning, Glanzman said, and PKM might be involved in that disruption.

Just as scientists are seeking to target and kill cancer cells without damaging healthy cells, Glanzman intends to study whether it is possible to weaken only certain synapses associated with traumatic memories, while leaving other memories intact.“The brain is the most complicated organ in the body,” Glanzman said, noting that the brain has many trillions of synapses. “The research is complex, but this is the way we are going to understand how memories in our brains last a lifetime, or at least part of the way. It will take a lot of research, but I think it will be feasible.”

Next steps include studying the relationship between PKM and the synapses and how the structure of synapses changes when PKM is inhibited.“That is going to tell us how long-term memories are maintained,” Glanzman said. “This is the first step. The more we know about how long-term memory is induced in the brain and how our memories are maintained in the brain, the more we are going to be able to treat long-term memory loss.” The experiments are very difficult, and Glanzman praised co-authors Cai, Pearce and Chen as “unbelievably skilled.”
For 28 years, Glanzman has studied learning and memory in the marine snail, which is substantially larger than its garden variety counterpart and has approximately 20,000 neurons in its central nervous system; humans have approximately 1 trillion. However, the cellular and molecular processes seem to be very similar between the marine snail and humans.“The fundamental mechanisms of learning and memory are identical, as far as we can tell,” Glanzman said. Glanzman’s research is funded by a Senator Jacob Javits Award in the Neurosciences from the National Institute of Neurological Disorders and Stroke (NINDS) and by the National Institute of Mental Health.
The marine snail processes information about its environment and is capable of learning when an environment is safe and when it is not, learning to escape from predators, and learning to identify food. The marine snail is native to California, living in tidal waters off the coast.
Glanzman is also studying learning at the synaptic level in the zebra fish.

In earlier research, Glanzman’s team identified a cellular mechanism in the Aplysia that plays an important role in learning and memory. A protein called the NMDA (N-methyl D-aspartate) receptor enhances the strength of synaptic connections in the nervous system and plays a vital role in memory and in certain kinds of learning in the mammalian brain as well. Glanzman’s demonstration that the NMDA receptor plays a critical role in learning in the marine snail was entirely unexpected.

Notes about this research article
Written by: Stuart Wolpert – UCLA Source: University of California – Los Angeles press release

Being overweight 'linked to dementia'By James Gallagher

Health reporter, BBC News

Middle aged people who are overweight but not obese, are 71% more likely to develop dementia than those with a normal weight, according to research. Previous studies have indicated a link between obesity and dementia.But a study 8,534 of Swedish twins, in the journal Neurology, suggests just being overweight is also a risk factor.About one out of every 20 people above the age of the 65 has dementia. The Alzheimer's Society said a healthy lifestyle could reduce the risk.

Those with a body mass index (BMI) - which measures weight relative to height - greater than 30, who are classified as obese, were 288% more likely to develop dementia than those with a BMI between 20 and 25, according to the study.

What is dementia?

Dementia is an umbrella term describing a serious deterioration in mental functions, such as memory, language, orientation and judgement. There are many types, but Alzheimer's disease, which accounts for two thirds of cases, is the most well-known.

The clinically overweight, who have a BMI between 25 and 30, were 71% more likely.Dr Weili Xu, from the Karolinska Institute in Stockholm, told the BBC: "We found in this study that being overweight is also a risk for dementia later in life.""The risk is not as substantial as for [the] obese, but it has public health importance because of this large number of people worldwide who are overweight," Dr Xu added.
The study says 1.6 billion adults are overweight worldwide.

Alzheimer's Society head of research, Dr Susanne Sorensen, said: "This robust study adds to the large body of evidence which suggests that if you pile on the pounds in middle age, your chances of developing dementia later in life are also increased."By eating healthily and exercising regularly, you can lessen your risk of developing dementia." Alzheimer's Research UK head of research, Dr Simon Ridley, said: "This study adds to existing evidence that excess weight in middle age could increase our risk of developing dementia.

"It's likely that dementia is caused by a complex mix of genetic, environmental and lifestyle factors. However, we still need to know much more about the causes of dementia if we are to find an effective treatment that is so desperately needed."

Brain Plasticity

The Discovery


The brain is adaptable throughout life

The image shows the addition of new neurons in the adult mouse hippocampus — the brain region involved in learning and memory. This birth of new cells is a major finding in showing how adaptable the brain is, even in adulthood. (Brain cells labeled blue-green are eight weeks old, while cells labeled red are at most four weeks old.) Credit: Reprinted with permission from Gage, F. and Zhao, C. Laboratory of Genetics LOG-G; The Salk Institute for Biological Studies. 2007.

