Do you know why you lose some of your memory function when you age? It’s because the brain actually shrinks. This, you are no doubt thinking, is something that most definitely can’t be reversed. Everyone should just accept that an agile brain and an excellent memory are things of the past once they hit middle age. But not so, according to a recent study done by researchers in Columbus, Ohio. Results show that a one-year period of exercise doesn’t only slow down brain shrinkage — it could also actually reverse it! For the study, Continue reading →
In an intriguing new health breakthrough, scientists have found that zinc plays a special role in our brains. The mineral — and popular natural supplement — seems to help brain cells communicate. This may mean it helps the brain form memories, and that it could even control epileptic seizures.
U.S. researchers watched zinc in action as it regulated communication between neurons in the hippocampus. This is the brain region where learning and memory processes occur, and where disrupted communication contributes to epilepsy.
Sometimes the disease itself doesn’t kill; the killer is the victim’s own immune system.
A growing amount of research shows that this can happen with certain infections, such as those that cause Lyme disease, syphilis, mycoplasmal pneumonia, and especially viral infections of the nervous system. Death and severe neurological damage come from an attack by our own body’s immune system and not from the damage done by the invading microorganism.
Activation of the body’s immune system triggers the release of glutamate which slowly kills brain cells by a process called excitotoxicity.
A recent study examined a viral infection of the central nervous system of mice which produced severe damage to the hippocampus area of the brain and to the spinal cord, and resulted in death in all of the mice in a little over a week. In some of the mice, researchers used an AMPA type glutamate receptor blocker, which prevented death in most of the animals and also prevented spinal cord damage.
Ironically, at the time the animals were protected from the damage by the glutamate receptor blocker, Continue reading →
Do you ever forget people’s names? Enter a room and forget why you went there? Forget a word mid-sentence? As we get older, these types of “senior moments” happen more often. Many of the people I evaluate worry that these slips mean they are getting Alzheimer’s disease. In most cases, they aren’t. They’re just part of normal, age-related memory decline. Starting at about age 30, our ability to process and remember information declines with age.
But though these cognitive changes are common, cognitive decline is not inevitable. Recent research has identified specific brain alterations that underlie this kind of age-related cognitive decline. And the good news is that many of these brain changes can be prevented with healthy lifestyle practices. A key finding: Elevated blood sugar contributes to cognitive decline.
The details: It has long been known that problems with short-term memory are related to age-related decreases in blood flow in a part of the brain called the hippocampus. Recently, researchers at Columbia University Medical Center discovered that decreased blood flow Continue reading →
Aerobics Exercise can keep your brain sharp as you age. A new study has shown that a program of exercise can, over the course of a year, increase the size of your hippocampus, a part of the brain key to memory and spatial navigation.
The hippocampus often shrinks in late adulthood, leading to memory impairment.
According to the Los Angeles Times:
“To complete the study, the team recruited 120 older people who didn’t exercise regularly. Half were randomly assigned to an aerobic exercise program Continue reading →
Push-ups, crunches, gyms, personal trainers – people have many strategies for building bigger muscles and stronger bones. But what can one do to build a bigger brain? Meditate.
That’s the finding from a group of researchers at UCLA who used high-resolution magnetic resonance imaging (MRI) to scan the brains of people who meditate. In a study published in the journal NeuroImage the researchers report that certain regions in the brains of long-term meditators were larger than in a similar control group.
Specifically, meditators showed significantly larger volumes of the hippocampus and areas within the orbital-frontal cortex, the thalamus and the inferior temporal gyrus — all regions known for regulating emotions.
“We know that people who consistently meditate have a singular ability to cultivate positive emotions retain emotional stability and engage in mindful behavior,” said Eileen Luders, lead author and a postdoctoral research fellow at the UCLA Laboratory of Neuro Imaging. “The observed differences in brain anatomy might give us a clue why meditators have these exceptional abilities.”
Research has confirmed the beneficial aspects of meditation. In addition to having better focus and control over their emotions, many people who meditate regularly have reduced levels of stress and bolstered immune systems. But less is known about the link between meditation and brain structure.
In the study, Luders and her colleagues examined 44 people — 22 control subjects and 22 who had practiced various forms of meditation, including Zazen, Samatha and Vipassana, among others. The amount of time they had practiced ranged from five to 46 years, with an average of 24 years.
More than half of all the meditators said that deep concentration was an essential part of their practice, and most meditated between 10 and 90 minutes every day.
