Could salmon and sunshine prevent brain damage?

Want to keep your brain in tip-top condition? Then you may want to put mackerel and mushrooms on your menu or start eating your salmon in the sun!

That’s because a new study led by University of Kentucky researchers suggests that a diet low in vitamin D causes damage to the brain.

In addition to being essential for maintaining bone health, new evidence shows that vitamin D serves important roles in other organs and tissue, including the brain.

The study, published in Free Radical Biology and Medicine showed that middle-aged rats that were fed a diet low in vitamin D for several months developed free radical damage to the brain. Additionally, many different brain proteins were damaged.  The vitamin D deficient rats also showed a significant decrease in cognitive performance on tests of learning and memory.

“Given that vitamin D deficiency is especially widespread among the elderly, we investigated how during aging from middle-age to old-age how low vitamin D affected the oxidative status of the brain,” said lead author on the paper Allan Butterfield, professor of Chemistry, director of the Center of Membrane Sciences, faculty of Sanders-Brown Center on Aging, and director of the Free Radical Biology in Cancer Core of the Markey Cancer Center. “Adequate vitamin D serum levels are necessary to prevent free radical damage in brain and subsequent deleterious consequences.”

Previously, low levels of vitamin D have been associated with Alzheimer’s disease, and it’s also been linked to the development of certain cancers and heart disease.

The elderly are particularly prone to have low vitamin D levels.

Butterfield recommends that people consult their physicians to have their vitamin D levels determined. If they turn out to be low it’s important to normalize them either through diet or sunlight exposure to help protect the brain.

low that they eat foods rich in vitamin D, take vitamin D supplements, and/or get at least 10-15 minutes of sun exposure each day to ensure that vitamin D levels are normalized and remain so to help protect the brain.
Surprisingly few foods contain vitamin D.  That’s because your body is built to get it from sunlight skin rather than from food. However, if your body has enough, it doesn’t matter whether you got it through your skin or through your stomach.

There are three vitamin D super foods:

• Salmon (especially wild-caught)
• Mackerel (especially wild-caught)
• Mushrooms (exposed to ultraviolet light)

Other food sources of vitamin D include:

• Cod liver oil
• Tuna canned in water
• Sardines canned in oil
• Milk or yogurt – fortified with vitamin D
• Beef or calf liver
• Egg yolks
• Cheese

If all that sounds a little too fishy for you, then you can boost your vitamin D from 10-15 minutes of sun exposure a day.

I’m off to get mine now!

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Does Double Dutch Delay Dementia?

G’day, Zao shang hao, Bonjour, Kalimera, Boker tov, God morgen, Buon giomo, Bom dia, Zdravstvuyitye, Buenos dias!

Or if you prefer – Good Morning!

No it’s not one of those guess the country viral Facebook quizzes (although we will print the answers at the bottom of this post for those of you who want to play along).  No, the reason for today’s multilingual greetings is because a new study has shown that speaking more than one language can delay the onset of, not one, not two…but three types of dementia.

In the largest study on the topic to date, published this week in the online issue of Neurology, researchers found that people who spoke two languages developed dementia four and a half years later than people who only spoke one language.

“Our study is the first to report an advantage of speaking two languages in people who are unable to read, suggesting that a person’s level of education is not a sufficient explanation for this difference,” said study author Suvarna Alladi. “Speaking more than one language is thought to lead to better development of the areas of the brain that handle executive functions and attention tasks, which may help protect from the onset of dementia.”

For the study, 648 people from India with an average age of 66 who were diagnosed with dementia were evaluated. Of those, 391 spoke two or more languages. A total of 240 had Alzheimer’s disease, 189 had vascular dementia and 116 had frontotemporal dementia, with the remainder having dementia with Lewy bodies and mixed dementia. Fourteen percent were illiterate.

People who spoke two languages had a later onset of Alzheimer’s disease, frontotemporal dementia and vascular dementia than people who spoke only one language. The difference was also found in those who could not read. There was no additional benefit in speaking more than two languages.

The two-language effect on age of dementia onset was shown separately of other factors such as education, gender, occupation and whether participants lived in the city or country.

