ScienceDaily (Nov. 24, 2008) — A study published in the online advance edition of The American Journal of Psychiatry for the first time reveals shape differences in the brains of children with ADHD, which could help pinpoint the specific neural circuits involved in the disorder. Researchers from the Kennedy Krieger Institute in Baltimore, Md. and the Johns Hopkins Center for Imaging Science used a new analysis tool, large deformation diffeomorphic mapping (LDDMM), which allowed them to examine the precise shape of the basal ganglia.
The study found boys with ADHD had significant shape differences and decreases in overall volume of the basal ganglia compared to their typically developing peers. Girls with ADHD did not have volume or shape differences, suggesting sex strongly influences the disorder's expression.
Previous studies examining the basal ganglia in children with ADHD were limited to volume analysis and had conflicting results, with some reporting a smaller volume and some reporting no difference in volume. LDDMM provides detailed analysis of the shape of specific brain regions, allowing for precise examination of brain structures well beyond what has been examined in previous MRI studies of ADHD. In this study, LDDMM was used to map the brains of typically developing children in order to generate a basal ganglia template. This is the first reported template of the basal ganglia. After creating LDDMM mappings of the basal ganglia of each child with ADHD, statistical analysis was conducted to compare them to the template.
In this study, the initial volume analysis revealed boys with ADHD had significantly smaller basal ganglia volumes compared with typically-developing boys. Moving beyond the standard volume analysis, the LDDMM revealed shape abnormalities in several regions of the basal ganglia. Comparison of the standard volume and LDDMM analysis of girls with ADHD and their typically developing peers failed to reveal any significant volume or shape differences.
The multiple shape differences found in boys with ADHD suggests that the disorder may not be associated with abnormalities in one specific neural circuit. Rather, it appears the disorder involves abnormalities in parallel circuits, including circuits important for the control of complex behavior and more basic motor responses, such as hitting the brake pedal when a traffic light turns yellow. Findings revealing abnormalities in circuits important for basic motor response control may be crucial to understanding why children with ADHD have difficulty suppressing impulsive actions.
"This study represents a major advancement in our ability to examine the neuroanatomic features of ADHD and other developmental disorders," said Dr. Stewart H. Mostofsky, senior study author and a pediatric neurologist in the Department of Developmental Cognitive Neurology at the Kennedy Krieger Institute. "Using LDDMM, we can more accurately measure the impact of ADHD on brain development, which will not only bring us closer to unlocking the biological basis of the disorder, but help us better diagnose and treat patients."
Researchers used MRI scans to examine children ages 8-13 years, including: 47 children with ADHD and a control group of 66 typically developing children. Researchers compared the LDDMM mappings of children with ADHD to their typically developing peers, and then went a step further by repeating the analysis separately for boys and girls. Children with ADHD who had a history of other neuropsychiatric diagnoses including conduct disorder, mood disorder, generalized anxiety disorder, separation anxiety disorder and/or obsessive-compulsive disorder were excluded from the study. Additionally, none of the children with ADHD had a learning disability or a history of speech/language disorders.
Potential next steps include research that carefully examines whether the brain abnormalities found in this study can predict certain behavioral features of ADHD. Future studies will also examine structural features associated with the ability to compensate and respond to therapy. The researchers also plan to use LDDMM analysis on children in a wider age range to see if changes in the basal ganglia occur over time.
The Center for Imaging Science at Johns Hopkins University, under the direction of Director Dr. Michael I. Miller, was a key collaborator in this study.
Tuesday, November 25, 2008
Tinnitus: Psychological Treatment and Neurostimulation Offer Hope
ScienceDaily (Nov. 24, 2008) — A remarkable number of patients with tinnitus demonstrate withdrawal behaviour and have a negative view of life. Feelings of anxiety and depression result in patients experiencing the complaint as a major burden on their quality of life. In addition to psychological treatment, neurostimulation now also appears to be a very promising therapy.
This is the result of research conducted by Hilke Bartels of the University Medical Center Groningen. She will be awarded a PhD by the University of Groningen on 26 November 2008.
Patients with tinnitus hear noises that do not originate outside but within the body itself. They can be squeaks, whistles or whooshing noises, or even rumbles, knocking or rustling sounds. It is estimated that 10-30 percent of the Dutch suffer from tinnitus. Four to five percent of these people feel seriously limited as a result; for example, they can’t concentrate properly anymore, or have trouble sleeping. The complaint usually starts when people are between the ages of 40 and 60 and their hearing is not what it used to be.
