Are you often tired after the big Thanksgiving meal? Do you blame the turkey? Well I am here to help vindicate the poor bird. There is a relationship between food and the human mind. To the body, food is chemistry - causing biochemical reactions that release enzymes, trigger hormones and stimulate neurotransmitter activity.
Every November, a common discussion arises involving the relationship of turkey and drowsiness. Here is the scientific explanation. Turkey happens to be high in an amino acid (a building block of protein) called tryptophan, which acts as a precursor to the neurotransmitter serotonin. As tryptophan crosses the blood-brain barrier, it is converted to serotonin with the assistance of the vitamins B6, B12 and folate. And, as serotonin levels increase, your food cravings are curbed, your mood improves and the feeling of sleepiness sets in.
Can the food you eat cause drowsiness? Of course! BUT do not blame the poor bird. Even though turkey does supply your body with tryptophan, your sleepiness is more likely the result of feasting on ample servings of stuffing, gravy, bread, rich side dishes and of course dessert! Next year resolve to eat less and leave the table for a little turkey trot. You will be glad that you did.
Thursday, November 30, 2006
Friday, November 17, 2006
Cell protein may explain diet link to longevity
In a finding that may explain why lower-calorie diets help people live longer, researchers report that a protein present in every organism from yeast to humans may be the genetic link between calorie intake and aging.
"For the past ten years, we've sought genes that confer longevity," Leonard Guarente, a professor of biology at Massachusetts Institute of Technology in Cambridge, told Reuters Health.
A gene that codes for the protein Sir2 appears to be one of them. In experiments with yeast, researchers have previously found that removing Sir2 from cells shortens their life spans, but adding an extra copy of the gene produces "superlong" cell lives, Guarente said.
Now he and his MIT colleagues have found in studies with yeast and mice that Sir2's activity seems to depend upon metabolism. They report their findings in the current issue of the journal Nature.
Sir2, explained Guarente, performs the necessary function of "silencing" genes, that is, it selectively turns off gene expression. All body cells contain the same DNA, yet these cells serve diverse purposes. A cell's identity -- for example, whether it's a blood cell or a skin cell -- depends on gene expression, Guarente noted. Some genes, he said, "need to be silenced, and some need to be active."
To their surprise, though, Guarente and his colleagues discovered that to do its job, Sir2 depends on a molecule known as nicotinamide adenine dinucleotide, or NAD. Present in all cells, NAD assists in breaking down food and aids metabolism.
This first coupling of metabolism and Sir2 is "incredibly exciting," Guarente said, because it could open up new avenues for slowing down the aging process.
"One of the few universals we know about aging is that calorie restriction can extend life," he noted.
This research offers an explanation: Cutting calories slows metabolism, which, Guarente said, may free up more NAD. In turn, the greater availability of NAD would keep Sir2 working properly. Moreover, keeping Sir2 in good shape should help keep the balance of silent and active genes in check, promoting the health of all body cells.
If further animal studies support this, the findings could do more than bolster the virtues of a lower-calorie diet, according to Guarente. Sir2 could become a drug target for preventing some of the degenerative diseases that come with aging, he said. A drug that, for example, binds with Sir2 and keeps it active may help protect bone and muscle mass from wearing down.
If such a drug is realized, however, it won't tack years onto anyone's life. Guarente said a Sir2-targeting drug would make little difference in longevity, but instead could help people "maintain their vitality longer."
"For the past ten years, we've sought genes that confer longevity," Leonard Guarente, a professor of biology at Massachusetts Institute of Technology in Cambridge, told Reuters Health.
A gene that codes for the protein Sir2 appears to be one of them. In experiments with yeast, researchers have previously found that removing Sir2 from cells shortens their life spans, but adding an extra copy of the gene produces "superlong" cell lives, Guarente said.
Now he and his MIT colleagues have found in studies with yeast and mice that Sir2's activity seems to depend upon metabolism. They report their findings in the current issue of the journal Nature.
Sir2, explained Guarente, performs the necessary function of "silencing" genes, that is, it selectively turns off gene expression. All body cells contain the same DNA, yet these cells serve diverse purposes. A cell's identity -- for example, whether it's a blood cell or a skin cell -- depends on gene expression, Guarente noted. Some genes, he said, "need to be silenced, and some need to be active."
To their surprise, though, Guarente and his colleagues discovered that to do its job, Sir2 depends on a molecule known as nicotinamide adenine dinucleotide, or NAD. Present in all cells, NAD assists in breaking down food and aids metabolism.
This first coupling of metabolism and Sir2 is "incredibly exciting," Guarente said, because it could open up new avenues for slowing down the aging process.
"One of the few universals we know about aging is that calorie restriction can extend life," he noted.
This research offers an explanation: Cutting calories slows metabolism, which, Guarente said, may free up more NAD. In turn, the greater availability of NAD would keep Sir2 working properly. Moreover, keeping Sir2 in good shape should help keep the balance of silent and active genes in check, promoting the health of all body cells.
If further animal studies support this, the findings could do more than bolster the virtues of a lower-calorie diet, according to Guarente. Sir2 could become a drug target for preventing some of the degenerative diseases that come with aging, he said. A drug that, for example, binds with Sir2 and keeps it active may help protect bone and muscle mass from wearing down.
If such a drug is realized, however, it won't tack years onto anyone's life. Guarente said a Sir2-targeting drug would make little difference in longevity, but instead could help people "maintain their vitality longer."
Football Players and Concussions: Too Much Too Soon?
Football players who sustain concussions have almost three times the risk of sustaining a second concussion during the same season compared with uninjured players, say investigators from the University of North Carolina at Chapel Hill.
Dr. Kevin M. Guskiewicz and his colleagues attribute this increased risk to the failure of clinicians to follow recommended return-to-play guidelines.
The researchers collected data from 242 high school and collegiate athletic trainers. Of 17,549 players, 5.1% sustained at least one concussion, and 14.7% of these sustained a second concussion during the same season. The second injury tended to be more severe.
The investigators report that 86% of concussed players reported headache, 67% reported dizziness, and 59% reported confusion. Headache persisted beyond 5 days in 10% of the injured players.
Although most grading scales are based on loss of consciousness and amnesia, in this study only 8.9% of those injured lost consciousness and 27.7% exhibited amnesia.
"Clinicians are usually forced to make decisions based on grading scales and return-to-play guidelines that are not inclusive of the most common signs and symptoms," Guskiewicz's group writes in the September-October issue of the American Journal of Sports Medicine.
Nearly a third of injured players returned to participation on the same day of injury, including 14.4% of those who sustained a grade II concussion. For the remainder of the injured players, return to play averaged nearly 3 days earlier than most of the recommended guidelines, the investigators note.
Guskiewicz and his associates conclude that "few clinicians are currently using assessment techniques...useful in identifying lingering signs and symptoms such as concentration deficits, blurred vision, (sensitivity to light), amnesia, dizziness and balance deficits."
