Reinventing the Fountain of Youth
Posts tagged Neuroprotector
Towards age-suppression
1388 days
The amino acid L-cysteine is one of the standard building blocks used by the body to produce the countless proteins it needs: enzymes, structural proteins, signalling molecules and their receptors, and small polypeptide molecules with specialized functions. One such polypeptide, ‘glutathione’, is an essential antioxidant that protects cells from being damaged or killed by stray free radicals.
Since glutathione is crucially important for preventing cellular damage and the diseases that result from such damage, there is good reason to increase the amount of L-cysteine available to the body for making it. The trouble is, if cysteine is used as a supplement, it can be neurotoxic. This toxicity can be avoided by using N-acetylcysteine (NAC) instead of cysteine itself.
NAC’s remarkable biological benefits
NAC is one of the most studied of all supplements. In the 1960s it was found to be useful for people with cystic fibrosis and other pulmonary ailments. It later garnered the attention of HIV researchers, and has now been investigated for many other medical conditions.
The list of medical applications of NAC is a very long one, and includes the following categories:
- Pulmonary and respiratory ailments
- Aging
- Muscle fatigue
- Neurological conditions
- Cancer
- Infections
- Neurodegenerative diseases
- Addictions
- Sickle cell disease
- Muscle-degenerative conditions
- Toxicity
- Cardiovascular ailments
- Immune system problems
- Diabetes
- Fatty liver disease
Let us look at one of the many intriguing applications of this supplement:
NAC interferes with cardiovascular damage.
Whenever food is cooked, some of the sugars in the food are converted into substances called ‘AGEs’ (Advanced Glycation Endproducts). These are inflammatory chemicals that, when consumed, cause damage to the walls of arteries and veins, as well as accelerated aging in other tissues in the body. The body actually produces its own AGEs from sugars, but usually in smaller amounts than are found in cooked food. Diabetics, however, have a much higher AGE burden than non-diabetics do, because diabetes causes spikes in blood sugar levels.
In an important 2004 paper, researchers reported that diabetics experience substantially less damage to arteries when their consumption of AGEs is reduced. Furthermore, NAC interferes with a key process through which AGEs produce inflammation and tissue damage, and actually prevents AGEs from damaging vascular cells.
NAC suppresses many other harmful processes taking place in the body. It is an inexpensive supplement that is safe and easy to obtain — so it would be foolish not to take advantage of it.
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Neurogenesis: How to Change Your Brain
148442 days
“In adult centers the nerve paths are something fixed, ended, immutable. Everything may die, nothing may be regenerated.”
– Santiago Ramon Y Cajal, “Degeneration and Regeneration in the Nervous System,” 1928
This long-held tenet, first proposed by Professor Cajal, held that brain neurons were unique because they lacked the ability to regenerate.
In 1998, the journal Nature Medicine published a report indicating that neurogenesis, the growth of new brain cells, does indeed occur in humans. As Sharon Begley remarked in her book, “Train Your Mind, Change Your Brain,” “The discovery overturned generations of conventional wisdom in neuroscience. The human brain is not limited to the neurons it is born with, or even the neurons that fill in after the explosion of brain development in early childhood.”
What the researchers discovered was that within each of our brains there exists a population of neural stem cells which are continually replenished and can differentiate into brain neurons. Simply stated, we are all experiencing brain stem cell therapy every moment of our lives.
As one might expect, the process of neurogenesis is controlled by our DNA. A specific gene codes for the production of a protein, brain-derived neurotrophic factor (BDNF) which plays a key role in creating new neurons. Studies reveal decreased BDNF in Alzheimer’s patients, as well as in a variety of neurological conditions including epilepsy, depression, schizophrenia and obsessive-compulsive disorder.
Fortunately, many of the factors that influence our DNA to produce BDNF factors are under our direct control. The gene that turns on BDNF is activated by a variety of factors including physical exercise, caloric restriction, curcumin and the omega-3 fat, DHA.
This is a powerful message. These factors are all within our grasp and represent choices we can make to turn on the gene for neurogenesis. Thus, we can treat ourselves to stem cell therapy by taking control of our gene expression.
Physical Exercise
Laboratory rats that exercise have been shown to produce far more BDNF in their brains compared to sedentary animals. And there is a direct relationship between elevation of BDNF levels in these animals and their ability to learn, as one might expect.