Overactive brains
For a long time it was assumed that the cause of tinnitus lay in the auditory organ itself. However, it is now clear that the brain is responsible: overactive parts of the brain in the auditory region emit continuous signals that are the cause of the ‘phantom noise’. This over-activity is usually the result of hearing loss. However, noise (buzzing in the ears after visiting a concert or discotheque), an infection or an operation on the ear, or a jaw or neck problem can also cause the symptoms.
With the help of the image-forming technologies PET and fMRI, Bartels mapped the over-activity of the relevant parts of the brain. She was thus able to confirm existing theories about the complaint.
Negative attitude
Bartels’s research has revealed that a remarkable number of tinnitus patients are depressed and have a negative attitude towards life. They do not dare to share these feelings with others, which means they experience little social support, which in turn leads to withdrawal behaviour. This is also described as the so-called ‘type D personality’. No fewer than 94 of the 265 tinnitus patients investigated had such a personality type. These patients experienced significantly more psychological discomfort, the research revealed. Anxiety and depression appear to strengthen the effect of tinnitus. People with a type D personality in particular should undergo treatment that concentrates on the reduction of anxiety and depression, according to Bartels.
Effective neurostimulation
A psychological approach is not the only light on the horizon, however. Between 2001 and 2003, the UMCG started an experimental treatment regime whereby the relevant brain areas were continuously stimulated with the help of a pulse generator, a sort of pacemaker. An evaluation revealed that four of the six patients treated in this way had significantly positive long-term results. The patients indicated that the ‘noise’ was reduced to manageable levels and awarded the treatment a mark of 7 out of 10. Neurostimulation with a magnet outside the skull also looks like an interesting treatment option. The tinnitus of 5 of the 24 patients who underwent this experimental treatment was temporarily suppressed.
Recommendations
Thus far no treatment has been shown to be effective for the majority of tinnitus patients. Current treatment options have either a medical, an audiological or a psychological basis. According to Bartels, a multidisciplinary approach is essential. She also calls for the use of validated questionnaires to chart the nature and the impact of tinnitus.
This is the result of research conducted by Hilke Bartels of the University Medical Center Groningen. She will be awarded a PhD by the University of Groningen on 26 November 2008.
Patients with tinnitus hear noises that do not originate outside but within the body itself. They can be squeaks, whistles or whooshing noises, or even rumbles, knocking or rustling sounds. It is estimated that 10-30 percent of the Dutch suffer from tinnitus. Four to five percent of these people feel seriously limited as a result; for example, they can’t concentrate properly anymore, or have trouble sleeping. The complaint usually starts when people are between the ages of 40 and 60 and their hearing is not what it used to be.
Overactive brains
For a long time it was assumed that the cause of tinnitus lay in the auditory organ itself. However, it is now clear that the brain is responsible: overactive parts of the brain in the auditory region emit continuous signals that are the cause of the ‘phantom noise’. This over-activity is usually the result of hearing loss. However, noise (buzzing in the ears after visiting a concert or discotheque), an infection or an operation on the ear, or a jaw or neck problem can also cause the symptoms.
With the help of the image-forming technologies PET and fMRI, Bartels mapped the over-activity of the relevant parts of the brain. She was thus able to confirm existing theories about the complaint.
Negative attitude
Bartels’s research has revealed that a remarkable number of tinnitus patients are depressed and have a negative attitude towards life. They do not dare to share these feelings with others, which means they experience little social support, which in turn leads to withdrawal behaviour. This is also described as the so-called ‘type D personality’. No fewer than 94 of the 265 tinnitus patients investigated had such a personality type. These patients experienced significantly more psychological discomfort, the research revealed. Anxiety and depression appear to strengthen the effect of tinnitus. People with a type D personality in particular should undergo treatment that concentrates on the reduction of anxiety and depression, according to Bartels.
Effective neurostimulation
A psychological approach is not the only light on the horizon, however. Between 2001 and 2003, the UMCG started an experimental treatment regime whereby the relevant brain areas were continuously stimulated with the help of a pulse generator, a sort of pacemaker. An evaluation revealed that four of the six patients treated in this way had significantly positive long-term results. The patients indicated that the ‘noise’ was reduced to manageable levels and awarded the treatment a mark of 7 out of 10. Neurostimulation with a magnet outside the skull also looks like an interesting treatment option. The tinnitus of 5 of the 24 patients who underwent this experimental treatment was temporarily suppressed.