Dr. Kevin M. Guskiewicz and his colleagues attribute this increased risk to the failure of clinicians to follow recommended return-to-play guidelines.
The researchers collected data from 242 high school and collegiate athletic trainers. Of 17,549 players, 5.1% sustained at least one concussion, and 14.7% of these sustained a second concussion during the same season. The second injury tended to be more severe.
The investigators report that 86% of concussed players reported headache, 67% reported dizziness, and 59% reported confusion. Headache persisted beyond 5 days in 10% of the injured players.
Although most grading scales are based on loss of consciousness and amnesia, in this study only 8.9% of those injured lost consciousness and 27.7% exhibited amnesia.
"Clinicians are usually forced to make decisions based on grading scales and return-to-play guidelines that are not inclusive of the most common signs and symptoms," Guskiewicz's group writes in the September-October issue of the American Journal of Sports Medicine.
Nearly a third of injured players returned to participation on the same day of injury, including 14.4% of those who sustained a grade II concussion. For the remainder of the injured players, return to play averaged nearly 3 days earlier than most of the recommended guidelines, the investigators note.
Guskiewicz and his associates conclude that "few clinicians are currently using assessment techniques...useful in identifying lingering signs and symptoms such as concentration deficits, blurred vision, (sensitivity to light), amnesia, dizziness and balance deficits."
Mind/Body Connection
Traditional systems of medicine such as Chinese medicine and Ayurveda have long claimed that the basis of good health lies in balance. In Chinese medicine it is the proper balance of the body’s vital energy (qi or chi), and in Ayurveda a balance among three physiological principles called doshas is required for optimum health. In the writings of the legendary ancient Greek physician, Hippocrates, we find a reference to the humors, four properties, which again, must be in balance for the patient to be in the best of health. In all of these systems, the balance between mind and body is a key factor, with a belief that state of mind can influence the state of the body, and vice versa.
Western science and medicine, heavily influenced by Cartesian philosophy, which makes a sharp distinction between mind and body, observer and observed, subject and object, has focused mainly on external causes and treatments for disease. Descartes’ most famous statement, “I think, therefore I am,” announces the basis of his philosophy and science, in which he views the outside world (the human body included) as a clockwork mechanism that can be objectively broken down into its component parts. The mind, in this view, is autonomous, neither altering the universe by observation, nor being altered by its interaction with its environment. Western science has largely adhered to this outlook, and has made tremendous progress in understanding the universe in which we live. In the last few decades, limitations have been recognized in sciences such as quantum physics, with the discovery that the role of the observer is not clearly distinct from the phenomenon being observed, and in medicine, where it is becoming clear that the mind and body cannot be so easily divided.
While many of the tenets of traditional medicine can be taken as philosophical or metaphorical, instead of scientific, there is evidence the balance between the mind and body that these ancient systems prescribe has a basis in modern Western medicine, in a balance between the brain and the immune system.
The body responds to stress by releasing hormones and other chemical agents that alter physiological processes in order to deal with the stressful situation. This biochemical/physiological process is known as the stress response. One key hormone in the stress response is cortico-releasing hormone (CRH). This hormone is released mainly by the hypothalamus in the brain, and, through a cascade of chemical events, leads to the release of cortisol by the adrenal glands. Cortisol causes elevation in heart rate, increased strength of heart contractions, and an array of other physiological events. Cortisol also seems to act as an important regulator of the immune system and as an anti-inflammatory agent. It plays a key role in keeping the immune system from over-reacting and damaging healthy tissues. Studies have also shown that white blood cells within the immune system produce molecules—called cytokines—that send signals to other parts of the immune system, and also to the brain. The brain then responds by inducing some of the behaviors associated with the stress response such as anxiety, and also the behaviors often associated with sickness such as lethargy and fatigue. Cortisol also has an inhibitory effect on the production of CRH, working in a feedback loop to shut off its own production.
Thus, through these chemical processes the brain and the immune system communicate and interact in order to regulate the body’s responses to stress, both external and internal. If this system is somehow altered or interrupted, miscommunications can occur and the body may respond improperly. For instance, continuous stress results in overproduction of cortisol, which in turn has a negative effect on the immune system, and may potentially lead to higher susceptibility to infection and disease.
Improper regulation of the stress response is associated with a number of conditions affecting the brain. For instance, people with classic depression have been shown to have high levels of cortisol in the blood. Depressed patients can often exhibit symptoms of the physiological stress response, such as anxiety and sleeplessness. Some studies have shown a correlation between the high level of cortisol and suppressed immune responses, but further study is needed to confirm these results. Also, patients who suffer from “atypical” depression often exhibit a reduced stress response and have impaired CRH production, which leads to fatigue and lethargy. Sufferers of seasonal affective disorder (SAD) also exhibit some of these symptoms. Chronic stress has also been shown to have other negative effects on brain function, such as impairment of learning and memory. Also, as mentioned above, stress, acting through the brain and immune system, has an effect on inflammatory responses in some diseases, such as arthritis. Stress can affect the level of inflammation, and thus the pain, associated with disease. The details of all the biochemical and physiological processes involved are far from worked out, but scientists are continuing research on the chemical pathways and interactions that take place between the brain and the immune system.
At the level of medical treatment, work is being done with several therapeutic techniques that integrate stress reduction and mind/body interaction. Traditional meditation techniques have been used to successfully reduce stress, high blood pressure, and chronic pain. It has helped Vietnam veterans deal with the effects of post-traumatic stress syndrome and may help reduce serum cholesterol levels and ease the struggle with substance abuse.
Guided imagery is a related technique in which the patient’s imagination is brought into play by using imagery and other imagined sensory experience to alter physiological processes. It has been used successfully to control pain and enhance immunity.
Biofeedback is a procedure that combines methods of relaxation and meditation with high-tech monitoring. A patient’s physiological functions are monitored, providing immediate feedback showing the effect of any relaxation techniques being practiced. Patients can learn to control heart rate, body temperature and brain wave activity, among other things. The use of monitoring devices lets the patients see the results of their thinking and mental efforts at controlling these physiological functions, and allows them to adjust their efforts accordingly to reach the maximum desired effect. With practice, a patient can learn to achieve the desired effect without the use of the monitoring devices. Biofeedback is used in the treatment of many disorders, including stress, high blood pressure, pain, epilepsy and sleep disorders.
Other therapies that aim to integrate body and mind and/or use the power of the mind to help treat illness include support groups, which have been shown to be highly successful in helping breast cancer patients confront their disease; yoga; art and dance therapy, which help patients express concerns and emotions and feelings related to their illness and to help improve self-image and self-understanding; music therapy; and hypnosis. This list is far from complete and many more new techniques and uses for the therapies listed here are being studied and developed.