The researchers used a high-resolution, three-dimensional form of MRI and two different approaches to measure differences in brain structure. One approach automatically divides the brain into several regions of interest, allowing researchers to compare the size of certain brain structures. The other segments the brain into different tissue types, allowing researchers to compare the amount of gray matter within specific regions of the brain.
The researchers found significantly larger cerebral measurements in meditators compared with controls, including larger volumes of the right hippocampus and increased gray matter in the right orbital-frontal cortex, the right thalamus and the left inferior temporal lobe. There were no regions where controls had significantly larger volumes or more gray matter than meditators.
Because these areas of the brain are closely linked to emotion, Luders said, “these might be the neuronal underpinnings that give meditators’ the outstanding ability to regulate their emotions and allow for well-adjusted responses to whatever life throws their way.”
What’s not known, she said, and will require further study, are what the specific correlates are on a microscopic level — that is, whether it’s an increased number of neurons, the larger size of the neurons or a particular “wiring” pattern meditators may develop that other people don’t.
Because this was not a longitudinal study — which would have tracked meditators from the time they began meditating onward — it’s possible that the meditators already had more regional gray matter and volume in specific areas; that may have attracted them to meditation in the first place, Luders said.
However, she also noted that numerous previous studies have pointed to the brain’s remarkable plasticity and how environmental enrichment has been shown to change brain structure.
LONDON – Scientists at the University College London have found that the hippocampus in the brain is responsible for our ability to organize the world into separate concepts.
Forming a concept involves selecting the important characteristics of our experiences and categorizing them.
The degree to do this effectively is a defining characteristic of human intelligence.
However, not much is known about how conceptual knowledge is created and used in the brain.
Thus, to identify the brain regions responsible, Dharshan Kumaran and colleagues at the Wellcome Trust Centre for Neuroimaging, UCL, showed 25 volunteers, pairs of fractal patterns that represented the night sky and asked them to forecast the weather – either rain or sun – based on the patterns.
Conceptual rules based on the positions and combinations of the patterns governed whether the resulting outcome would be rain or sun, but the volunteers were not told this.
Instead, they rewarded correct predictions with cash prizes, encouraging the volunteers to deduce these conceptual rules.
In an initial learning phase, the different possible combinations were repeatedly shown to the participants, so that they could make their predictions by simply memorizing previous outcomes and could also begin to realize that rules based on the positions and combinations of the patterns governed whether the result would be rain or sun.
In a second phase, the volunteers were provided with less information to encourage them to apply the rules they had identified, which made the researchers to separate those volunteers who had formed the concept in the learning phase from those who hadn’t.
During both experiments FMRI scanning was used to identify areas of brain activity.
It was found that in the first phase, they could tell if a volunteer would go on to apply concepts in the second phase by the degree of activity in their hippocampus, which is known to be responsible for learning and memory.
In the second phase, activity centered on the ventromedial prefrontal cortex (VMPFC), important in decision-making, was active.
The team concluded that the hippocampus creates and stores concepts, and passes this information onto the VMPFC where it is put to use during the making of decisions.
People with amnesia are also known to have problems forming concepts, so Kumaran is expecting his findings to lead to the development of improved teaching methods and other tools for the treatment of amnesiacs.
The study has been published in the journal Neuron.
TRENTON – Scientists from University of Medicine and Dentistry of New Jersey have identified a protein that can repair brain damage in Alzheimer’s patients.
They said that a protein called vimentin normally appears twice in a lifetime – when neurons in the brain are forming during the first years of life and, years later when the brain’s neurons are under siege from Alzheimer’s or other neurodegenerative diseases.
“Vimentin is expressed by neurons in regions of the brain where there is Alzheimer’s damage but not in undamaged areas of the brain,” said DrRobertNagele, a professor at UMDNJ and the study’s corresponding author.
“When the patient shows up at the doctor’s office with symptoms of cognitive impairment, the neurons have reached the point where they can no longer keep pace with the ever-increasing damage caused by Alzheimer’s,” he added.
While explaining the study results, Nagele likened neurons to a tree with long strands called dendrites branching off from the main part of the cell.
The dendrite branches are covered with 10,000 tiny “leaves” called synapses that allow neurons to communicate with each other. Vimentin is an essential protein for building the dendrite branches that support the synapses.
“A hallmark of Alzheimer’s is the accumulation of amyloid deposits that gradually destroy the synapses and cause the collapse of dendrite branches,” he said.
“When the dendrites and synapses degenerate, the neuron releases vimentin in an attempt to re-grow the dendrite tree branches and synapses. It’s a rerun of the embryonic program that allowed the brain to develop in the early years of life,” Nagele added.
