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Persons with higher levels of leptin, a protein hormone produced by fat cells and involved in the regulation of appetite, may have an associated reduced incidence of Alzheimer disease and dementia, according to a study in the December 16 issue of JAMA.
Previous studies have shown that overweight and obesity in mid-life are associated with poorer cognitive function in the general population and an increased risk of dementia. There has been evidence that leptin exerts additional functions on the brain outside the hypothalamus (a region of the brain that controls body temperature, hunger, and thirst), according to background information in the article.
The researchers found that higher leptin levels were associated with a lower incidence of dementia and AD. The incidence of dementia decreased gradually across increasing levels of leptin: a person with a baseline leptin level in the lowest quartile group had a 25 percent risk of developing AD after 12 years of follow-up, whereas the corresponding risk for a person in the top quartile group was only 6 percent.
“These findings are consistent with recent experimental data indicating that leptin improves memory function in animals through direct effects on the hippocampus and strengthens the evidence that leptin is a hormone with a broad set of actions in the central nervous system. Due to the exploratory character of the present analyses, we did not adjust for multiple comparisons and acknowledge that our findings require confirmation in independent samples,” the authors write.
“If our findings are confirmed by others, leptin levels in older adults may serve as one of several possible biomarkers for healthy brain aging and, more importantly, may open new pathways for possible preventive and therapeutic intervention. Further exploration of the molecular and cellular basis for the observed association may expand our understanding of the pathophysiology underlying brain aging and the development of AD.”
(JAMA 2009;302[23]:2565-2572. )
Understanding exactly how the brain encodes and stores memories is one of the central, unsolved mysteries in neuroscience. Currently the most widely accepted theory is long-term potentiation (LTP)—the lasting communication established between two neurons when they are stimulated simultaneously.
As a person processes an event, two neurons pass information through a small space called a synapse. This chemical conversation triggers an intricate cascade, inviting nearby neurons to fire and ultimately creating a network of connections with varying strengths. Afterward, this pattern of connections, or memory, remains within the network of neurons that processed the event.
Although many areas of the brain contain synapses capable of creating strong patterns of connectivity, the hippocampus is a particularly favorable spot for recording memories. This brain region plays a critical role in learning new information, forming spatial memories and storing short-term memories as long-term ones.
Memories formed with the hippocampus are especially rich because they integrate input from several areas of the brain, and the hippocampus contains densely packed layers of neurons. In addition, damage to this region and nearby areas causes profound and permanent amnesia—an inability to store new memories or to recall old ones—and is observed in patients who have Alzheimer’s disease.
The discovery of stem cells in the adult brain has generated a great deal of excitement in the neurosciences. Thousands of new cells are produced each day in a healthy hippocampus, a key brain area for learning and memory. However, soon after the cells are born, many of them die unless they are exposed to a learning experience. Thus, new neurons in the adult are rescued from death by learning. With this award, a number of important questions about the relationship between learning and neurogenesis will be answered: What do new neurons do once they are rescued from death? Are they used for memory or for acquiring new information? Are new cells retained with each new learning experience and if so, do they then contribute to learning in the future? Also, do the absolute numbers that are born relate to the numbers kept alive by learning? And finally, what physiological mechanisms and brain rhythms keep them alive? To answer these questions, behavioral, electrophysiological, molecular and biochemical techniques will be used. These studies are important because they will identify the critical features of learning that keep new neurons alive and in turn how those new neurons then contribute to optimal learning in the future. The discovery of neurogenesis has transformed the way we think about the adult brain and generated much interest in the public, especially educators of children and young adults. These findings will be disseminated to the public with writings in lay magazines (i.e. Shors, Scientific American, 2009) and public presentations (i.e. Quark Park, a public art installation about science). The project will train postdoctoral, graduate and undergraduate students in this new field of research which intersects biology, psychology, physiology, as well as biomedical and stem cell engineering.
Every day, new brain cells (neurons) are born in the brains of adult mammals, a process called neurogenesis (neuro = neurons, genesis = birth). These newborn cells appear particularly in the hippocampus – a brain area that is important for new memory formation. Over the next few weeks, many of these newborn cells die off again. But studies show that, if a rat has been exercising or has been exposed to new learning, more of the newborn cells survive. The rate of survival of these new cells also depends on sleep.
As we sleep, we (like rats) cycle through several “stages,” including rapid-eye movement (REM) sleep, which is believed to be when we dream, and several kinds of non-REM sleep.