When scientists discovered that the brain could create new brain cells in adulthood, they introduced a new way of thinking that could one day help treat or delay onset of Alzheimer’s disease (AD). AD is the most common form of cognitive dementia, the loss of higher mental functions like memory.

New Discovery, New Belief

Researchers in the 1960s were curious to understand more about growth and repair in the adult brain, and conducted a number of experiments with rodents to help illuminate these processes. They made an amazing and unexpected discovery: newly created cells that later transformed into what appeared to be neurons, or brain cells.


The discovery was not initially recognized for the breakthrough it was because most experts thought that the brain finished developing and changing early in life and did not produce more neurons. Additionally, scientists faced the challenge of proving that the newly created cells were neurons.Further advances came from explorations of learning conducted by researchers lured by birdsong. Years after the initial discoveries, advanced brain imaging techniques helped establish the existence, in adult canaries, of these precursor cells, or stem cells, that reproduced, migrated to other brain areas, and matured into neurons. This process, called neurogenesis, is just one example of how plastic or adaptable the brain is.

Human Discoveries

Further research has proved that the brains of adult humans also undergo neurogenesis, revealing the plasticity of the brain throughout our lives. Scientists located adult human neurogenesis sites in the dentate gyrus of the hippocampus — the brain region involved in learning and memory — and the subventricular zone in the region where fluid that helps protect the brain and spinal cord is made.Indeed, scientists worldwide, working in many different specialties, have found that the human brain is highly plastic, possessing the ability not only to create new neurons, but to modify networks of neurons to better cope with new circumstances.

These collective discoveries may pave the way for further understanding of how old age and conditions like AD affect plasticity, and may help researchers find ways to preserve it.

New Application

Enhancing the brain’s plasticity

 These three-dimensional projections of brain positron emission tomography scans (outer brain surface) show amyloid plaques and tau tangles labeled by a chemical marker — the first developed to tag physical evidence of Alzheimer’s disease (AD) in living people. The control image is from an older person without AD. Warmer colors (red, yellow)indicate higher levels of plaques and tangles. Credit: Reprinted from Lancet Neurology, 7, G. Small et al., Current and future uses of neuroimaging for cognitively impaired patients, 161–72, © (2008), with permission from Elsevier.
 This figure shows the effects of exercise on levels of brain-derived neurotrophic factor (BDNF) in the hippocampus of rats. Growth factors like BDNF help many neurons survive. Levels of the message that makes BDNF are much higher in exercising rats(A) than in sedentary animals (B). Red and yellow denote the highest level of BDNF, while green and blue denote the lowest. Credit: Alzheimer’s Disease Education and Referral Center, a service of the National Institute on Aging.

As Alzheimer’s disease progresses, it kills brain cells mainly in the hippocampus and cortex, which leads to impairments in learning, memory, and thinking. Harnessing thebrain’s capacity to adapt in adulthood may one day help prevent and treat Alzheimer’s disease.

Once scientists realized the adult brain’s enormous capacity for plasticity, they could study the effects of aging and Alzheimer’s disease on that capability and explore ways to maintain healthy brain function.

Declining Plasticity in Old Age and in People with Alzheimer’s Disease

Brain deterioration begins well before old age. Scientists believe that changes in plasticity at brain synapses — the junctions where neurons signal to each other — and the loss of neurons may be responsible for this decline in function.

Interestingly, these changes also precede AD impairments and many harmful precursors of AD, like amyloid beta deposits, tau tangles, ApoE4 proteins, and brain inflammation. These AD hallmarks damage areas of the brain responsible for learning, memory, and cognition by further impairing synapses and contributing to cell death. With AD patients, early neuron loss and changes in synapse function have been observed in the hippocampus and neocortex — the very brain regions involved in language, memory, and other higher cognitive functions.

An Enriched Environment Plays a Role

Researchers have found at least one clear link between brain plasticity and healthy aging: They know that a rich, stimulating environment can enhance and maintain brain plasticity, even in old age and with AD patients. Studies of aged rodents modeled with and without AD show that regular social interaction, exercise, and a healthful diet, as well as cardiovascular exercise, can increase neurogenesis, neuron communication, and hippocampus-related learning, and can decrease levels of amyloid beta deposits. In addition, exercise has been shown to help increase production of proteins and blood vessels that support the growth and survival of cells.

In humans, research has revealed that exercise enhances cognitive function and protects against dementia and neurodegenerative diseases like AD — just one line of discovery that shows promise against these debilitating conditions.