With this understanding of the relationship of BDNF to exercise, researchers in a report in the Journal of the American Medical Association, entitled “Effect of Physical Activity in Cognitive Function in Older Adults at Risk for Alzheimer’s Disease,” found that elderly individuals engaged in regular physical exercise for a 24-week period had an improvement of an astounding 1,800 percent on measures of memory, language ability, attention and other important cognitive functions compared to an age-matched group not involved in the exercise program.
The mechanism by which exercise enhances brain performance is described in these and other studies as sitting squarely with increased production of BDNF. Just by engaging in regular physical exercise, you open the door to the possibility of actively taking control of your mental destiny.
Caloric Restriction
In January, 2009, the Proceedings of the National Academy of Science published a study entitled “Caloric Restriction Improves Memory in Elderly Humans.” In this study, German researchers imposed a 30 percent calorie reduction on the diets of elderly individuals and compared their memory function with a similar age group who basically ate whatever they wanted. At the conclusion of the three-month study, those who ate without restriction experienced a small, but clearly defined decline in memory function, while memory function in the group consuming the calorie-reduced diet actually increased, and fairly profoundly. In recognition of the obvious limitations of current pharmaceutical approaches to brain health, the authors concluded, “The present findings may help to develop new prevention and treatment strategies for maintaining cognitive health into old age.” What a concept. Preventive medicine for the brain.
Curcumin
Because curcumin, the main active ingredient in the spice turmeric, increases BDNF, it has attracted the interest of neuroscientists around the world. Interestingly, in evaluating villages in India where turmeric is used in abundance in curried recipes, epidemiological studies have found that Alzheimer’s disease is only about 25 percent as common as in the U.S. There is little doubt that the positive effects of enhanced BDNF production on brain neurons is at least part of the reason why those consuming curcumin are so resistant to this brain disorder.
DHA
Like curcumin, DHA enhances gene expression for the production of BDNF. In a recently completed double-blind interventional trial, 485 healthy older individuals (average age 70 years) with mild memory problems were given a supplement containing DHA from marine algae or placebo for six months. Lead researcher of the study, Dr. Karin Yurko-Mauro, commented, “In our study, healthy people with memory complaints who took algal DHA capsules for six months had almost double the reduction in errors on a test that measures learning and memory performance versus those who took a placebo … The benefit is roughly equivalent to having the learning and memory skills of someone three years younger.”
Harnessing the expression of our DNA is empowering, and the tools to better brain health are available to us all — right now!
Sources:
Results of the MIDAS trial: Effects of docosahexaenoic acid on physiological and safety parameters in age-related cognitive decline. Karin Yurko-Mauro, Deanna McCarthy, Eileen Bailey-Hall, Edward B. Nelson, Andrew Blackwell, MIDAS Investigators
Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, July 2009 (Vol. 5, Issue 4, Supplement, Page P84).
David Perlmutter, MD, FACN, ABIHM is a Board-Certified Neurologist and Fellow of the American College of Nutrition who received his M.D. degree from the University of Miami School of Medicine where he was awarded the Leonard G. Rowntree Research Award. After completing residency training in Neurology, also at the University of Miami, Dr. Perlmutter entered private practice in Naples, Florida.
http://www.huffingtonpost.com/
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Lithium increases gray matter in the brain
0498 days
Able to stabilize the mood swings of many people with manic depression, lithium revolutionized psychiatric therapy when the drug came on the scene several decades ago. Yet neuroscientists remain perplexed at how this potent medication works.
Scientists in Detroit have now provided a clue that could help resolve that mystery. They find that about a month of treatment with the drug increases the volume of gray matter in a person’s brain. Gray matter, the so-called thinking part of the brain, is made up primarily of the main bodies of nerve cells and their short connections.
“This is a highly significant finding and may shed light on the therapeutic mechanism of lithium,” says De-Maw Chuang of the National Institute of Mental Health in Bethesda, Md.
Another study by some of the Detroit scientists hints that lithium stimulates production of new brain cells. This observation raises hope that the drug can treat strokes, Alzheimer’s disease, and other conditions that kill brain cells. It may also support a radical new theory that the birth and death of brain cells underlie depression.
There have been hints before that lithium safeguards nerve cells. Two years ago, Chuang’s group showed that the drug protects nerve cells from fatal over-stimulation by the brain chemical glutamate. Husseini K. Manji of Wayne State University in Detroit and his colleagues then found that lithium-treated nerve cells overproduce a protein, bcl-2, that helps cells resist signals to commit suicide.
Manji next joined with his colleague Gregory J. Moore to carry out a brain-imaging study of people starting lithium treatment for manic depression. After 4 weeks, about the time it takes for lithium’s mood-stabilizing effects to emerge, the drug had increased the volume of brain gray matter by about 3 percent in 8 of the 10 people studied, the researchers report this week at the Society for Neuroscience meeting in New Orleans.