Recommendations
Thus far no treatment has been shown to be effective for the majority of tinnitus patients. Current treatment options have either a medical, an audiological or a psychological basis. According to Bartels, a multidisciplinary approach is essential. She also calls for the use of validated questionnaires to chart the nature and the impact of tinnitus.
Tuesday, November 18, 2008
Unraveling Mystery of Brain Aneurysms
ScienceDaily (Nov. 15, 2008) — Yale researchers have taken the first critical steps in unraveling the mysteries of brain aneurysms, the often fatal rupturing of blood vessels that afflicts 500,000 people worldwide each year and nearly killed Vice President-elect Joseph Biden two decades ago.
An international team — led by Murat Gunel, professor of neurosurgery and neurobiology, and Richard Lifton, Sterling Professor and chair of genetics, and a Howard Hughes Medical Institute investigator — scanned the genomes of more than 2,000 individuals suffering from intracranial aneurysms along with 8,000 healthy subjects. They discovered three chromosome segments, or loci, where common genetic variations can create significant risk for ruptured aneurysms, which in turn cause strokes.
The subjects came from hospitals in Finland, the Netherlands and Japan, and the results were similar in all groups, indicating that these variations increase risk among diverse human populations.
The findings, reported online in the journal Nature Genetics, could lead to new screening tests to identify hundreds of thousands of people at risk for strokes caused by bleeding and point to new therapies that might be able to strengthen blood vessels in the brain before they burst.
"Even though we have made significant strides in treating unruptured aneurysms, until now we have not had an effective means of identifying the majority of individuals at risk of developing this deadly problem. These genetic findings provide a starting point for changing that equation," Gunel said.
The median age when hemorrhagic stroke occurs is 50 years old, and usually there are no warning signs. In the majority of cases, the resulting strokes cause death or severe brain damage. Without an understanding of the cause of these events, physicians have been left to respond after the fact, once the damage has largely been done. Biden was one of the lucky individuals who survived a ruptured aneurysm with minimal damage — although at the time he was stricken, his condition was thought to be grave enough that a priest was summoned to confer last rites.
The Yale study showed that the risk of harboring an aneurysm increased with the number of risk variants, or alleles. Individuals with the highest number of risk alleles tripled their risk of an aneurysm, researchers found.
Based on this large collaborative study, a screening test may one day be able to identify those who are at higher risk of forming brain aneurysms or suffering a bleeding stroke as a result.
"These findings provide fundamental insights into the genetic and biochemical changes that cause this devastating brain disease, providing hope that we may also be able to provide preventive therapy before rupture occurs," Lifton said.
For instance, the new findings implicate variations in the gene SOX17, which is known to play a crucial role in the early development and repair of endothelial cells that make up the arterial walls of blood vessels. "These variations may interfere with the ability to produce cells that repair damage to the blood vessels, suggesting a path forward for developing new approaches to prevention," Gunel said.
Kaya Bilguvar of Yale was first author of the paper. Other Yale researchers included Shrikant Mane, Christopher E. Mason, Murim Choi, Emilia Gaal, Yasa Bayri, Luis Kobl, Zulfikar Arlier, Sudhakar Ravuri, and Matthew W. State.
The work was funded by the National Institutes of Health, the Yale Center for Human Genetics and Genomics, the Yale Program on Neurogenetics and the Howard Hughes Medical Institute.
Citation: Nature Genetics, Nov. 9, 2008
An international team — led by Murat Gunel, professor of neurosurgery and neurobiology, and Richard Lifton, Sterling Professor and chair of genetics, and a Howard Hughes Medical Institute investigator — scanned the genomes of more than 2,000 individuals suffering from intracranial aneurysms along with 8,000 healthy subjects. They discovered three chromosome segments, or loci, where common genetic variations can create significant risk for ruptured aneurysms, which in turn cause strokes.
The subjects came from hospitals in Finland, the Netherlands and Japan, and the results were similar in all groups, indicating that these variations increase risk among diverse human populations.
The findings, reported online in the journal Nature Genetics, could lead to new screening tests to identify hundreds of thousands of people at risk for strokes caused by bleeding and point to new therapies that might be able to strengthen blood vessels in the brain before they burst.