“These results offer strong evidence for the protective effect of bilingualism against dementia in a population very different from those studied so far in terms of its ethnicity, culture and patterns of language use,” Alladi said.

While the study didn’t show any additional benefit in speaking more than two languages, we don’t think it hurts to try.

How many languages do you speak?

Answers:

G’day [Australia] Zao shang hao [China], Bonjour [France] Kalimera [Greece] Boker tov [Israel] ,God morgen [Denmark], Buon giomo [Italy], Bom dia [Portugal], Zdravstvuyitye [Russia], Buenos dias [Spain]

Snuffing Out Alzheimer’s

Hot on the heels of Friday’s blog – Sniffing Out Alzheimer’s, British scientists just announced a major breakthrough that could, one day, result in a treatment for Alzheimer’s, Parkinson’s, Huntington’s and other neurodegenerative diseases.

In tests on mice, researchers from the toxicology unit of the Medical Research Council showed brain cell death from prion disease could be prevented.

Professor Roger Morris, from King’s College London, said: “This finding, I suspect, will be judged by history as a turning point in the search for medicines to control and prevent Alzheimer’s disease.”

It is rare to get cautious scientists keen to describe any study as a turning point in history, let alone a study in mice.

Not only is it is early science, a lot can go wrong between a drug for mice and a drug for humans and the only published data is for prion disease, not even Alzheimer’s.

So why the excitement?

It is the first time that any form of neurodegeneration has been completely halted, so it is a significant landmark. It shows that the process being targeted has serious potential.

The research team focused on the natural defense mechanisms built into brain cells. When a virus hijacks a brain cell it leads to a build-up of viral proteins. Cells respond by shutting down nearly all protein production in order to halt the virus’s spread.

However, many neurodegenerative diseases involve the production of faulty or “misfolded” proteins. These activate the same defenses, but with more severe consequences. The misfolded proteins linger and the brain cells shut down protein production for so long that they eventually starve themselves to death.

This process, repeated in neurons throughout the brain, can destroy movement or memory or even kill, depending on the disease.  It  is thought to take place in many forms of neurodegeneration, so safely disrupting it could treat a wide range of diseases.

The researchers used a compound which prevented those defense mechanisms kicking in and in turn halted neurodegeneration.

The study showed mice with prion disease developed severe memory and movement problems. They died within 12 weeks. However, those given the compound showed no sign of brain tissue wasting away.

Lead researcher Professor Giovanna Mallucci says: “They were absolutely fine, it was extraordinary. What’s really exciting is a compound has completely prevented neurodegeneration and that’s a first. This isn’t the compound you would use in people, but it means we can do it and it’s a start.“

She said the compound offered a “new pathway that may well give protective drugs” and the next step was for drug companies to develop a medicine for use in humans.

Side effects are an issue. The compound also acted on the pancreas, meaning the mice developed a mild form of diabetes and lost weight. Any human drug would need to act only on the brain.

David Allsop, professor of neuroscience at Lancaster University described the results as “very dramatic and highly encouraging.”

SRxA’s Word on Health agrees.  We look forward to seeing further research and how these findings could apply to diseases such as Alzheimer’s and Parkinson’s.

Sniffing Out Alzheimer’s

A dollop of peanut butter and a ruler might be a way to confirm a diagnosis of early-stage Alzheimer’s disease.

Jennifer Stamps, a graduate student in the McKnight Brain Institute Center for Smell and Taste, came up with the idea of using peanut butter to test for smell sensitivity.  when she was working with Kenneth Heilman MD, a professor of neurology at the University of Florida.

One of the first places in the brain to degenerate in people with Alzheimer’s disease is the front part of the temporal lobe that evolved from the smell system. This portion of the brain is also involved in forming new memories. The ability to smell is associated with the first cranial nerve – the olfactory nerve.

Because peanut butter is a “pure odorant,” it is only detected by the olfactory nerve.

In a small pilot study, patients sat down with a clinician, a tablespoon of peanut butter and a metric ruler.

The patient closed his or her eyes and mouth and blocked one nostril. The clinician opened the peanut butter container and held the ruler next to the open nostril while the patient breathed normally. The clinician then moved the peanut butter up the ruler one centimeter at a time during the patient’s exhale until the person could detect an odor.