There is still a long way to go and much left to learn, both at the biological level and at level of medical treatment, about the interactions of the mind and body. Many medical institutions have created centers to study and utilize alternative types of therapy, including therapies intended to bring the mind and body into balance and to use the power of the mind to aid in healing and recovery. The National Center for Complementary and Alternative Medicine (NCCAM), part of the National Institute of Health, conducts and supports research on a wide variety of alternative treatments. Many feel that the wisdom of traditional medicine is largely in its recognition of the importance of balance within the mind and body. Modern medicine is recognizing some of the benefits of mind/body interactions, and the balance of traditional and modern techniques may lead to treatments that neither system alone could achieve.
Sources
American Psychological Association. Rallying the troops inside our bodies.
Available at: http://helping.apa.org/mind_body/pnia.html
Association for Applied Psychophysiology and Biofeedback Website. Available at: http://www.AAPB.org
Damasio AR. Descartes’ Error. New York: Avon Books; 1994: 223-267.
Sternberg EM. Emotions and disease: From balance of humors to balance of molecules. Nature Medicine. 1997;3(3):264-267.
Sternberg EM, Gold PW. The mind-body interaction in disease. Scientific American (special issue: Mysteries of the Mind). 1997;7(1):8-15.
Western science and medicine, heavily influenced by Cartesian philosophy, which makes a sharp distinction between mind and body, observer and observed, subject and object, has focused mainly on external causes and treatments for disease. Descartes’ most famous statement, “I think, therefore I am,” announces the basis of his philosophy and science, in which he views the outside world (the human body included) as a clockwork mechanism that can be objectively broken down into its component parts. The mind, in this view, is autonomous, neither altering the universe by observation, nor being altered by its interaction with its environment. Western science has largely adhered to this outlook, and has made tremendous progress in understanding the universe in which we live. In the last few decades, limitations have been recognized in sciences such as quantum physics, with the discovery that the role of the observer is not clearly distinct from the phenomenon being observed, and in medicine, where it is becoming clear that the mind and body cannot be so easily divided.
While many of the tenets of traditional medicine can be taken as philosophical or metaphorical, instead of scientific, there is evidence the balance between the mind and body that these ancient systems prescribe has a basis in modern Western medicine, in a balance between the brain and the immune system.
The body responds to stress by releasing hormones and other chemical agents that alter physiological processes in order to deal with the stressful situation. This biochemical/physiological process is known as the stress response. One key hormone in the stress response is cortico-releasing hormone (CRH). This hormone is released mainly by the hypothalamus in the brain, and, through a cascade of chemical events, leads to the release of cortisol by the adrenal glands. Cortisol causes elevation in heart rate, increased strength of heart contractions, and an array of other physiological events. Cortisol also seems to act as an important regulator of the immune system and as an anti-inflammatory agent. It plays a key role in keeping the immune system from over-reacting and damaging healthy tissues. Studies have also shown that white blood cells within the immune system produce molecules—called cytokines—that send signals to other parts of the immune system, and also to the brain. The brain then responds by inducing some of the behaviors associated with the stress response such as anxiety, and also the behaviors often associated with sickness such as lethargy and fatigue. Cortisol also has an inhibitory effect on the production of CRH, working in a feedback loop to shut off its own production.
Thus, through these chemical processes the brain and the immune system communicate and interact in order to regulate the body’s responses to stress, both external and internal. If this system is somehow altered or interrupted, miscommunications can occur and the body may respond improperly. For instance, continuous stress results in overproduction of cortisol, which in turn has a negative effect on the immune system, and may potentially lead to higher susceptibility to infection and disease.
Improper regulation of the stress response is associated with a number of conditions affecting the brain. For instance, people with classic depression have been shown to have high levels of cortisol in the blood. Depressed patients can often exhibit symptoms of the physiological stress response, such as anxiety and sleeplessness. Some studies have shown a correlation between the high level of cortisol and suppressed immune responses, but further study is needed to confirm these results. Also, patients who suffer from “atypical” depression often exhibit a reduced stress response and have impaired CRH production, which leads to fatigue and lethargy. Sufferers of seasonal affective disorder (SAD) also exhibit some of these symptoms. Chronic stress has also been shown to have other negative effects on brain function, such as impairment of learning and memory. Also, as mentioned above, stress, acting through the brain and immune system, has an effect on inflammatory responses in some diseases, such as arthritis. Stress can affect the level of inflammation, and thus the pain, associated with disease. The details of all the biochemical and physiological processes involved are far from worked out, but scientists are continuing research on the chemical pathways and interactions that take place between the brain and the immune system.
At the level of medical treatment, work is being done with several therapeutic techniques that integrate stress reduction and mind/body interaction. Traditional meditation techniques have been used to successfully reduce stress, high blood pressure, and chronic pain. It has helped Vietnam veterans deal with the effects of post-traumatic stress syndrome and may help reduce serum cholesterol levels and ease the struggle with substance abuse.
Guided imagery is a related technique in which the patient’s imagination is brought into play by using imagery and other imagined sensory experience to alter physiological processes. It has been used successfully to control pain and enhance immunity.
Biofeedback is a procedure that combines methods of relaxation and meditation with high-tech monitoring. A patient’s physiological functions are monitored, providing immediate feedback showing the effect of any relaxation techniques being practiced. Patients can learn to control heart rate, body temperature and brain wave activity, among other things. The use of monitoring devices lets the patients see the results of their thinking and mental efforts at controlling these physiological functions, and allows them to adjust their efforts accordingly to reach the maximum desired effect. With practice, a patient can learn to achieve the desired effect without the use of the monitoring devices. Biofeedback is used in the treatment of many disorders, including stress, high blood pressure, pain, epilepsy and sleep disorders.
Other therapies that aim to integrate body and mind and/or use the power of the mind to help treat illness include support groups, which have been shown to be highly successful in helping breast cancer patients confront their disease; yoga; art and dance therapy, which help patients express concerns and emotions and feelings related to their illness and to help improve self-image and self-understanding; music therapy; and hypnosis. This list is far from complete and many more new techniques and uses for the therapies listed here are being studied and developed.
There is still a long way to go and much left to learn, both at the biological level and at level of medical treatment, about the interactions of the mind and body. Many medical institutions have created centers to study and utilize alternative types of therapy, including therapies intended to bring the mind and body into balance and to use the power of the mind to aid in healing and recovery. The National Center for Complementary and Alternative Medicine (NCCAM), part of the National Institute of Health, conducts and supports research on a wide variety of alternative treatments. Many feel that the wisdom of traditional medicine is largely in its recognition of the importance of balance within the mind and body. Modern medicine is recognizing some of the benefits of mind/body interactions, and the balance of traditional and modern techniques may lead to treatments that neither system alone could achieve.
Sources
American Psychological Association. Rallying the troops inside our bodies.