"Even though we have made significant strides in treating unruptured aneurysms, until now we have not had an effective means of identifying the majority of individuals at risk of developing this deadly problem. These genetic findings provide a starting point for changing that equation," Gunel said.
The median age when hemorrhagic stroke occurs is 50 years old, and usually there are no warning signs. In the majority of cases, the resulting strokes cause death or severe brain damage. Without an understanding of the cause of these events, physicians have been left to respond after the fact, once the damage has largely been done. Biden was one of the lucky individuals who survived a ruptured aneurysm with minimal damage — although at the time he was stricken, his condition was thought to be grave enough that a priest was summoned to confer last rites.
The Yale study showed that the risk of harboring an aneurysm increased with the number of risk variants, or alleles. Individuals with the highest number of risk alleles tripled their risk of an aneurysm, researchers found.
Based on this large collaborative study, a screening test may one day be able to identify those who are at higher risk of forming brain aneurysms or suffering a bleeding stroke as a result.
"These findings provide fundamental insights into the genetic and biochemical changes that cause this devastating brain disease, providing hope that we may also be able to provide preventive therapy before rupture occurs," Lifton said.
For instance, the new findings implicate variations in the gene SOX17, which is known to play a crucial role in the early development and repair of endothelial cells that make up the arterial walls of blood vessels. "These variations may interfere with the ability to produce cells that repair damage to the blood vessels, suggesting a path forward for developing new approaches to prevention," Gunel said.
Kaya Bilguvar of Yale was first author of the paper. Other Yale researchers included Shrikant Mane, Christopher E. Mason, Murim Choi, Emilia Gaal, Yasa Bayri, Luis Kobl, Zulfikar Arlier, Sudhakar Ravuri, and Matthew W. State.
The work was funded by the National Institutes of Health, the Yale Center for Human Genetics and Genomics, the Yale Program on Neurogenetics and the Howard Hughes Medical Institute.
Citation: Nature Genetics, Nov. 9, 2008
Exercise Increases Brain Growth Factor and Receptors, Prevents Stem Cell Drop in Middle Age
The American Physiological Society released the following announcement:
Exercise increases brain growth factor and receptors, prevents stem celldrop in middle age
BETHESDA, Md. (Nov. 18, 2008)
A new study confirms that exercise canreverse the age-related decline in the production of neural stem cellsin the hippocampus of the mouse brain, and suggests that this happensbecause exercise restores a brain chemical which promotes the productionand maturation of new stem cells.Neural stem cells and progenitor cells differentiate into a variety ofmature nerve cells which have different functions, a process calledneurogenesis. There is evidence that when fewer new stem or progenitorcells are produced in the hippocampus, it can result in impairment ofthe learning and memory functions. The hippocampus plays an importantrole in memory and learning.The study, "Exercise enhances the proliferation of neural stem cells andneurite growth and survival of neuronal progenitor cells in dentategyrus of middle-aged mice," was carried out by Chih-Wei Wu, Ya-TingChang, Lung Yu, Hsiun-ing Chen, Chauying J. Jen, Shih-Ying Wu, Chen-PengLo, Yu-Min Kuo, all of the National Cheng Kung University MedicalCollege in Taiwan. The study appears in the November issue of theJournal of Applied Physiology, published by The American PhysiologicalSociety.
Rise in corticosterone or fall in nerve growth factor?The researchers built on earlier studies that found that the productionof stem cells in the area of the hippocampus known as the dentate gyrusdrops off dramatically by the time mice are middle age and that exercisecan slow that trend. In the current study, the researchers wanted totrack these changes in mice over time, and find out why they happen.
One hypothesis the researchers investigated is that the age-relateddecline in neurogenesis is tied to a rise in corticosterone in middleage. Elevation of corticosterone has been associated with a drop in theproduction of new stem cells in the hippocampus.The second hypothesis is that nerve growth factors -- which encouragenew neural cell growth but which decrease with age -- account for thedrop in neurogenesis. Specifically, the study looked at whether adecrease in brain-derived neurotrophic growth factor leads to a declinein new neural stem cells.Variables studied.