The distance was recorded and the procedure repeated on the other nostril after a 90-second delay.

The clinicians running the test did not know the patients’ diagnoses, which were not usually confirmed until weeks after the initial clinical testing.

Patients in the early stages of Alzheimer’s disease had a dramatic difference in detecting odor between the left and right nostril – their left nostril did not detect the smell until it was an average of 10 centimeters (almost 4 inches) closer to the nose than the right nostril.

This was not the case in patients with other kinds of dementia. These patients had either no differences in odor detection between nostrils or the right nostril was worse at detecting odor than the left one.

Of the 24 patients tested who had mild cognitive impairment, which sometimes signals Alzheimer’s disease and sometimes turns out to be something else, about 10 patients showed a left nostril impairment and 14 patients did not. The researchers said more studies must be conducted to fully understand the implications.

“At the moment, we can use this test to confirm diagnosis,” Stamps says. “But we plan to study patients with mild cognitive impairment to see if this test might be used to predict which patients are going to get Alzheimer’s disease.”

Many of the tests used to confirm a diagnosis of Alzheimer’s disease or other dementias can be time-consuming, costly, or invasive.  In contrast, according to the researchers their peanut butter and ruler test could be used by clinics that don’t have access to the personnel or equipment to run other, more elaborate tests required for a specific diagnosis.

And of course there’s the benefit that you can eat the test afterwards!

Like this post?  Check back on Monday for more ground breaking Alzheimer’s news.

10 Brain Damaging Habits

According to the World Health Organization here’s 10 habits that can severely damage your brain:

1.  No Breakfast – Skipping breakfast in order to lose weight or save time is totally wrong and directly affects our brain. Those who don’t take breakfast or take unhealthy breakfast having lower blood sugar level and sometime it may cause overweight.

2. Overreacting – causes hardening of the brain arteries, leading to a decrease in mental power.

3. High Sugar consumption – Too much sugar will interrupt the absorption of proteins and nutrients causing malnutrition and may interfere with brain development by reducing the production of Brain Derived Neutrotrophic Factor, without which the brain cannot learn.

4. Smoking – causes brain shrinkage, damages memory, judgment, learning and thinking powers and may even lead to dementia and Alzheimer’s disease.

5. Air Pollution – The brain is the largest oxygen consumer in our body. Inhaling polluted air decreases the supply of oxygen to the brain, bringing about a decrease in brain efficiency.

6. Sleep Deprivation – Sleep allows our brain to rest. Long term deprivation from sleep will accelerate the death of brain cells.

7. Head covered while sleeping – Sleeping with the head covered decreases available air space and forces you to start breathing carbon dioxide instead of oxygen. This leads to a rise in intracranial pressure and results in brain hypoxia which may lead to brain damaging effects.

8. Working your brain during illness – Working hard or studying with sickness may lead to a decrease in effectiveness of the brain. When we are sick the brain is at its weakest and becomes more easily stressed. This stress can also affect memory.

9. Drinking too little water – Water is the main source of energy and is essential for brain function and activity of neurotransmitters. Dehydration can lead to anger, stress, exhaustion, depression and lack of mental clarity.

10. Rarely Talking – Intellectual conversations help to train and promote efficiency of the brain. Conversely, lack of stimulating thoughts may cause brain shrinkage. Reading SRxA’s Word on Health and discussing the content with friends is an excellent way to avoid this!  So grab a glass of water and subscribe today. Consider it free brain fuel!

Out Pacing Alzheimer’s

Alzheimer’s disease is the most common form of degenerative dementia, afflicting about 5.5 million Americans and costing more than $100 billion per year. In terms of U.S. health care expenditure it now ranks as the third costliest disease.

Alzheimer’s disease is not easily managed. It becomes progressively disabling with loss of memory, cognition, worsening behavioral function and a gradual loss of independent functioning. Currently there is no cure.

But this may be all about to change. Last October, during a five-hour surgery at The Ohio State University Wexner Medical Center, Kathy Sanford became the first Alzheimer’s patient in the United States to have a pacemaker implanted in her brain.

Could this be the dramatic shift in the disappointing struggle to find something to slow the damage of this epidemic?  As yet, no one knows if it might work, and if it does, how long the effects might last.  Research is still in its infancy.