Available at: http://helping.apa.org/mind_body/pnia.html
Association for Applied Psychophysiology and Biofeedback Website. Available at: http://www.AAPB.org
Damasio AR. Descartes’ Error. New York: Avon Books; 1994: 223-267.
Sternberg EM. Emotions and disease: From balance of humors to balance of molecules. Nature Medicine. 1997;3(3):264-267.
Sternberg EM, Gold PW. The mind-body interaction in disease. Scientific American (special issue: Mysteries of the Mind). 1997;7(1):8-15.
Monday, November 13, 2006
Worried about lapses in your memory?
If you're worried about lapses in your memory, you're in good company: About 80% of people feel they have a problem remembering names, and about 60% say they forget phone numbers and misplace items such as keys often enough to consider it a problem.
It's true that memory slightly declines after age 30, but it usually doesn't become noticeably impaired until after age 75. Instead, memory problems seem to come to light in middle age because people tend to be more aware of their memory shortcomings when they need it the most -- at an age when they have more responsibilities and need to remember more.
On average, most people forget names or misplace items an average of once a week to once a month. They recheck something, such as checking to make sure they've turned off the stove or locked the door, about once a week.
If you're concerned about your memory, that's a good sign. If you had a real memory problem, you wouldn't remember that you couldn't remember. But here's how you can help ease your mind and get the most from your memory:
Try to stay calm. Being worried or anxious can temporarily impair your memory. Some people find their memories "freeze up" under stressful situations. The harder they try to remember, the worse their memory is. The trick is to relax and refocus your mind -- the memory usually returns.
Practice a healthy lifestyle. Eating a low-fat diet, exercising regularly and practicing other so-called "heart-smart" strategies helps to keep your arteries open and functioning optimally, so your brain will get a steady flow of blood to supply oxygen and nutrients. Regular exercise has been shown to improve some mental abilities by an average of 20 to 30%.
Monitor your senses. You can't remember something if you never learned it in the first place. If you're having trouble paying attention because of poor eyesight or poor hearing, see a doctor about getting glasses or a hearing aid.
Don't test yourself needlessly. You likely have enough to remember without testing yourself with trivial matters, and the act of remembering doesn't improve memory. Instead of trying to "cram," make lists, write yourself notes, keep a journal or diary of important facts and dates or tell a friend or spouse. Interestingly, the act of writing things down helps you remember, and having the list or a stack of Post-It notes will jog your memory.
Get into a routine. You'll have a better chance of remembering to do something if you do it the same way every day. Put your car keys in the same place; go through the same sequence of actions before you leave the house. After a while you'll be able to put yourself on automatic pilot for these simple tasks.
Rekindle your memories. When you need to remember something, try to make connections with already existing memories. It's easier for experts to learn a new fact in their field because they already have a framework of knowledge on which to hang the new piece of information. For names, try to connect the name to someone you know or a character in a movie or book. For example, if you meet a woman named Sandra, you might make a mental connection to your favorite actress, Sandra Bullock or Sandra Dee.
Barry Gordon, M.D., Ph.D., a Professor of Neurology and Cognitive Science at the School of Medicine and Director of the Memory Clinic at the Johns Hopkins Medical Institutions, is among the nation's foremost authorities on memory. He is author of Memory: Remembering and Forgetting in Everyday Life, available through amazon.com or barnesandnoble.com, or by calling 410-435-2865.
It's true that memory slightly declines after age 30, but it usually doesn't become noticeably impaired until after age 75. Instead, memory problems seem to come to light in middle age because people tend to be more aware of their memory shortcomings when they need it the most -- at an age when they have more responsibilities and need to remember more.
On average, most people forget names or misplace items an average of once a week to once a month. They recheck something, such as checking to make sure they've turned off the stove or locked the door, about once a week.
If you're concerned about your memory, that's a good sign. If you had a real memory problem, you wouldn't remember that you couldn't remember. But here's how you can help ease your mind and get the most from your memory:
Try to stay calm. Being worried or anxious can temporarily impair your memory. Some people find their memories "freeze up" under stressful situations. The harder they try to remember, the worse their memory is. The trick is to relax and refocus your mind -- the memory usually returns.
Practice a healthy lifestyle. Eating a low-fat diet, exercising regularly and practicing other so-called "heart-smart" strategies helps to keep your arteries open and functioning optimally, so your brain will get a steady flow of blood to supply oxygen and nutrients. Regular exercise has been shown to improve some mental abilities by an average of 20 to 30%.
Monitor your senses. You can't remember something if you never learned it in the first place. If you're having trouble paying attention because of poor eyesight or poor hearing, see a doctor about getting glasses or a hearing aid.
Don't test yourself needlessly. You likely have enough to remember without testing yourself with trivial matters, and the act of remembering doesn't improve memory. Instead of trying to "cram," make lists, write yourself notes, keep a journal or diary of important facts and dates or tell a friend or spouse. Interestingly, the act of writing things down helps you remember, and having the list or a stack of Post-It notes will jog your memory.
Get into a routine. You'll have a better chance of remembering to do something if you do it the same way every day. Put your car keys in the same place; go through the same sequence of actions before you leave the house. After a while you'll be able to put yourself on automatic pilot for these simple tasks.
Rekindle your memories. When you need to remember something, try to make connections with already existing memories. It's easier for experts to learn a new fact in their field because they already have a framework of knowledge on which to hang the new piece of information. For names, try to connect the name to someone you know or a character in a movie or book. For example, if you meet a woman named Sandra, you might make a mental connection to your favorite actress, Sandra Bullock or Sandra Dee.
Barry Gordon, M.D., Ph.D., a Professor of Neurology and Cognitive Science at the School of Medicine and Director of the Memory Clinic at the Johns Hopkins Medical Institutions, is among the nation's foremost authorities on memory. He is author of Memory: Remembering and Forgetting in Everyday Life, available through amazon.com or barnesandnoble.com, or by calling 410-435-2865.
The Pain Game
Are you in pain? It’s a standard question to ask someone who looks uncomfortable. Note the intriguing use of language. You don’t ask someone, are you in pneumonia, or in flu? However, when pain occurs it can take over and occupy your life – you are in pain – a captive, trapped by your body’s own alarm system.
"The relief of pain remains a major challenge in modern medicine," says University College London’s Professor of Neuropharmacology, Anthony Dickenson. However, pain has proved to be remarkably difficult to tackle.
Pain is a very personal experience, partly because there is no truly objective way of measuring it. However, in the last decade scientists have gained a more thorough understanding of the mechanisms that trigger pain and the neural pathways that transmit pain signals to the brain, raising hopes for more effective treatment strategies in the future.
The pain pathway
Exposure to heat or damage to tissues stimulates C-fibers, a set of fine nerve fibers that run from the skin and other tissues to the spinal cord. Within the spinal cord, they form connections with other fibers in a structure called the dorsal horn. These fibers then carry the pain signals on to the brain. This route, from tissue through the spinal cord to the brain is called the pain pathway, and there are numerous ways of potentially blocking or disrupting it.