The researchers trained young (3 months), adult (7 months), early middle-aged (9 months), middle-aged (13 months) and old (24 months) mice to runa treadmill for up to one hour a day.The study tracked neurogenesis, age, exercise, serum corticosteronelevels and brain-derived neurotrophic factor (BDNF) and its receptorTrkB levels in the hippocampus. The researchers focused on middle age asa critical stage for the decline of neurogenesis in the mice. As expected, the study found that neurogenesis drops off sharply inmiddle-aged mice. For example, the number of neural progenitor andmitotic (dividing) cells in the hippocampus of middle-aged mice was only5% of that observed in the young mice.The researchers also found that exercise significantly slows down the loss of new nerve cells in the middle-aged mice. They found thatproduction of neural stem cells improved by approximately 200% comparedto the middle-aged mice that did not exercise. In addition, the survivalof new nerve cells increased by 170% and growth by 190% compared to thesedentary middle-aged mice.
Exercise also significantly enhanced stemcell production and maturation in the young mice. In fact, exerciseproduced a stronger effect in younger mice compared to the older mice.How does this happen?Based on these results, it appears that nerve growth factor has more todo with these findings than the corticosterone:
* The middle-aged exercisers had more brain-derived neurotrophicfactor and its receptor, TrkB, compared to the middle-aged mice that didnot exercise. This suggests that exercise promotes the production ofbrain-derived neurotrophic factor which, in turn, promotesdifferentiation and survival of new brain cells in the hippocampus.
* Exercise did not change the basal level of serum corticosterone inmiddle-aged mice. This suggests that the reduction of neurogenesisduring aging is not due to the drop in corticosterone levels.
Exercise increases brain growth factor and receptors, prevents stem celldrop in middle age
BETHESDA, Md. (Nov. 18, 2008)
A new study confirms that exercise canreverse the age-related decline in the production of neural stem cellsin the hippocampus of the mouse brain, and suggests that this happensbecause exercise restores a brain chemical which promotes the productionand maturation of new stem cells.Neural stem cells and progenitor cells differentiate into a variety ofmature nerve cells which have different functions, a process calledneurogenesis. There is evidence that when fewer new stem or progenitorcells are produced in the hippocampus, it can result in impairment ofthe learning and memory functions. The hippocampus plays an importantrole in memory and learning.The study, "Exercise enhances the proliferation of neural stem cells andneurite growth and survival of neuronal progenitor cells in dentategyrus of middle-aged mice," was carried out by Chih-Wei Wu, Ya-TingChang, Lung Yu, Hsiun-ing Chen, Chauying J. Jen, Shih-Ying Wu, Chen-PengLo, Yu-Min Kuo, all of the National Cheng Kung University MedicalCollege in Taiwan. The study appears in the November issue of theJournal of Applied Physiology, published by The American PhysiologicalSociety.
Rise in corticosterone or fall in nerve growth factor?The researchers built on earlier studies that found that the productionof stem cells in the area of the hippocampus known as the dentate gyrusdrops off dramatically by the time mice are middle age and that exercisecan slow that trend. In the current study, the researchers wanted totrack these changes in mice over time, and find out why they happen.
One hypothesis the researchers investigated is that the age-relateddecline in neurogenesis is tied to a rise in corticosterone in middleage. Elevation of corticosterone has been associated with a drop in theproduction of new stem cells in the hippocampus.The second hypothesis is that nerve growth factors -- which encouragenew neural cell growth but which decrease with age -- account for thedrop in neurogenesis. Specifically, the study looked at whether adecrease in brain-derived neurotrophic growth factor leads to a declinein new neural stem cells.Variables studied.
The researchers trained young (3 months), adult (7 months), early middle-aged (9 months), middle-aged (13 months) and old (24 months) mice to runa treadmill for up to one hour a day.The study tracked neurogenesis, age, exercise, serum corticosteronelevels and brain-derived neurotrophic factor (BDNF) and its receptorTrkB levels in the hippocampus. The researchers focused on middle age asa critical stage for the decline of neurogenesis in the mice. As expected, the study found that neurogenesis drops off sharply inmiddle-aged mice. For example, the number of neural progenitor andmitotic (dividing) cells in the hippocampus of middle-aged mice was only5% of that observed in the young mice.The researchers also found that exercise significantly slows down the loss of new nerve cells in the middle-aged mice. They found thatproduction of neural stem cells improved by approximately 200% comparedto the middle-aged mice that did not exercise. In addition, the survivalof new nerve cells increased by 170% and growth by 190% compared to thesedentary middle-aged mice.