A recent study has suggested that REM is particularly important for neurogenesis in the hippocampus. One group of rats were given four days of REM deprivation, by putting the rats in a small chamber where the floor was a treadmill that automatically activated whenever the rats entered REM sleep – forcing them to step forward to avoid being carried into the wall of the chamber. (Non-REM sleep didn’t activate the treadmill.) For comparison, a group of control rats were placed in the same type of chamber, but treadmill activation was unrelated to sleep cycle.
The REM-deprived rats showed much less neurogenesis than controls. Both groups showed similar amounts of total sleep, and similar levels of stress hormones, indicating that the stress of being periodically awoken was similar for the REM-deprived and control rats. This study therefore suggests that REM sleep is particularly important for the birth and survival of new neurons in the adult brain.
There are two important implications of this study. The first is that it adds to a growing literature suggesting that relatively short-term periods of sleep deprivation (equivalent to a few nights’ insomnia or intentional wakefulness) can significantly affect the brain. This is a cautionary finding for those of us who routinely don’t get a full night’s sleep.
The second implication is that not all sleep is equal. This study also adds to a growing literature suggesting that REM sleep has some special functions, particularly contributing to learning and memory. Many medications, including some over-the-counter sleeping aids, disrupt REM sleep. If REM sleep is indeed important for neurogenesis, then disrupting REM may disrupt neurogenesis – which might in turn have consequences for a person’s learning and memory abilities.
Further Reading:
R. Guzman-Marin et al. (2008). Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat. Sleep, 31(2):167-175.
Help your brain cells to survive with novel learnings from Myfitbrain
Our brains are continually in the process of growing, shrinking, and killing neurons. By the way, that three-pound mass of tissue and fluid in our skulls consists of some 100 billion of them. And they’re party to an estimated 40 quadrillion, that’s 15 zeros, potential synaptic connections. Wow!
The activity of the brain is a miraculous never-ending balancing act, and problems arise when the scale is tipped toward neural shrinkage or death. The result can be anxiety and mood issues, as well as other mind variances. For example, brain imaging has revealed key-area brain shrinkage of as much as 10%-15% in chronic depression sufferers.
The term used for neural shrinkage is atrophy, and the chemicals that cause atrophy are known as atrophics. So, for example, the chemicals generated and released as a result of stress, most notably cortisol, are atrophics. Chemicals that foster neural growth, such as the antidepressants so often used in the treatment of panic and depression, are known as trophics. In short, then, neural growth, shrinkage, and death are to a large degree caused by the action of atrophic and trophic agents.
Neurogenesis is the process by which neurons are created. And though it makes perfect sense that it’s most active during prenatal development, the process continues on a much smaller scale into adulthood, even our senior years.
It’s so important to understand the dynamics of neurogenesis actually have the ability to reverse, if you will, all sorts of mental and emotional distress. That’s correct, in the face of targeted and appropriate intervention our brains can grow fresh neurons that serve to facilitate, enhance, and support newly learned coping skills, allowing us to feel one heck of a lot better. But, think about it, if one’s mental or emotional state improves, didn’t something brain-biological have to have happened?
For instance, the dentate gyrus of the hippocampus is an area of the brain in which neurogenesis is particularly active. See, the hippocampus, a component of the limbic system, is all about memory, learning, and emotion; all of which play major roles in anxiety and mood. Indeed, it’s been suggested that decreased hippocampal neurogenesis may be linked to increases in depression, which can be reversed by, say, the use of antidepressants – trophics.
So how ‘bout a short list of neurogenesis friendly factors. First of all, we have to include any medication with anti-panic, antidepressant, mood-stabilizing, and atypical antipsychotic characteristics. Incidentally, I’m not recommending these meds, just stating biochemical fact. And neurogenesis is also encouraged by mentally, emotionally, and physically healthy environments and lifestyle habits. Included are exercise, learning and memory work, spirituality, and psychotherapy. By the way, research has shown that one of the reasons all of these factors support neural growth and survival is because they increase levels of brain-derived neurotrophic factor (BDNF). Note the word, “neuroTROPHIC.”
On the other side of the fence, neurogenesis has its enemies. First in line is any sort of over-the-top or chronic stress. And that’s because it results in the secretion of the glucocorticoids, a family of steroids produced in the adrenal glands necessary for the regulation of energy metabolism and immune and inflammatory responses. The “stress hormone,” cortisol, is responsible for the vast majority of glucocorticoid activity. And though we need cortisol to increase our blood sugar and blood pressure levels in response to stress, too much of it for a long period of time can be a major problem.