Blocking pain in the periphery
One possibility is preventing the C-fibers from being stimulated. All nerves conduct messages by allowing minute pores to open and close in their membranes. These pores regulate the flow of sodium ions in and out of the nerve fiber, allowing signals to pass along. Local anesthetics block these sodium channels, and if their action is blocked, the nerve can no longer transmit signals, including pain. However, local anesthetics have drawbacks. If they escape into the blood circulation, the anesthetics can block sodium channels in other areas, including the heart and brain.
C-fibers are triggered by excessive heat. "The issue is, why don’t C-fibers respond until the temperature is up to 42 degrees centigrade – an extreme temperature – why don’t they respond before?" asks Dickenson. The answer, he explains, is that C-fibers contain a specialized form of sodium channel that only opens at temperatures that are likely to cause damage. Working at University College London, Dr John Wood has thoroughly analyzed this channel. It has been isolated and genetically engineered into bacteria so that large quantities can be produced and studied. The race is now on to find a chemical that can block its action while leaving all other sodium channels unaffected. "How many companies are chasing this idea is anyone’s guess, but you can guarantee that they are," says Dickenson with a smile.
An interesting note: These channels also respond to capsacin, the hot component of chili peppers, which explains why a curry feels ‘hot’ rather than feeling like you are chewing glass.
Another approach to preventing C-fiber stimulation is to block the production of prostaglandin, a chemical released from a tissue as part of its inflammatory response to damage. One of its actions is to stimulate C-fibers. A group of drugs called non-steroidal painkillers blocks the action of the prostaglandin-producing cyclooxygenase enzymes COX1 and COX2. However, a major problem with these compounds is that they are indiscriminate in their action, and block the enzymes in locations like the blood vessels and stomach wall, where prostaglandins play an important role in maintaining healthy tissue. In blocking chronic pain, you can end up causing stomach ulcers.
However, there is renewed hope that this approach may work. It now appears that while COX1 is present in almost all tissues, COX2 is present in particularly high concentrations in damaged tissues. There are now some drugs that are capable of specifically blocking COX2.
Dickenson points out that COX2 is also constantly present in the brain, although no one is quite sure what function it has there. Its presence, though, could explain why non-steroidal painkillers like paracetamol, which can block COX2, are pretty good at inhibiting pain in situations like fever, even though they do nothing to reduce inflammation.
Dickenson comments that a big issue with new generations of painkillers will be their high price relative to the cost of drugs like aspirin and paracetamol.
Dealing with pain that results directly from injured nerves is also a major clinical problem. Most of the drugs that are showing signs of tackling this neuropathic pain were originally designed as anticonvulsants, antidepressants, and antiepileptics. Among the newcomers to the field, gabapentin appears to present the most hope. Its mode of action is unclear, but it probably operates by blocking calcium channels in the neurons, and clinical trials show that it can be quite effective. The sodium channel blockers discussed above could also be of great importance in treating neuropathic pain.
Blocking pain in the spinal cord
Yet another approach to blocking pain is to allow the C-fibers to become stimulated, but block the transmission of their signal within the dorsal horn of the spinal cord. The major neurotransmitter involved in this process is glutamate, and there are many pharmaceutical companies focussing on the task of blocking the N-methyl-D-aspartate (NMDA) receptor that glutamate binds to. The problem is that these drugs currently have many adverse side effects, such as sedation, so at the moment they are given as a last resort. However, there appear to be many sub-types of the receptor, raising the hope that it might be possible to block the NMDA receptors that mediate pain without inducing side effects.
Within the spinal cord, a peptide known as substance P plays an important role in transmitting pain signals from one neuron to another. Speaking at the Society for Neuroscience held in Miami in October 1999, Dr Ronald Wiley of Vanderbilt University and Veteran Affairs Medical Center, Nashville, explained that when substance P becomes attached to its receptor on the surface of a neuron, the receptor-substance P conjugate is drawn inside the cell. This has given a number of researchers the idea of attaching a toxin to substance P and injecting it alongside the pain pathway. The theory is that the toxin will be drawn only into fibers associated with transmitting pain and will selectively kill them. Work in laboratory animals indicates that this approach has a potentially powerful effect. Dickenson, however, is skeptical about any approach aimed at destroying elements of the nervous system in order to reduce pain. "The idea seems great," he says, "but prior to this modern wave of intervention in pain, surgeons used to treat chronic pain by cutting nerve tracts in the spinal cord - the pain went away for a bit and then returned with a vengeance. I’m not sure that these toxins will fare any better."
Blocking pain in the brain
Drugs acting in the periphery are useful because they don’t need to get into the central nervous system and so don’t cause side effects associated with central nervous system function. However, as we have seen there are multiple peripheral mechanisms that trigger pain, and you can only block one at a time. Drugs like the opioid morphine, which acts within the brain, can block all pain. "Opioid-like drugs have been around for at least three millennia and are arguably the most valuable drugs in medicine," claims Dickenson.
The trouble with opioids is their side effects of addiction, euphoria, and a reduced ability to think clearly. Opioids bind to receptors in the membranes of neurons and prevent the neurons from firing. Morphine works on the mu-receptor, but delta-receptors, kappa-receptors, and, more recently, opioid receptor-like 1 receptors (ORL1) have been discovered. The hope is that a drug will be developed that can bind to the correct ratio of the different types of opioid receptors so that it kills pain without inducing the adverse side effects of morphine. "At the moment it looks as though concentrating on the delta-receptors could provide the best way forward," says Dickenson.
The neurotransmitter serotonin (also known as 5-HT) is involved in some cases of migraine, and drugs that block its ability to bind to nerves are capable of blocking migraine-associated pain. This role of serotonin also explains why some people suffer from migraines after consuming red wine or chocolate, as both of these contain high quantities of chemicals that the body can turn into serotonin. It also explains why migraines are one of the potential side effects of specific serotonin re-uptake inhibitors (such as Prozac) used as antidepressants, as they allow the concentration of serotonin in the brain to increase.
Finally, cannabis may prove useful in the fight against pain. This compound stimulates two different receptors named cannabis 1 and cannabis 2, although it appears that cannabis 1 is the predominant receptor in the brain. Dickenson is keen to see the results of a number of Canadian trials that are testing to see if the drug operates predominantly through its mood altering properties or whether it really is a potent analgesic.
Conclusion
Pain plays a useful role in that it alerts us to damage to our bodies. Problems arise when the siren sounds too loud and for too long. The next few years should see new drugs that promise a more intelligent and directed approach to releasing hundreds of thousands of people from the captivity of being in pain.
"The relief of pain remains a major challenge in modern medicine," says University College London’s Professor of Neuropharmacology, Anthony Dickenson. However, pain has proved to be remarkably difficult to tackle.