Exercise also significantly enhanced stemcell production and maturation in the young mice. In fact, exerciseproduced a stronger effect in younger mice compared to the older mice.How does this happen?Based on these results, it appears that nerve growth factor has more todo with these findings than the corticosterone:
* The middle-aged exercisers had more brain-derived neurotrophicfactor and its receptor, TrkB, compared to the middle-aged mice that didnot exercise. This suggests that exercise promotes the production ofbrain-derived neurotrophic factor which, in turn, promotesdifferentiation and survival of new brain cells in the hippocampus.
* Exercise did not change the basal level of serum corticosterone inmiddle-aged mice. This suggests that the reduction of neurogenesisduring aging is not due to the drop in corticosterone levels.
Saturday, November 15, 2008
Bad Health Habits and Lifestyle Choices Are Among Alzheimer's Causes
Stress, inactivity and even certain medications can weaken memory.
By Melissa Healy November 17, 2008
When it comes to preserving memories, we are sometimes our own worst enemies. The lives we lead often undermine the complex process of creating and retrieving memories. And they can boost the odds of our developing diseases -- including Alzheimer's -- that further ravage the brain's mechanisms of memory. Here are things that science tells us pose the greatest threat to our memories: Knowing them, says UCLA neurologist Dr. Gary Small, may allow us "to act early to prevent."Medications
Want a healthier brain for clearer thinking and better memory?Researcher says this nutrient may reverse "up to 12 years of decline"
www.hsibaltimore.com
Brain Food
Attend 4 Stimulating Lectures by Ivy League Profs - Stay Sharp
www.onedayu.com
Many medications prescribed widely in the U.S. can cause memory problems. Among the most likely to disrupt memory are benzodiazepines (including Ativan, Valium and Xanax). Any drug that can cause drowsiness can disturb concentration and absorption of new facts -- there are legions of those, including over-the-counter antihistamines.Some drugs have been discovered by accident to have memory-disrupting qualities and have been hailed as possible treatments for those at risk of post-traumatic stress disorder. Beta blockers, prescribed widely, have been shown to reduce the emotional power of certain memories and are being investigated by the U.S. military. Propofol, a sedative colloquially known as "milk of amnesia," can also erase a few minutes of memory.Untreated heart disease
High blood pressure, high cholesterol, Type 2 diabetes and obesity all raise the risk of stroke, which can affect memory profoundly. Studies have also found those with Type 2 diabetes at three times greater risk for Alzheimer's as the general population. Those with high cholesterol and blood pressure in midlife are also at greater risk. And obesity (particularly excess fat around the middle) has been linked to higher dementia rates 30 years later.
StressResearchers know that high emotion surrounding an event assures that it will be committed to memory. As the brain floods with adrenaline and norepinephrine, the mechanisms of memory are excited. Episodes of high stress, intense happiness, love and sadness can preserve a sharp memory. But when stress is constant and the brain is bathed chronically in stress hormones such as cortisol, attention grows weak and events are stored fitfully in short-term memory and fitfully committed to long-term memory. Established memories are poorly retrieved.Cortisol overload will cause many of the brain cells with memory functions to power down. And over time, chronic stress will degrade communications between cells in brain regions important to learning and memory. Even several hours of steady stress can flood the brain with hormones that disrupt memory, according to a March report by UC Irvine researchers in the Journal of Neuroscience.
Alcoholism causes progressive brain shrinkage and disrupts communications between regions involved in storing and retrieving memories. In the extreme, an alcoholic can exhibit total loss of long-term memories. But memory "blackouts" and fragmented recollection are common even among social drinkers, researchers have found. Heavy alcohol use can also cause vitamin B1 deficiencies, which along with vitamin B12 deficiencies can negatively affect memory.
epression sabotages concentration and with it, memory. Brain-imaging reveals that depression decreases activity in the brain's frontal lobes, a linchpin of memory-making.A study reported in 2006 by University of Rochester researcher Mark Mapstone found that among middle-aged women, those with depressive symptoms had more complaints of memory lapses and poorer performance registering new information than those without mood disturbance.Mapstone found that the women did not show cognitive problems on neuropsychological tests. With their attention spread thin by competing demands and mood disturbances affecting concentration, many fear they have Alzheimer's when in fact they may have problems getting information into the memory stream, rather than storing or retrieving it. Attention-deficit disorder and sleep deprivation are thought to have similar effects.