Dr. Douglas Scharre, neurologist and director of the division of cognitive neurology, and Dr. Ali Rezai, neurosurgeon and director of the neuroscience program are jointly conducting the study.

Sanford is the first of up to 10 patients who will be enrolled in the FDA-approved study to determine if using a brain pacemaker can improve cognitive and behavioral functioning in people with Alzheimer’s disease.

The study employs the use of deep brain stimulation (DBS), the same technology used to successfully treat patients with movement disorders such as Parkinson’s disease.

First, holes are drilled into the patient’s skull so tiny pacemaker wires can be implanted into just the right spot. A battery-powered generator near her collarbone then sends tiny shocks up her neck and into her brain.

It is hoped that zapping the brain with mild jolts of electricity will make the brain work better and stave off the cognitive, behavioral and functional effects of Alzheimer’s disease.

“If the early findings that we’re seeing continue to be robust and progressive, then I think that will be very promising and encouraging for us,” says Ali Rezai MD, “But so far we are cautiously optimistic.”

Kathy Sanford says she volunteered for the study to help others avoid the angst she has suffered as Alzheimer’s slowly disrupted her life.  The Ohio woman’s early stage Alzheimer’s was gradually getting worse. She still lived independently, posting reminders to herself, but no longer could work. The usual medicines weren’t helping.
Her father is proud that his daughter is participating in the study. “What’s our choice? To participate in a program or sit here and watch her slowly deteriorate?” asked Joe Jester, 78.  He drives his daughter to follow-up testing, hoping to spot improvement.

Since having the surgery last October Sanford has undertaken a number of problem-solving tests while neurologists adjusted the voltage and frequency and watched her reactions.

She was cheered to see her test scores climb a bit during those adjustments. While she knows there are no guarantees, she says “if we can beat some of this stuff, or at least get a leading edge on it, I’m in for the whole deal.”

Her optimism and hope is shared by her neurologist. “We’re getting tired of not having other things work” said Douglas Scharre MD.  Alzheimer’s doesn’t just steal memories. It eventually robs sufferers of the ability to do the simplest of tasks.

Here’s hoping these brain pacemakers can reconnect some of the circuits and diminish such losses.

iPods help Seniors re live their past and regain memories

For as long as humans have pounded drums and plucked strings, listening to music has affected people’s sense of well-being, lifting their spirits, and calming their nerves.  Now, a new film suggests that the right music can change the lives of people suffering from Alzheimer’s and dementia.

The documentary “Alive Inside” shows the transformative power of music as several elderly dementia patients are given iPods loaded with their favorite music.

The film follows social worker Dan Cohen, who decides on a whim to bring iPods to a nursing home.  To his and the staff’s surprise many residents suffering from memory loss seem to “awaken” when they are able to listen to music from their past.  The previously unresponsive seniors quickly start to tap their toes, swing their hands, and, incredibly, start having long discussions about their passion for music and its role in their lives.

One man – Henry – becomes especially impassioned when he is asked what music means to him. “It gives me the feeling of love, romance,” he says. “I figure right now the world needs to come into music. The Lord came to me and made me holy, I’m a holy man. So he give me these sounds.”

With great excitement, Dan turns to renowned neurologist Dr. Oliver Sacks, and the film follows them both as they investigate the mysterious way music functions inside our brains and our lives.

Sacks best known as the author of 12 books, including: The Mind’s Eye, Awakenings, The Man Who Mistook His Wife for a Hat and Musicophilia says “Music imprints itself on the brain deeper than any other human experience. Music evokes emotion and emotion can bring with it memory and the feeling of life when nothing else can.”

Besides telling a moving story, the film’s producers hope it will encourage widespread adoption of personalized music programs in nursing homes and that it will inspire and educate the millions of people burdened by diseases that affect memory.  They also hope to create a grassroots demand for music therapy and potentially help not only patients but also caregivers across the globe.

Although Alive Inside focuses on one man’s journey, it raises many questions about what it means to be Alive Inside. It questions when we stop being human, and what it takes to re-start a life that has faded away. It asks questions about how we see our elderly, and how we are going to treat an epidemic of these degenerative diseases.