Pain is a very personal experience, partly because there is no truly objective way of measuring it. However, in the last decade scientists have gained a more thorough understanding of the mechanisms that trigger pain and the neural pathways that transmit pain signals to the brain, raising hopes for more effective treatment strategies in the future.
The pain pathway
Exposure to heat or damage to tissues stimulates C-fibers, a set of fine nerve fibers that run from the skin and other tissues to the spinal cord. Within the spinal cord, they form connections with other fibers in a structure called the dorsal horn. These fibers then carry the pain signals on to the brain. This route, from tissue through the spinal cord to the brain is called the pain pathway, and there are numerous ways of potentially blocking or disrupting it.
Blocking pain in the periphery
One possibility is preventing the C-fibers from being stimulated. All nerves conduct messages by allowing minute pores to open and close in their membranes. These pores regulate the flow of sodium ions in and out of the nerve fiber, allowing signals to pass along. Local anesthetics block these sodium channels, and if their action is blocked, the nerve can no longer transmit signals, including pain. However, local anesthetics have drawbacks. If they escape into the blood circulation, the anesthetics can block sodium channels in other areas, including the heart and brain.
C-fibers are triggered by excessive heat. "The issue is, why don’t C-fibers respond until the temperature is up to 42 degrees centigrade – an extreme temperature – why don’t they respond before?" asks Dickenson. The answer, he explains, is that C-fibers contain a specialized form of sodium channel that only opens at temperatures that are likely to cause damage. Working at University College London, Dr John Wood has thoroughly analyzed this channel. It has been isolated and genetically engineered into bacteria so that large quantities can be produced and studied. The race is now on to find a chemical that can block its action while leaving all other sodium channels unaffected. "How many companies are chasing this idea is anyone’s guess, but you can guarantee that they are," says Dickenson with a smile.
An interesting note: These channels also respond to capsacin, the hot component of chili peppers, which explains why a curry feels ‘hot’ rather than feeling like you are chewing glass.
Another approach to preventing C-fiber stimulation is to block the production of prostaglandin, a chemical released from a tissue as part of its inflammatory response to damage. One of its actions is to stimulate C-fibers. A group of drugs called non-steroidal painkillers blocks the action of the prostaglandin-producing cyclooxygenase enzymes COX1 and COX2. However, a major problem with these compounds is that they are indiscriminate in their action, and block the enzymes in locations like the blood vessels and stomach wall, where prostaglandins play an important role in maintaining healthy tissue. In blocking chronic pain, you can end up causing stomach ulcers.
However, there is renewed hope that this approach may work. It now appears that while COX1 is present in almost all tissues, COX2 is present in particularly high concentrations in damaged tissues. There are now some drugs that are capable of specifically blocking COX2.
Dickenson points out that COX2 is also constantly present in the brain, although no one is quite sure what function it has there. Its presence, though, could explain why non-steroidal painkillers like paracetamol, which can block COX2, are pretty good at inhibiting pain in situations like fever, even though they do nothing to reduce inflammation.
Dickenson comments that a big issue with new generations of painkillers will be their high price relative to the cost of drugs like aspirin and paracetamol.
Dealing with pain that results directly from injured nerves is also a major clinical problem. Most of the drugs that are showing signs of tackling this neuropathic pain were originally designed as anticonvulsants, antidepressants, and antiepileptics. Among the newcomers to the field, gabapentin appears to present the most hope. Its mode of action is unclear, but it probably operates by blocking calcium channels in the neurons, and clinical trials show that it can be quite effective. The sodium channel blockers discussed above could also be of great importance in treating neuropathic pain.
Blocking pain in the spinal cord
Yet another approach to blocking pain is to allow the C-fibers to become stimulated, but block the transmission of their signal within the dorsal horn of the spinal cord. The major neurotransmitter involved in this process is glutamate, and there are many pharmaceutical companies focussing on the task of blocking the N-methyl-D-aspartate (NMDA) receptor that glutamate binds to. The problem is that these drugs currently have many adverse side effects, such as sedation, so at the moment they are given as a last resort. However, there appear to be many sub-types of the receptor, raising the hope that it might be possible to block the NMDA receptors that mediate pain without inducing side effects.
Within the spinal cord, a peptide known as substance P plays an important role in transmitting pain signals from one neuron to another. Speaking at the Society for Neuroscience held in Miami in October 1999, Dr Ronald Wiley of Vanderbilt University and Veteran Affairs Medical Center, Nashville, explained that when substance P becomes attached to its receptor on the surface of a neuron, the receptor-substance P conjugate is drawn inside the cell. This has given a number of researchers the idea of attaching a toxin to substance P and injecting it alongside the pain pathway. The theory is that the toxin will be drawn only into fibers associated with transmitting pain and will selectively kill them. Work in laboratory animals indicates that this approach has a potentially powerful effect. Dickenson, however, is skeptical about any approach aimed at destroying elements of the nervous system in order to reduce pain. "The idea seems great," he says, "but prior to this modern wave of intervention in pain, surgeons used to treat chronic pain by cutting nerve tracts in the spinal cord - the pain went away for a bit and then returned with a vengeance. I’m not sure that these toxins will fare any better."
Blocking pain in the brain
Drugs acting in the periphery are useful because they don’t need to get into the central nervous system and so don’t cause side effects associated with central nervous system function. However, as we have seen there are multiple peripheral mechanisms that trigger pain, and you can only block one at a time. Drugs like the opioid morphine, which acts within the brain, can block all pain. "Opioid-like drugs have been around for at least three millennia and are arguably the most valuable drugs in medicine," claims Dickenson.
The trouble with opioids is their side effects of addiction, euphoria, and a reduced ability to think clearly. Opioids bind to receptors in the membranes of neurons and prevent the neurons from firing. Morphine works on the mu-receptor, but delta-receptors, kappa-receptors, and, more recently, opioid receptor-like 1 receptors (ORL1) have been discovered. The hope is that a drug will be developed that can bind to the correct ratio of the different types of opioid receptors so that it kills pain without inducing the adverse side effects of morphine. "At the moment it looks as though concentrating on the delta-receptors could provide the best way forward," says Dickenson.
The neurotransmitter serotonin (also known as 5-HT) is involved in some cases of migraine, and drugs that block its ability to bind to nerves are capable of blocking migraine-associated pain. This role of serotonin also explains why some people suffer from migraines after consuming red wine or chocolate, as both of these contain high quantities of chemicals that the body can turn into serotonin. It also explains why migraines are one of the potential side effects of specific serotonin re-uptake inhibitors (such as Prozac) used as antidepressants, as they allow the concentration of serotonin in the brain to increase.
Finally, cannabis may prove useful in the fight against pain. This compound stimulates two different receptors named cannabis 1 and cannabis 2, although it appears that cannabis 1 is the predominant receptor in the brain. Dickenson is keen to see the results of a number of Canadian trials that are testing to see if the drug operates predominantly through its mood altering properties or whether it really is a potent analgesic.