Health Implications

Promise for treating Alzheimer’s disease

With new knowledge of how normal aging and conditions like Alzheimer’s disease affect plasticity and how environment can enhance brain function, scientists can investigate the power of plasticity in treating AD.

Maintaining Healthy Brain Function

Targeting areas in the brain that may be more vulnerable to aging and AD, such as the hippocampus, may enhance overall brain function and help slow or stop the natural decline in brain plasticity.

Using strategies to maintain healthy brain function in youth and increasingly in old age may also help delay or prevent decreasing brain plasticity. Cardiovascular exercise and other behavioral changes — such as switching to a more healthful diet — may stave off cognitive decline, keep brain networks flexible, increase neurogenesis, and enhance processes that aid in the growth and survival of both existing and new cells.

Boosting Brain Plasticity as Treatment

For now, encouraging efforts to enhance brain plasticity at the first sign of neuron dysfunction, before AD impairments develop, may be the best bet in treating or delaying onset of the disease.

For example, brain plasticity exercises may one day help AD patients. These include demanding sensory, cognitive, and motor activities that reengage and strengthen the brain systems involved in learning. Such brain plasticity training has helped normal aging adults improve memory.

Many drug trials also are underway that target the early development of amyloid beta, tau, ApoE4, and brain inflammation to prevent or reverse their negative effects on brain plasticity and cell loss, and ultimately on learning and memory.
Researchers have much more to learn about preserving and enhancing plasticity as a way to defend against memory-robbing conditions that strike in old age. The discovery of adult neurogenesis is spurring significant progress, but only continued research will help scientists harness the adult brain’s enormous capacity for plasticity to prevent or delay the onset of AD, and to treat the more than 4.5 million Americans diagnosed with it.

US stem cell research funding ban lifted by court

A US appeals court has overturned an earlier order to suspend federal funding of stem cell research.
The Washington court said opponents of the research, who say it is illegal because it involves the destruction of human embryos, were unlikely to succeed in their lawsuit to stop the funding.
The ruling marks a significant victory for US President Barack Obama, correspondents say.
President Obama lifted a ban on funding for stem cell research in March 2009.Soon after, US District Judge Royce Lamberth issued a temporary injunction on the move while a legal challenge went ahead - although this suspension was itself overruled on appeal, pending a final decision. The US Court of Appeals in Washington ruled 2-1 on Friday that a 1996 US law against federal funding of embryo destruction was "ambiguous", and "did not prohibit funding a research project in which an ESC (embryonic stem cell) will be used".

'Momentous day'

Scientists say the research could lead to breakthroughs for treatments of spinal cord injuries and diseases including Alzheimer's and Parkinson's.Opponents, who include religious groups, argue that the research is unethical and illegal.The suit opposing federal funding, which was also backed by some Christian groups, was brought against the National Institutes of Health (NIH).
The NIH and the White House both welcomed Friday's ruling.

"This is a momentous day - not only for science, but for the hopes of thousands of patients and their families who are relying on NIH-funded scientists to pursue life-saving discoveries and therapies that could come from stem cell research," NIH Director Francis Collins said in a statement.

White House spokesman Nick Papas said the decision was a victory for scientists and patients.
"Responsible stem cell research has the potential to treat some of our most devastating diseases and conditions and offers hope to families across the country and around the world," he said.

Bullying tendency wired in brain

Bullies' brains may be wired differently, the research suggests. Bullies' brains may be hardwired to have sadistic tendencies, US imaging research suggests. An area of the brain associated with reward lit up in scans when aggressive boys watched a video of someone inflicting pain. Boys without a history of unusual aggression had no such response, the study in Biological Psychology found. The aggressive teenagers also reacted more strongly to pain that was accidentally caused.

The small study of 16-18 year olds - eight with a "conduct disorder" and eight with no aggressive tendency - suggests in some boys, natural empathetic impulses may be disrupted in ways that increase aggression, the researchers said. A better understanding of the biological basis of these things is good to have but the danger is it causes people to leap to biological solutions - drugs - rather than other behavioural solutions
Dr Michael Eslea

Those with the conduct disorder had exhibited disruptive behaviour such as starting a fight, using a weapon and stealing after confronting a victim. Tests were done using functional MRI scans while the participants looked at video clips in which people endured pain accidentally, such as when a heavy bowl was dropped on their hands, and intentionally, such as when a person stepped on another's foot.