Couch potato lifestylePhysical and mental exercises are essential to keeping memory functioning: Lack of either is associated with memory problems, especially as we age.The brain, like any organ, benefits from improved blood flow that comes with aerobic activity. And its tissues are strengthened with increased use. Plus, studies show that those with higher education levels and a habit of mental stimulation build up a "cognitive reserve" that reduces the symptom severity even when their brains are under attack by Alzheimer's. "It's a common sense expression, but it seems to be true: A huge amount of data says use it or lose it," says UC Irvine neuroscientist James McGaugh
By Melissa Healy November 17, 2008
When it comes to preserving memories, we are sometimes our own worst enemies. The lives we lead often undermine the complex process of creating and retrieving memories. And they can boost the odds of our developing diseases -- including Alzheimer's -- that further ravage the brain's mechanisms of memory. Here are things that science tells us pose the greatest threat to our memories: Knowing them, says UCLA neurologist Dr. Gary Small, may allow us "to act early to prevent."Medications
Want a healthier brain for clearer thinking and better memory?Researcher says this nutrient may reverse "up to 12 years of decline"
www.hsibaltimore.com
Brain Food
Attend 4 Stimulating Lectures by Ivy League Profs - Stay Sharp
www.onedayu.com
Many medications prescribed widely in the U.S. can cause memory problems. Among the most likely to disrupt memory are benzodiazepines (including Ativan, Valium and Xanax). Any drug that can cause drowsiness can disturb concentration and absorption of new facts -- there are legions of those, including over-the-counter antihistamines.Some drugs have been discovered by accident to have memory-disrupting qualities and have been hailed as possible treatments for those at risk of post-traumatic stress disorder. Beta blockers, prescribed widely, have been shown to reduce the emotional power of certain memories and are being investigated by the U.S. military. Propofol, a sedative colloquially known as "milk of amnesia," can also erase a few minutes of memory.Untreated heart disease
High blood pressure, high cholesterol, Type 2 diabetes and obesity all raise the risk of stroke, which can affect memory profoundly. Studies have also found those with Type 2 diabetes at three times greater risk for Alzheimer's as the general population. Those with high cholesterol and blood pressure in midlife are also at greater risk. And obesity (particularly excess fat around the middle) has been linked to higher dementia rates 30 years later.
StressResearchers know that high emotion surrounding an event assures that it will be committed to memory. As the brain floods with adrenaline and norepinephrine, the mechanisms of memory are excited. Episodes of high stress, intense happiness, love and sadness can preserve a sharp memory. But when stress is constant and the brain is bathed chronically in stress hormones such as cortisol, attention grows weak and events are stored fitfully in short-term memory and fitfully committed to long-term memory. Established memories are poorly retrieved.Cortisol overload will cause many of the brain cells with memory functions to power down. And over time, chronic stress will degrade communications between cells in brain regions important to learning and memory. Even several hours of steady stress can flood the brain with hormones that disrupt memory, according to a March report by UC Irvine researchers in the Journal of Neuroscience.
Alcoholism causes progressive brain shrinkage and disrupts communications between regions involved in storing and retrieving memories. In the extreme, an alcoholic can exhibit total loss of long-term memories. But memory "blackouts" and fragmented recollection are common even among social drinkers, researchers have found. Heavy alcohol use can also cause vitamin B1 deficiencies, which along with vitamin B12 deficiencies can negatively affect memory.
epression sabotages concentration and with it, memory. Brain-imaging reveals that depression decreases activity in the brain's frontal lobes, a linchpin of memory-making.A study reported in 2006 by University of Rochester researcher Mark Mapstone found that among middle-aged women, those with depressive symptoms had more complaints of memory lapses and poorer performance registering new information than those without mood disturbance.Mapstone found that the women did not show cognitive problems on neuropsychological tests. With their attention spread thin by competing demands and mood disturbances affecting concentration, many fear they have Alzheimer's when in fact they may have problems getting information into the memory stream, rather than storing or retrieving it. Attention-deficit disorder and sleep deprivation are thought to have similar effects.
Couch potato lifestylePhysical and mental exercises are essential to keeping memory functioning: Lack of either is associated with memory problems, especially as we age.The brain, like any organ, benefits from improved blood flow that comes with aerobic activity. And its tissues are strengthened with increased use. Plus, studies show that those with higher education levels and a habit of mental stimulation build up a "cognitive reserve" that reduces the symptom severity even when their brains are under attack by Alzheimer's. "It's a common sense expression, but it seems to be true: A huge amount of data says use it or lose it," says UC Irvine neuroscientist James McGaugh
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