Conclusion
Pain plays a useful role in that it alerts us to damage to our bodies. Problems arise when the siren sounds too loud and for too long. The next few years should see new drugs that promise a more intelligent and directed approach to releasing hundreds of thousands of people from the captivity of being in pain.
New Neurons Grow in Adult Brains
The longstanding belief that the adult brains do not produce new neurons is being challenged by current research. Adults may indeed be able to generate new neurons, in a process called neurogenesis, throughout life and at the rate of thousands per day. These findings could radically alter the way scientists look at the brain and could eventually lead to new methods of treating brain disease and injury.
In the most recent study, published in the October 15, 1999 issue of Science, researchers showed that new neurons are continually being added to the cerebral cortex of adult monkeys. The cerebral cortex is the largest and most complex region of the brain and is the seat of high-level decision-making, thinking, and personality.
The discovery, made by Elizabeth Gould and Charles Gross of Princeton’s Department of Psychology, along with graduate student Alison Reeves and research staff member Michael Graziano, is likely to translate to humans. Monkeys and humans, as fellow primates, have fundamentally similar brains.
Gould and Gross point out that it’s not yet known what purpose the new cells serve in the cortex, but if the newly formed neurons are found to have a functional role, scientists may have to re-examine current theories about how the brain works. For instance, it’s been known for some time that the adult brain displays a certain degree of plasticity, that is an ability to change, but traditional thought is that the brain handles processes like learning and memory by altering the nature of the connections, called synapses, between neurons. If new cells are being generated on a regular basis, a whole new level of complexity is opened up.
“We know that the brain is plastic and can change as a result of experience,” says Allan Tobin, director of the Brain Research Institute at UCLA, “but what we don’t know is whether these changes are mediated by pre-synaptic changes, post-synaptic changes, or now, by the generation of new cells.”
If the results are confirmed in humans, they could have major implications for the treatment of neurodegenerative diseases like Parkinson’s, Huntington’s, or Alzheimer’s disease. In these diseases neurons either die or lose their normal function. When a critical number of cells have been lost, symptoms arise and continue to worsen as more and more neurons are effected. While practical applications are years away, physicians may one day find ways to influence the process of neurogenesis in order to generate more neurons in a particular region of the brain.
“With the idea that new cells themselves can be generated in the adult brain,” says Tobin, “maybe you can find signals that will differentiate a whole cohort of cells to replace those that have died.”
Finding New Neurons:
In order to test for the presence of new neurons in the adult brain, Gould and Gross injected rhesus monkeys with a chemical called BrdU. Cells that are dividing incorporate BrdU into their DNA and pass it on to the newly formed cells. At different time points after the injection, ranging from two hours to seven days, the researchers examined the cerebral cortex and found evidence of BrdU containing cells in three different regions. Because BrdU is only incorporated into the DNA of cells that are actively dividing, the cells with DNA containing the chemical had to have formed after the injection.
The researchers conducted additional experiments to determine that these newly formed cells had the characteristics of neurons. They were able to detect several different proteins in the cells that are found specifically in neurons. Also, they showed that the cells containing BrdU had the long extensions, called axons, characteristic of neurons. To do this Gould and Gross used a technique called fluorescent retrograde tracing. In this technique a chemical dye is applied to a small region of the brain, and the dye travels from the end of the axon back to the cell body, making the axon visible under a microscope.
According to Gould and Gross, the new cells appeared to originate in a region called the subventricular zone (svz) and then migrated outward in a stream through the cerebral cortex to specific locations, where they differentiated into mature neurons. The svz was previously identified by other researchers as a source of neuronal stem cells—cells capable of dividing and differentiating into a variety of specialized brain cells.
The new cells were found in three of the four regions that were examined—the prefrontal region, the inferior temporal region, and the posterior parietal region. These three brain areas are involved in the complex cognitive tasks of decision making and short-term memory, recognition of objects and faces, and the representation of objects in space, respectively. No new cells were found in the striate cortex, which is responsible for the initial, basic steps of visual processing.
The observation that new cells were found in regions important for cognitive functioning and not in an area involved in more rudimentary processing suggests that neurogenesis may play a role in higher brain functions. Gould and Gross speculate that the new neurons could play a role in learning and memory by “marking the temporal dimension of memory” and serving as “a substrate for learning.” In a sense, the new neurons may be timekeepers, somehow helping keep memories in the right order and marking them in time. They could also be serving as a blank slate, on which new memories could be written and new skills learned.
A Brief History:
“It’s a surprise,” says Tobin of UCLA, referring to the Gould and Gross experiments, “but it’s a surprise that’s been growing on us for the last couple of years.”
In fact, evidence that neurogenesis occurs in the adult brains of some animals, such as rats and birds, has been around for many years. In 1965, Joseph Altman and his colleagues showed that new neurons were regularly produced by adult rats in the hippocampus, a region of the brain important for the early phases of learning and memory.
In the 1980’s Fernando Nottebohm, of Rockefeller University, discovered that songbirds, such as the canary, produced new neurons during the time they were learning new songs. This was particularly interesting work as it suggested that the production of new neurons was connected with a particular behavior. Nottebohm’s continuing research has shown that birds add new neurons to their hippocampal complexes throughout their lives.
Studies of neurogenesis in primates during the 1980s turned up only negative results, and it was perhaps because of these results that the study of neurogenesis in higher mammals remained largely unexplored until now.
In any case, more recent evidence of neurogenesis has been found in the hippocampi of adult primates, including humans. In 1998, Fred Gage of the Salk Institute for Biological Studies in La Jolla, California, and Peter Eriksson at the Sahlgrenska University Hospital in Goteborg, Sweden, looked at hippocampal tissue from five patients that had died of cancer. These cancer patients had received an earlier injection of BrdU for diagnostic purposes (since BrdU labels dividing cells, it can also help in the detection of growing cancer cells). Gage and Eriksson found BrdU labeled neurons in the hippocampi of all five patients, who ranged in age from 57 to 72 years old.
Still, it was unclear whether neurogenesis occurs in the higher parts of the brain like the cerebral cortex. Evolutionarily speaking, the hippocampus is a very old structure, present in brains from reptilian to human. The newer structures, such as the cerebral cortex were still thought to lack the ability to grow new neurons.
That’s where the new experiments by Gould and Gross come in. By showing that neurogenesis occurs in the cerebral cortex of primates, they have shown that the brain is a much more dynamic organ than previously believed. The next steps will include proving that similar results can be found in humans and discovering the functional role of the newly generated neurons.
Sources:
Eriksson PS, Perfilieva E, Bjork-Eriksson T, Alborn AM, Nordborg C, Peterson DA, Gage FH. Neurogenesis in the adult human hippocampus. Nature Medicine. 1998;4(11):1313-1317.