The filmmakers have had an early trailer online for more than a year, but it recently premiered in New York and interest has exploded in recent days, thanks to social media sites such as Facebook and Reddit  They have also been able to raise over $50,000 to make an edited version of the film and obtain copyright approval for songs heard on the film.

Producer /  Director Michael Rossato-Bennett says following the work of Cohen and Sacks was one of the most fulfilling things he has done during his 30-year filmmaking and photography career.

“Usually when you make a film you wait for a moment to make you cry and it might take three months,” he said. “On the first day of filming I cried like five times. There is something in seeing another person awaken. That does something to all of us.”

For more information about the film and music and memory please click here.

Keeping harmful protein fibers at bay

Misfolded clothes, are the bane of many a fashion retail worker’s existence; misfolded proteins on the other hand are not just useless,  they can also be toxic. When proteins in the human body get out of alignment they form linear aggregates known as amyloid fibers that can lead to disorders such as Alzheimer’s and Parkinson’s diseases.

So SRxA’s Word on Health was interested to learn that US researchers have discovered a protein machinery that inhibits the formation and helps to dissolve such fibers.

The researchers set out to study whether two small heat shock proteins (HSPs) – proteins that assist other proteins in folding – could affect the generation of amyloid fibres by a misfolded protein of the same organism (Sup35). Using purified proteins, derived from baker’s yeast they showed that Hsp26 and Hsp42 inhibited amyloid formation.

Even cleverer still, they were able to determine exactly which steps of the process were affected. Hsp42 slowed down early structural reorganization of small aggregates before the fibers were formed, whereas Hsp26 inhibited fiber growth.

All of which, we’re sure you’re saying, is great news for baker’s yeast, but you’ve never seen a loaf of bread with Alzheimer’s!

And here’s the problem.   Humans and other animals lack the yeast enzyme – Hsp104 – that rapidly dissolves amyloid.  As such, it was unclear if and how our cells could get rid of amyloid fibres.

Undeterred, the scientists started to experiment further.  They showed that Sup35 fibers can be dissolved by a combination of several yeast HSPs (Hsp40, Hsp70 and Hsp110) in the absence of Hsp104.  And, the effect was even better if the fibers were pretreated with Hsp26 and Hsp42.

What’s more, they obtained similar results when using the equivalent human HSPs to disaggregate the amyloid fibres involved in Parkinson’s disease. Although amyloid disassembly took many days, the researchers propose that such system could work in long-lasting cells such as neurons.

The full results are published here.

While their findings suggest that enhancing the activity of certain HSPs in affected cells and/or introducing yeast Hsp104 could help to dissolve the amyloid in disorders such as Parkinson’s disease, additional research would be needed to assess the efficacy and safety of such treatments before human testing can begin.

Nevertheless it’s a step in the right direction.  Now, if only we could find an answer to misfolded clothes!

Diabetes Drug may Repair Injured Brains

Here’s a good brain teaser for a Wednesday.  What do an old diabetes drug, brain injury and Alzheimer’s Disease have in common?

Here’s some clues to help you solve the riddle.

(i)           Metformin is a widely used treatment for type II diabetes

(ii)          An increasing proportion of people with Alzheimer’s Disease also have diabetes

(iii)         Hyperinsulinemia (excess levels of insulin in the blood) may enhance the onset and progression of neurodegeneration

Have you solved it?  If so, congratulations!

If not, the answer, according to data just published in the journal Cell Stem Cell is that the former may hold the clue to treating the latter.

In other words, the study suggests that metformin, an anti-diabetes drug first discovered in the 1920’s, is able to help activate the mechanism that signals stem cells to generate brain cells.

Principal investigator, Freda Miller, a Professor from the Department of Molecular Genetics at the University of Toronto
says “If you could take stem cells that normally reside in our brains and somehow use drugs to recruit them into becoming appropriate neural cell types, then you may be able to promote repair and recovery in at least some of the many brain disorders and injuries for which we currently have no treatment.”

The research involved laboratory experiments using both mouse and human brain stem cells, as well as learning and memory tests performed on live mice given the drug.