Strong response

Aggressive adolescents showed "a specific and very strong" activation of the amygdala and ventral striatum - areas of the brain that respond to feeling rewarded - when watching pain inflicted on others, suggesting they enjoyed watching pain, the researchers said. And unlike the control group, the boys with conduct disorder did not show activation of the parts of the area of the brain involved in self-regulation - known as the the medial prefrontal cortex and the temporoparietal junction. Using the same type of research, study leader Jean Decety, professor in psychology and psychiatry at the University of Chicago, has previously shown that seven to 12 year olds have naturally empathy for people in pain. This is the first study to use fMRI to study situations which would normally prompt people to be sympathetic.

"This work will help us better understand ways to work with juveniles inclined to aggression and violence."
Dr Michael Eslea, senior lecturer in psychology at the University of Central Lancashire said the research was interesting but needed to be repeated in a larger sample.

"A better understanding of the biological basis of these things is good to have but the danger is it causes people to leap to biological solutions - drugs - rather than other behavioural solutions."

Autism Checklist

A simple checklist that parents fill out in the waiting room may help doctors someday screen for warning signs of autism as early as a baby's first birthday. San Diego pediatricians tested the tool with more than 10,000 babies at their one-year checkups, looking for such things as how the tots babble, gesture and interact with others.The research, being published Thursday, is a first step in the quest for earlier autism screening. It's not ready for routine use, as more work is needed to verify its accuracy. But it also may prove valuable in finding more at-risk babies to study what causes the developmental disorder.
"There are subtle signs of autism at one year if you just look for them," said neuroscientist Karen Pierce of the University of California, San Diego, who led the study. "Let's just get these kids detected early and treated early." Recent data suggest about one in 100 U.S. children has some form of autism, which ranges from mild to severe problems with behaviour, communication and socialization. The American Academy of Pediatrics already urges autism screening during regular doctor visits at ages 18 months and 24 months. Yet a 2009 study found that on average, children aren't diagnosed until they're five.
Experts say early therapy can lessen autism's severity, even if they don't know exactly what types will prove best. "The earlier you start, the better," said Dr. Lisa Gilotty of the National Institute of Mental Health, which helped fund the study.

Hence the interest in younger screening.

"This is very exciting work, to think we may be able to identify children with autism this early," said Dr. Susan Hyman of the University of Rochester and a pediatrics academy autism specialist, who wasn't involved in the new study.But, she cautioned, it's not clear how best to do that: "I don't think screening for autism at 12 months is ready for prime time." Thursday's study uses a 24-question checklist written in easy-to-understand terms that parents can answer in about five minutes. It was developed a few years ago to detect broader signs of language or developmental delays.

Pierce signed up 137 pediatricians to use the questionnaire during every one-year checkup and refer babies who failed for further testing. Those youngsters were re-evaluated every six months to age three, when a diagnosis could be certain. Of 10,479 babies screened, 184 who were sent for further testing followed through — and 32 eventually were diagnosed with autism, Pierce reported Thursday in the Journal of Pediatrics.

That's consistent with expected rates of detection that young; Rochester's Hyman said some forms of autism don't become apparent until age two or even later.Numerous other children were diagnosed with language delay or some other developmental problems, so that in the end, the screening accurately predicted some problem in 75 per cent of those kids, Pierce calculated. But there were false alarms for one in four, who had no problems. The children began treatment at around 19 months. In addition, Pierce's program does MRI scans and other tests as part of broader research into autism's biological underpinnings, studies now limited by the few numbers of babies being identified as at risk when they're so young.

One big puzzle: Only a fraction of the total 1,318 babies who failed the initial screening were referred for follow-up. The study couldn't tell how much of that gap was recording error, or if doctors or parents weren't worried enough to follow up right away, or if families went elsewhere. Still, the study shows early screening is feasible in the hectic everyday offices of regular pediatricians. That's important as scientists now develop various screening tests, said Geraldine Dawson, chief science officer of Autism Speaks, which co-funded the work.

Pierce says other cities should consider the screening — but doctors first must know where to send families for follow-up testing. That can cost several thousand dollars, and state programs for free evaluation of at-risk children may have waiting lists.

For now, what should worry parents? Pierce's top concerns:

Lack of what she calls "shared attention." Around age one, babies should try to "pull your attention into their world," pointing to a bird and watching to see if you look, for example, or bringing you a toy, she said.


Lack of shared enjoyment, where a baby may smile at mom but not engage if other people try peek-a-boo.


Repetitive behaviours like spinning a car wheel rather than playing with the toy.


Language delays are worrisome if they accompany other problem signs, she said: "If they wave and they point, that's a good sign the brain is readying itself to be ready to speak."