Gould E, Reeves AJ, Graziano MSA, Gross CG. Neurogenesis in the neocortex of adult primates. Science. 1999;286:548-552.
Gould E, Tanapat P, Hastings NB, Shors TJ. Neurogenesis in adulthood: a possible role in learning. Trends Cog Sci. 1999;3(5):186-1992.
In the most recent study, published in the October 15, 1999 issue of Science, researchers showed that new neurons are continually being added to the cerebral cortex of adult monkeys. The cerebral cortex is the largest and most complex region of the brain and is the seat of high-level decision-making, thinking, and personality.
The discovery, made by Elizabeth Gould and Charles Gross of Princeton’s Department of Psychology, along with graduate student Alison Reeves and research staff member Michael Graziano, is likely to translate to humans. Monkeys and humans, as fellow primates, have fundamentally similar brains.
Gould and Gross point out that it’s not yet known what purpose the new cells serve in the cortex, but if the newly formed neurons are found to have a functional role, scientists may have to re-examine current theories about how the brain works. For instance, it’s been known for some time that the adult brain displays a certain degree of plasticity, that is an ability to change, but traditional thought is that the brain handles processes like learning and memory by altering the nature of the connections, called synapses, between neurons. If new cells are being generated on a regular basis, a whole new level of complexity is opened up.
“We know that the brain is plastic and can change as a result of experience,” says Allan Tobin, director of the Brain Research Institute at UCLA, “but what we don’t know is whether these changes are mediated by pre-synaptic changes, post-synaptic changes, or now, by the generation of new cells.”
If the results are confirmed in humans, they could have major implications for the treatment of neurodegenerative diseases like Parkinson’s, Huntington’s, or Alzheimer’s disease. In these diseases neurons either die or lose their normal function. When a critical number of cells have been lost, symptoms arise and continue to worsen as more and more neurons are effected. While practical applications are years away, physicians may one day find ways to influence the process of neurogenesis in order to generate more neurons in a particular region of the brain.
“With the idea that new cells themselves can be generated in the adult brain,” says Tobin, “maybe you can find signals that will differentiate a whole cohort of cells to replace those that have died.”
Finding New Neurons:
In order to test for the presence of new neurons in the adult brain, Gould and Gross injected rhesus monkeys with a chemical called BrdU. Cells that are dividing incorporate BrdU into their DNA and pass it on to the newly formed cells. At different time points after the injection, ranging from two hours to seven days, the researchers examined the cerebral cortex and found evidence of BrdU containing cells in three different regions. Because BrdU is only incorporated into the DNA of cells that are actively dividing, the cells with DNA containing the chemical had to have formed after the injection.
The researchers conducted additional experiments to determine that these newly formed cells had the characteristics of neurons. They were able to detect several different proteins in the cells that are found specifically in neurons. Also, they showed that the cells containing BrdU had the long extensions, called axons, characteristic of neurons. To do this Gould and Gross used a technique called fluorescent retrograde tracing. In this technique a chemical dye is applied to a small region of the brain, and the dye travels from the end of the axon back to the cell body, making the axon visible under a microscope.
According to Gould and Gross, the new cells appeared to originate in a region called the subventricular zone (svz) and then migrated outward in a stream through the cerebral cortex to specific locations, where they differentiated into mature neurons. The svz was previously identified by other researchers as a source of neuronal stem cells—cells capable of dividing and differentiating into a variety of specialized brain cells.
The new cells were found in three of the four regions that were examined—the prefrontal region, the inferior temporal region, and the posterior parietal region. These three brain areas are involved in the complex cognitive tasks of decision making and short-term memory, recognition of objects and faces, and the representation of objects in space, respectively. No new cells were found in the striate cortex, which is responsible for the initial, basic steps of visual processing.
The observation that new cells were found in regions important for cognitive functioning and not in an area involved in more rudimentary processing suggests that neurogenesis may play a role in higher brain functions. Gould and Gross speculate that the new neurons could play a role in learning and memory by “marking the temporal dimension of memory” and serving as “a substrate for learning.” In a sense, the new neurons may be timekeepers, somehow helping keep memories in the right order and marking them in time. They could also be serving as a blank slate, on which new memories could be written and new skills learned.
A Brief History:
“It’s a surprise,” says Tobin of UCLA, referring to the Gould and Gross experiments, “but it’s a surprise that’s been growing on us for the last couple of years.”
In fact, evidence that neurogenesis occurs in the adult brains of some animals, such as rats and birds, has been around for many years. In 1965, Joseph Altman and his colleagues showed that new neurons were regularly produced by adult rats in the hippocampus, a region of the brain important for the early phases of learning and memory.
In the 1980’s Fernando Nottebohm, of Rockefeller University, discovered that songbirds, such as the canary, produced new neurons during the time they were learning new songs. This was particularly interesting work as it suggested that the production of new neurons was connected with a particular behavior. Nottebohm’s continuing research has shown that birds add new neurons to their hippocampal complexes throughout their lives.
Studies of neurogenesis in primates during the 1980s turned up only negative results, and it was perhaps because of these results that the study of neurogenesis in higher mammals remained largely unexplored until now.
In any case, more recent evidence of neurogenesis has been found in the hippocampi of adult primates, including humans. In 1998, Fred Gage of the Salk Institute for Biological Studies in La Jolla, California, and Peter Eriksson at the Sahlgrenska University Hospital in Goteborg, Sweden, looked at hippocampal tissue from five patients that had died of cancer. These cancer patients had received an earlier injection of BrdU for diagnostic purposes (since BrdU labels dividing cells, it can also help in the detection of growing cancer cells). Gage and Eriksson found BrdU labeled neurons in the hippocampi of all five patients, who ranged in age from 57 to 72 years old.
Still, it was unclear whether neurogenesis occurs in the higher parts of the brain like the cerebral cortex. Evolutionarily speaking, the hippocampus is a very old structure, present in brains from reptilian to human. The newer structures, such as the cerebral cortex were still thought to lack the ability to grow new neurons.
That’s where the new experiments by Gould and Gross come in. By showing that neurogenesis occurs in the cerebral cortex of primates, they have shown that the brain is a much more dynamic organ than previously believed. The next steps will include proving that similar results can be found in humans and discovering the functional role of the newly generated neurons.
Sources:
Eriksson PS, Perfilieva E, Bjork-Eriksson T, Alborn AM, Nordborg C, Peterson DA, Gage FH. Neurogenesis in the adult human hippocampus. Nature Medicine. 1998;4(11):1313-1317.
Gould E, Reeves AJ, Graziano MSA, Gross CG. Neurogenesis in the neocortex of adult primates. Science. 1999;286:548-552.
Gould E, Tanapat P, Hastings NB, Shors TJ. Neurogenesis in adulthood: a possible role in learning. Trends Cog Sci. 1999;3(5):186-1992.
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