“This is the first demonstration of a pharmacological increase of human brain matter,” says Moore.
The researchers propose that most of the increased volume results from nerve cells sprouting additional branches to nearby cells, a sign of healthy brain cells. A small part of the increased gray matter may even consist of new brain cells.
In New Orleans, Manji’s group reported that lithium boosted new nerve cell production in one brain region of rodents. Mice receiving lithium had about 25 percent more new brain cells in the hippocampus than untreated mice did.
In past mouse studies, a diverse slate of proven antidepressant therapies, including electroconvulsive therapy, exercise, and drugs such as Prozac, has triggered the birth of nerve cells in the hippocampus.
This earlier work and other evidence have prompted some scientists to theorize that depression stems from problems with a brain’s natural ability to generate new cells in the hippocampus. That remains speculation, however. Indeed, only recently have scientists accepted that the adult human brain can grow new cells.
Lithium‘s ability to protect nerve cells and increase production of new ones may make the drug useful in more illnesses than manic depression, suggests Moore. Chuang, for example, reported last year that lithium reduces brain-cell loss in a rodent version of Huntington’s disease.
The drug also protects rodent brains from cell death after a stroke, even if researchers wait to administer the drug. “We can give lithium up to 3 hours after the onset of stroke,” says Chuang.
Manji proposes testing lithium in people with Alzheimer’s and Parkinson’s diseases and amyotrophic lateral sclerosis, more commonly known as Lou Gehrig’s disease.
J. Travis, Reprinted from Science News
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Low Vitamin D Linked to Schizophrenia
3500 days
There may be a link between sunlight, vitamin D and children’s brain development.
- Babies born with low vitamin D levels are shown to be twice as likely to develop schizophrenia.
- The finding may mean there could be a way to prevent cases of the disease.
- Scientists caution more research needs to be done to confirm the link.
Babies born with low vitamin D levels are twice as likely to develop schizophrenia later in life, researchers from the Queensland Brain Institute have found.
But the researchers say the good news from the study is that it suggests it may be possible to prevent schizophrenia.
John McGrath from the Queensland Brain Institute says there have been suggestions for some time that there may be a link between sunlight, vitamin D and brain development. He says it is increasingly clear children with low vitamin D levels are more likely to develop schizophrenia.
“For the babies who had very low vitamin D, their risk was about twice as high as those babies who had optimal vitamin D,” said McGrath.
But the amazing thing was that the study that was based in Denmark, where low vitamin D is quite common, we found that if vitamin D is linked to schizophrenia our statistics suggest that it could explain about 40 percent of all schizophrenias. That’s a much bigger effect than we’re used to seeing in schizophrenia research.
While the simplest way to get enough vitamin D is to spend more time in the sun, it remains unclear whether there are fewer cases of schizophrenia in a country like Australia which sees a lot more sunlight.
“We don’t have high-quality data on that, but some statistics suggest we do have slightly lower incidences and prevalence of schizophrenia,” said McGrath.
Like many other diseases, like multiple sclerosis, schizophrenia tends to be more common in places further away from the equator. And if you’re born in winter and spring you tend to have a slightly increased risk of schizophrenia also, and that was one of the original pieces of the jigsaw puzzle that led us to wonder maybe vitamin D could be implicated.
Ian Hickie from the Brain and Mind Research Institute in Sydney says he is not surprised by the results, however he says more research is needed.
So the real acid test is going to be trying to lift vitamin D levels in pregnant women and newborns and see whether there’s an effect on later schizophrenia,” said Hickie. “Or even in fact, looking at providing higher levels of vitamin D by vitamin D supplementation in other ways later in life and particularly childhood and the teenage years, to see whether you might reduce the risk of onset of schizophrenia.
Vitamin D supplements may prove an effective way to prevent schizophrenia. But McGrath agrees there is only a statistical link at the moment and that does not prove vitamin D deficiencies are to blame for schizophrenia.
“Because the treatment and the outcome can be separated by about 20, 30 years, we need to treat pregnant women and then wait for their offspring to develop schizophrenia,” he said. “It will be a very challenging study to do.”
It could be decades before scientists know for sure.
“But medical research tends to move at a steady pace. I think the other thing is that there are many other studies suggesting that vitamin D is good for baby’s bone health,” McGrath said.
So it may well be that recommendations will be made to women to increase their vitamin D status for more obvious outcomes, like baby’s rickets for example. If that happened then it may well be that schizophrenia would start to fall in decades to come.