The researchers also reported some initial findings that indicated a similar damage response mechanism takes place following traumatic brain injury, suggesting the possibility that similar therapeutic agents could be developed to enhance repair both for sudden brain trauma and for progressive neurodegenerative diseases.
The findings are published in journal Brain Research.
Kava is a tall shrub in the pepper family that grows in the South Pacific islands. It has been used there for thousands of years as a folk remedy and as a social and ceremonial beverage.
The part of the plant used medicinally is the root. Although the root was traditionally chewed or made into a beverage, kava is now available in capsule, tablet, beverage, tea, and liquid extract forms.
Why People Use Kava:
Because kava can cause sedation, and in high amounts, intoxication, kava drinks are consumed in some parts of the world in much the same way as alcohol.
How Kava Works:
The main active components in kava root are called kavalactones. Specific types of kavalactones include dihydrokavain, methysticin, kavain, dihydromethysticin, dihydrokawain, yangonin and desmethoxyyangonin.
Although it’s not clear exactly how kava works, kavalactones may affect the levels of neurotransmitters (chemicals that carry messages from nerve cells to other cells) in the blood. Kava has been found to affect the levels of specific neurotransmitters, including norepinephrine, gamma aminobutyric acid (GABA) and dopamine.
Scientific Evidence for Kava:
A number of well-designed studies have examined kava’s ability to relieve anxiety compared to anxiety medication or a placebo. The results have been promising.
In 2003, a review by the Cochrane Collaboration examined the existing research to see how kava fared compared to a placebo in treating anxiety. After analyzing the 11 studies (involving a total of 645 people) that met the criteria, the researchers concluded that kava “appears to be an effective symptomatic treatment option for anxiety.” However, they added that it seemed to be a small effect.
Concerns About Kava and the Liver:
Although rare, case reports have linked kava use with liver toxicity, including hepatitis, cirrhosis, and liver failure.
As a result, the FDA issued a warning about kava in 2002. Several countries have banned or restricted the sale of kava.
Clinical trials have not found liver toxicity. Adverse liver reactions appear to be linked to factors such as pre-existing liver disease, alcohol consumption, excessive doses, genetic variations in the cytochrome P450 enzymes, consumption of other drugs or herbs that, combined, may have a toxic effect, or the use of stem or leaf extracts or extracts made with acetone or ethanol.
Potential Side Effects of Kava:
Side effects include indigestion, mouth numbness, skin rash, headache, drowsiness and visual disturbances. Chronic or heavy use of kava has linked to pulmonary hypertension, skin scaling, loss of muscle control, kidney damage, and blood abnormalities.
Kava may lower blood pressure and it also may interfere with blood clotting, so it shouldn’t be used by people with bleeding disorders. People with Parkinson’s disease shouldn’t use kava because it may worsen symptoms.
Kava should not be taken within 2 weeks of surgery. Pregnant and nursing women, children, and people with liver or kidney disease shouldn’t use kava.
Possible Drug Interactions:
Kava shouldn’t be taken by people who are taking Parkinson’s disease medications, antipsychotic drugs, or any medication that influences dopamine levels.
Kava shouldn’t be combined with alcohol or medications for anxiety or insomnia, including benzodiazepines such as Valium (diazepam) or Ativan (lorazepam). It may have an additive effect if taken with drugs that cause drowsiness.
Kava may have an additive effect if combined with antidepressant drugs called monoamine oxidase inhibitors (MAOI).
Kava shouldn’t be taken with any drug or herb that impairs liver function. Kava also may interfere with blood clotting, so people taking Coumadin (warfarin) or any drug that influences blood clotting should avoid it unless under a doctor’s supervision.
Kava is a diuretic, so it may have an additive effect if combined with drugs or herbs that have diuretic properties.
BEVERLY HILLS – An estimated 10 per cent of American adults have mood disorders — 21 million. Another five million have Alzheimer’s disease.
Interest in cognitive health is also expanding to the younger populations, ages 25—50 years. Many younger people are more receptive to ‘keeping their brain sharp’ as they find themselves taking care of an elderly parent suffering from age-related mental decline and realise that they might have a similar condition in a few decades.
One of the primary ingredients marketed for cognitive health is the omega-3 fatty acid DHA. Martek’s life’sDHA is used in many infant formulas for improved cognitive function (and eye health), and through this platform is finding a home elsewhere. Its success is demonstrated with Martek’s second quarter financial 2009 results, which showed revenues up two per cent to $92.4 million.