Miller and her colleagues started by adding metformin to stem cells from the brains of mice, then repeated the experiment with human brain stem cells generated in the lab. In both cases, the stem cells gave rise to new brain cells.

They then tested the drug in lab mice and found that those given daily doses of metformin for two or three weeks had increased brain cell growth and outperformed rodents not given the drug in learning and memory tasks.

In the key experiment, mice were forced to learn the position of a platform hidden under the surface of a water-filled maze and then asked rapidly to learn a new position.

Mice were injected with either metformin or saline for 38 days. On days 22 through 38, they learned the initial position of the platform, which provided an escape from the water-filled maze.  Then the platform was moved to the opposite side of the maze, and the animals were asked again to learn its position. In both tasks, the mice learned the platform positions with equivalent speed.

But when they were put back in the maze – this time with the platform removed – control mice spent more time searching for it in the original position, while the metformin-treated animals preferentially looked in the new region.

The implication  is that metformin helped the mice form their new memories of the second platform position. Further analysis showed that their enhanced ability was paralleled by an increase in the number of  neurons.

In a separate study researchers have shown that metformin can increase lifespan and delay the onset of cognitive impairment in a mouse model of Huntington’s disease.

Taken together, these findings raise the possibility that metformin’s ability to enhance neurogenesis might have a positive impact in some nervous system disorders.

Miller’s team is already planning a pilot study to test metformin in young patients with acquired brain damage, either as result of treating a childhood brain tumor or from a traumatic head injury.

We will report back to you with results, as they are published.

Nutty about Brain Health?

Last year, we posted news of an epigenetic diet rich in broccoli, cauliflower, cabbage, fava beans and kale that claimed to reduce cancer and degenerative brain changes.  Despite its alleged health benefits, the diet has found few followers among your average American carnivore.

And although it’s unlikely that we will ever see nutritionists advocating a hamburger, beer and potato chip diet, maybe more people will be tempted to reduce their risk of Alzheimer’s disease and memory problems by following the dietary advice of a new study published in the May 2, 2012, online issue of Neurology®.

This research showed shows that eating foods such as fish, chicken, salad dressing and nuts, which contain omega-3 fatty acids, is associated with lower blood levels of beta-amyloid, a protein related to Alzheimer’s.

The study followed 1,219 people 65 and older, who were free of dementia. Participants, provided information about their diet for an average of 1.2 years before their blood was tested for beta-amyloid.

The researchers looked specifically at 10 nutrients, including saturated fatty acids, omega-3 and omega-6 polyunsaturated fatty acids, mono-unsaturated fatty acid, vitamin E, vitamin C, beta-carotene, vitamin B12, folate and vitamin D.

They found that the more omega-3 fatty acids a person ate, the lower their blood beta-amyloid levels. Consuming one gram of omega-3 per day – the equivalent of approximately half a fillet of salmon per week, lowered blood beta-amyloid levels by 20-30%.

“It was a continuous association.  More and more intake of omega-3s was associated with lower and lower levels of beta-amyloid in the blood.  There was no threshold effect,” author Nikolaos Scarmeas, MD, from  Columbia University Medical Center

The association between omega-3 consumption and beta-amyloid was unaffected by whether or not a person took supplements – meaning if two people consumed the same amount of omega-3s, one through food and the other through supplements, the person who consumed more omega-3 rich foods typically had lower blood levels of beta-amyloid.

Other nutrients were not associated with changes in plasma beta-amyloid levels. And results stayed the same after adjusting for age, education, gender, ethnicity, amount of calories consumed and presence of the APOE gene, a risk factor for Alzheimer’s disease.

The beneficial impact of omega-3 on brain health would fall in line with past studies of the nutrient.  “Previous studies have suggested that omega-3s and other aspects of diet may be related to brain function,” Scarmeas said. “Here we demonstrate one possible mechanism could be through amyloid, the main biological mechanism that relates to Alzheimer’s disease.”

Scarmeas speculated that omega-3s may be able to reduce oxidative stress on the brain and the resulting vascular damage, or even have some kind of impact on beta-amyloid in the brain.

And although there is not enough data yet to suggest omega 3’s and beta-amyloid are directly related, I, for one, will be ordering the pecan crusted chicken salad for lunch today, dressing on the plate!