But Hickie warns against spending too much time in the sun to get more vitamin D because that could increase the risk of skin cancer.
“Rates of melanoma and skin cancer are obviously very high in our country and directly related to sun exposure, particularly in childhood,” he said.
So on the one hand we need to be careful about over exposure to sunlight, on the other hand it may well be that in some places, or in some individuals, low levels of vitamin D may constitute a risk factor, particularly in pregnancy and therefore affecting the rates of vitamin D in newborn children.
So this is one of the issues that we’re going to need to look at clearly. I don’t think it means that everyone should be rushing out into the sun and necessarily putting themselves at risk of other sun-related cancers.
Even if vitamin D does make a difference, there are several other factors that may play a part.
A predisposition to the illness can run in families, chemical imbalances in the brain may be responsible and stressful events are often thought to play a role in the onset of the schizophrenia.
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Why Fish Oils Work Swimmingly Against Inflammation and Diabetes
0504 days
Researchers at the University of California, San Diego School of Medicine have identified the molecular mechanism that makes omega-3 fatty acids so effective in reducing chronic inflammation and insulin resistance.
The discovery could lead to development of a simple dietary remedy for many of the more than 23 million Americans suffering from diabetes and other conditions.
Writing in the advance online edition of the September 3 issue of the journal Cell, Jerrold Olefsky, MD, and colleagues identified a key receptor on macrophages abundantly found in obese body fat. Obesity and diabetes are closely correlated. The scientists say omega-3 fatty acids activate this macrophage receptor, resulting in broad anti-inflammatory effects and improved systemic insulin sensitivity.
Macrophages are specialized white blood cells that engulf and digest cellular debris and pathogens. Part of this immune system response involves the macrophages secreting cytokines and other proteins that cause inflammation, a method for destroying cells and objects perceived to be harmful. Obese fat tissue contains lots of these macrophages producing lots of cytokines. The result can be chronic inflammation and rising insulin resistance in neighboring cells over-exposed to cytokines. Insulin resistance is the physical condition in which the natural hormone insulin becomes less effective at regulating blood sugar levels in the body, leading to myriad and often severe health problems, most notably type 2 diabetes mellitus.
Olefsky and colleagues looked at cellular receptors known to respond to fatty acids. They eventually narrowed their focus to a G-protein receptor called GPR120, one of a family of signaling molecules involved in numerous cellular functions. The GPR120 receptor is found only on pro-inflammatory macrophages in mature fat cells. When the receptor is turned off, the macrophage produces inflammatory effects. But exposed to omega-3 fatty acids, specifically docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), the GPR120 receptor is activated and generates a strong anti-inflammatory effect.
“It’s just an incredibly potent effect,” said Olefsky, a professor of medicine and associate dean of scientific affairs for the UC San Diego School of Medicine. “The omega-3 fatty acids switch on the receptor, killing the inflammatory response.”
The scientists conducted their research using cell cultures and mice, some of the latter genetically modified to lack the GPR120 receptor. All of the mice were fed a high-fat diet with or without omega-3 fatty acid supplementation. The supplementation treatment inhibited inflammation and enhanced insulin sensitivity in ordinary obese mice, but had no effect in GPR120 knockout mice. A chemical agonist of omega-3 fatty acids produced similar results.
“This is nature at work,” said Olefsky. “The receptor evolved to respond to a natural product — omega-3 fatty acids — so that the inflammatory process can be controlled. Our work shows how fish oils safely do this, and suggests a possible way to treating the serious problems of inflammation in obesity and in conditions like diabetes, cancer and cardiovascular disease through simple dietary supplementation.”
However, Olefsky said more research is required. For example, it remains unclear how much fish oil constitutes a safe, effective dose. High consumption of fish oil has been linked to increased risk of bleeding and stroke in some people.
Should fish oils prove impractical as a therapeutic agent, Olefsky said the identification of the GPR120 receptor means researchers can work toward developing an alternative drug that mimics the actions of DHA and EPA and provides the same anti-inflammatory effects.
Co-authors of the paper are Da Young Oh, Saswata Talukdar, Eun Ju Bae, Hidetaka Morinaga, WuQuiang Fan, Pingping Li and Wendell J. Lu, all in the Department of Medicine, Division of Endocrinology and Metabolism at the University of California, San Diego; Takeshi Imamura, Division of Pharmacology, Shiga University of Medical Science; and Steven M. Watkins, Lipomics Technologies, Inc.
ScienceDaily (Sep. 2, 2010)