“Our success within the infant formula market has provided us credibility with the food companies. If we are good enough for babies, we must be good enough for the rest of the population,” says SarahSullivan, senior manager of marketing at Martek Biosciences. “We market DHA based on the available science. And because DHA has brain, eye and heart-health benefits, there are many directions we can go. Ultimately, it’s up to the CPG company and how they want to position the ingredient within their food. But, because there isn’t as much competition within the ‘brain-health’ space, we generally recommend that they go that route.”
Other ingredients are hopping on the DHA bandwagon. Ocean Nutrition Canada, a major supplier of fish oil, has partnered with KyowaHakko USA and its Cognizin ingredient, which is GRAS and water-soluble.
Gamma amino butyric acid (GABA)
St John’s wort
“We wanted to leverage both companies’ ingredients for brain health,” says KarenETodd, RD, director of marketing for KyowaHakko USA. “We have found that Cognizin not only supports memory function and healthy cognition, but crosses over many functions — increasing levels of critical neurotransmitters such as dopamine and acetylcholine, enhancing cellular integrity by increasing phospholipids synthesis, and supporting cellular activity by increasing levels of adenosine triphosphate (ATP).”
ChemiNutra combined omega-3 fatty acids with phosphatidylserine (PS) to form a new offering. “OmegaAid PS is the natural evolution of combining marine-sourced omega-3 fatty acids with PS, utilizing Chemi’s proprietary manufacturing expertise, and supported by Chemi’s numerous patents,” says ScottHagerman, president of ChemiNutra and ChemiPharma.
Hagerman says the company works to leverage market interest into successful new ingredients. “We first look at market attractiveness, long-term prospects of selling, production capabilities and, finally, patent opportunities, since we have to make substantial investments in identifying and developing new ingredient product opportunities.”
One new entrant to the field is Vivimind by Ovos Natural Health. The ingredient, derived from homotaurine found in seaweed, has a great deal of research behind it, on more than 2,000 individuals. It is set to launch in the US market by the end of the year.
“Vivimind has received scientific support and has been embraced by consumers in the Canadian market since its launch in September 2008,” says JimStitley, general manager of US commercial operations for Ovos.
Other emerging ingredients include vinpocetine, curcumin and turmeric. And — surprise, surprise — vitamin D. A May 2009 study in Europe of more than 3,000 men aged 40-79 found those with high vitamin D levels performed better on memory and information processing tes
CHICAGO (Reuters) – Prolonged exposure to cocaine can cause permanent changes in the way genes are switched on and off in the brain, a finding that may lead to more effective treatments for many kinds of addiction, U.S. researchers said on Thursday.
A study in mice by IanMaze of Mount Sinai School of Medicine in New York and colleagues found that chronic cocaine addiction kept a specific enzyme from doing its job of shutting off other genes in the pleasure circuits of the brain, making the mice crave the drug even more.
The study helps explain how cocaine use changes the brain, said Dr. Nora Volkow, director of the National Institute on Drug Abuse, part of the National Institutes of Health, which funded the study published in the journal Science.
“This finding is opening up our understanding about how repeated drug use modifies in long-lasting ways the function of neurons,” Volkow said in a telephone interview.
For the study, the team gave one group of young mice repeated doses of cocaine and another group repeated doses of saline, then a single dose of cocaine.
They found that one way cocaine alters the reward circuits in the brain is by repressing gene 9A, which makes an enzyme that plays a critical role in switching genes on and off.
Other studies have found that animals exposed to cocaine for a long period of time undergo dramatic changes in the way certain genes are turned on and off, and they develop a strong preference for cocaine.
This study helps explain how that occurs, Volkow said, and may even lead to new ways of overcoming addiction.
In the study, Maze and colleagues showed these effects could be reversed by increasing the activity of gene 9A.
“When they do that, they completely reverse the effects of chronic cocaine use,” Volkow said.
She said this mechanism is likely not confined to cocaine addiction, and could lead to a new area of addiction research for other drugs, alcohol and even nicotine addition.
“One of the questions we’ve had all along is, after discontinuing a drug, why do you continue to be addicted?
“This is one of the mechanisms that probably is responsible for these long-lasting modifications to the way people who are addicted to drugs perceive the world and react to it,” she said.
CHAROLETTE – Scientists from University of North Carolina have identified a gene that controls the number of cells composing brain.
Called GSK-3, the gene has been found to strike a balance between two key processes – proliferation, in which the cells multiply to provide plenty of starting materials, and differentiation, in which those materials evolve into functioning neurons.