One other neurogenesis adversary worth mentioning is excesses of glutamate, the brain’s most abundant excitatory, action-generating, neurotransmitter. It’s especially a factor during trauma and hypoglycemic events.
Absolutely, neurogenesis is a marvelous biochemical phenomenon that can really work to our advantage. And choice directs the outcome.
Animal studies conducted at the National Institute on Aging Gerontology Research Center and the Johns Hopkins UniversitySchool of Medicine, for example, have shown that both calorie restriction and intermittent fasting along with vitamin and mineral intake, increase resistance to disease, extend lifespan, and stimulate production of neurons from stem cells.
In addition,
fasting has been shown to enhance synaptic elasticity, possibly increasing the ability for successful re-wiring following brain injury. These benefits appear to result from a cellular stress response, similar in concept to the greater muscular regeneration that results from the stress of regular exercise.
Additional research suggests that increasing time intervals between meals might be a better choice than chronic calorie restriction, because the resultant decline in sex hormones may adversely affect both sexual and brain performance. Sex steroid hormones testosterone and estrogen are positively impacted by an abundant food supply. In other words, you might get smarter that way, but it might adversely affect your fun in the bedroom, among other drawbacks.
But if your not keen on starving yourself, there are other options. Another recent finding, stemming from the Burnham Institute for Medical Research and Iwate University in Japan, reports that the herb rosemary contains an ingredient that fights off free radical damage in the brain. The active ingredient, known as carnosic acid (CA), can protect the brain from stroke and neurodegeneration such as Alzheimer’s and from the effects of normal aging.
Although researchers are patenting more potent forms of isolated compounds in this herb, unlike most new drugs, simply using the rosemary in its natural state may be the most safe and clinically tolerated because it is known to get into the brain and has been consumed by people for over a thousand years. The herb was used in European folk medicine to help the nervous system.
Another brain booster that Bruce N. Ames, Ph.D., a professor of biochemistry and molecular biology at the University of California, Berkeley, swears by his daily 800 mg of alpha-lipoic acid and 2,000 mg of acetyl-L-carnitine, chemicals which boost the energy output of mitochondria that power our cells. Mitochondrial decay is a major factor in aging and diseases such as Alzheimer’s and diabetes. Elderly rats on these supplements had more energy and ran mazes better.
Omega-3s fatty acids DHA and EPA found in walnuts and fatty fish (such as salmon, sardines, and lake trout) are thought to help ward off Alzheimer’s disease. (In addition, they likely help prevent depression and have been shown to help prevent sudden death from heart attack).
Turmeric, typically found in curry, contains curcumin, a chemical with potent antioxidant and anti-inflammatory properties. In India, it is even used as a salve to help heal wounds. East Asians also eat it, which might explain their lower rates (compared to the United States) of Parkinson’s disease and Alzheimer’s disease, in addition to various cancers. If curry isn’t part of your favorite cuisines, you might try a daily curcumin supplement of 500 to 1,000 mg.
Physical exercise may also have beneficial effects on neuron regeneration by stimulating regeneration of brain and muscle cells via activation of stress proteins and the production of growth factors. But again, additional research suggests that not all exercise is equal. Interestingly, some researchers found that exercise considered drudgery was not beneficial in neuronal regeneration, but physical activity that was engaged in purely for fun, even if equal time was spent and equal calories were burned, resulted in neuronal regeneration.
Exercise can also help reduce stress, but any stress-reducing activity, such as meditation and lifestyle changes, can help the brain. There is some evidence that chronic stress shrinks the parts of the brain involved in learning, memory, and mood. (It also delays wound healing, promotes atherosclerosis, and increases blood pressure.)
It should go without saying that short-term cognitive and physical performance is not boosted by
fasting, due to metabolic changes including decrease in body temperature, decreased heart rate and blood pressure and decreased glucose and insulin levels, so you’re better off not planning a marathon or a demanding work session during a
fasting period.
As part of a healthy lifestyle the prescription of moderating food intake, exercising, and eating anti-oxidant rich foods is what we’ve long known will boost longevity, but it’s good to know that we can bring our brains along with us as we make it into those golden years without being the 1 in 7 who suffers from dementia. Keep your fingers crossed and eat some rosemary chicken.
Professor Elizabeth Gould received the prestigious Benjamin Franklin from the RSA organization for her groundbreaking work on neurogenesis. Her research into the effect of environments on the neuronal composition of the brain has profound and far-reaching societal implications.
Good video on how neurogenesis works in the hippocampus and why working out your brain helps it to improve for the long run. Also how anxiety can inhibit neurogenesis which inhibits your ability to learn.