If the stem cells proliferate too much, they could grow out of control and produce a tumour. If they proliferate too little, there may not be enough cells to become the billions of neurons of the brain.
The study showed that GSK-3 controls the signals that determine how many neurons actually end up composing the brain.
The novel findings may have significant implications for people suffering from neuropsychiatric illness like schizophrenia, depression, and bipolar disorder.
“I don’t believe anyone would have imagined that deleting GSK-3 would have such dramatic effects on neural stem cells,” Nature quoted senior study author Dr William D. Snider, professor of neurology and cell and molecular physiology, and director of the UNC Neuroscience Centre, as saying
“People will have to think carefully about whether giving a drug like lithium to children could have negative effects on the underlying structure of the nervous system,” he added.
During the study, the researchers genetically engineered mice to lack both forms of the GSK-3 gene, designated alpha and beta.
They further used a “conditional knock-out” strategy to remove GSK-3 at a specific time in the development of the mouse embryo, when a type of cell called a radial progenitor cell had just been formed.
“It was really quite striking,” said Snider.
“Without GSK-3, these neural stem cells just keep dividing and dividing and dividing. The entire developing brain fills up with these neural stem cells that never turn into mature neurons,” he added.
GSK-3 is known to coordinate signals for proliferation and differentiation within nerve cells through multiple “signalling pathways.”
They found that every one of the pathways that they studied went awry after deleting the GSK-3 gene.
The study has been published in the journal Nature Neuroscience.
GLASGOW – A British study suggests that the ability to identify a face, when it is shown for only a fraction of a second, reduces as people age.
Lead researcher Guillaume Rousselet, from the University of Glasgow, came to this conclusion after analysing electric activity from the brains of young and old people as they watched pictures of faces with cloud-like noise.
He said: “Very few studies have attempted to measure the effect of ageing on the time-course of visual processing in response to complex stimuli like faces. We found that, as well as a general reduction in speed in the elderly, one particular component of the response to a face, the N170, is less sensitive to faces in the elderly.”
The N170 occurs 170 milliseconds after a stimulus is presented.
The researchers revealed that it was more closely associated with the appearance of a face among the young subjects.
However, in older subjects, the researcher said that it occurred also in response to noise, perhaps implying reduced ability to differentiate faces from noise.
Revealing the findings of the study, Rousselet said: “Our data support the common belief that as we get older we get slower. Beyond this general conclusion, our research provides new tools to quantify by how much the brain slows down in the particular context of face perception. Now, we need to identify the reasons for the speed reduction and for the heterogeneity of the effects – indeed, why the brains of some older subjects seem to tick as fast as the brains of some young subjects is, at this point, a complete mystery.”
The study has been published in the journal BMC Neuroscience.
HOUSTON – In a new study on mice, researchers have found why and how the use of addictive drugs take control of reward signals and influence neural processes associated with learning and memory.
The study could help explain how drug-associated memories, such as the place of drug use, drive and perpetuate the addiction.
It is known that the neurochemical dopamine, a key player in the brain’s reward system, is involved in the process of addiction.
Research has indicated that dopamine participates in neural processes associated with learning, such as the strengthening of neuronal connections, called synaptic potentiation.
Evidence has also implicated the hippocampus, a deep-brain structure that is critical for formation of new memories, in the development of drug addiction.
“Although addictive drugs like nicotine have been shown to influence the induction of synaptic potentiation, there has been little or no research in freely moving animals that monitors ongoing induction of synaptic potentiation by a biologically relevant drug dose,” explains senior author Dr.JohnDani from the Department of Neuroscience at the Baylor College of Medicine in Houston, Texas.
The researchers recorded from the brains of freely moving mice while applying physiologically relevant concentrations of nicotine, the addictive component in tobacco.
The researchers found that nicotine induced synaptic potentiation correlated with the mice learning to prefer a place associated with the nicotine dose.
Importantly, these effects required a local dopamine signal within the hippocampus.
The finding reinforces the view that dopamine enables memory for specific events.
Overall, the results point to some intriguing possibilities about how drug-associated memories might contribute to behaviors associated with addiction.
“An animal’s memories or feelings about the environment are updated when the dopamine signal labels a particular event as important, new, and salient. Normally these memories help us to perform successful behaviors, but in our study, those memories were linked to the addictive drug.
When specific environmental events occur, such as the place or people associated with drug use, they are capable of cuing drug-associated memories or feelings that motivate continued drug use or relapse,” concluded Dani.
The study has been published in the latest issue of the journal Neuron.