PASADENA, Calif.—Biologists at the California Institute of Technology (Caltech) have demonstrated a connection between multiple sclerosis (MS)—an autoimmune disorder that affects the brain and spinal cord-and gut bacteria.
The work—led by Sarkis K. Mazmanian, an assistant professor of biology at Caltech, and postdoctoral scholar Yun Kyung Lee—appears online the week of July 19-23 in the Proceedings of the National Academy of Sciences.
Our modern sterile environments might have shifted the make-up of our intestinal flora in a direction that causes immune system changes that increase the odds of MS.
Segmented filamentous bacteria induce an inflammatory cascade that leads to MS in lab animals created to study MS.
To find out, Mazmanian and his colleagues tried to induce MS in animals that were completely devoid of the microbes that normally inhabit the digestive system. "Lo and behold, these sterile animals did not get sick," he says.
Then the researchers decided to see what would happen if bacteria were reintroduced to the germ-free mice. But not just any bacteria. They inoculated mice with one specific organism, an unculturable bug from a group known as segmented filamentous bacteria. In prior studies, these bacteria had been shown to lead to intestinal inflammation and, more intriguingly, to induce in the gut the appearance of a particular immune-system cell known as Th17. Th17 cells are a type of T helper cell—cells that help activate and direct other immune system cells. Furthermore, Th17 cells induce the inflammatory cascade that leads to multiple sclerosis in animals.
"The question was, if this organism is inducing Th17 cells in the gut, will it be able to do so in the brain and central nervous system?" Mazmanian says. "Furthermore, with that one organism, can we restore to sterile animals the entire inflammatory response normally seen in animals with hundreds of species of gut bacteria?"
The answer? Yes on all counts. Giving the formerly germ-free mice a dose of one species of segmented filamentous bacteria induced Th17 not only in the gut but in the central nervous system and brain—and caused the formerly healthy mice to become ill with MS-like symptoms.
So this brings up the obvious question: Which types of bacteria will reduce our risks of MS? Anyone know much about popular yogurt bacteria? Which ones would be better to get more of? Any ones to avoid?
Update: A research report about probiotic (live lactic acid bacteria) use in pregnancy to cut the incidence of eczema in babies highlights how intestinal bacteria can influence immune system function.
(20.07.2010) Mothers who drank milk with a probiotic supplement during and after pregnancy were able to cut the incidence of eczema in their children by almost half, a new study published in the British Journal of Dermatology has shown.
The randomized, double-blind study, conducted by researchers at the Norwegian University of Science and Technology (NTNU), compared mothers who drank one glass of probiotic milk a day to women who were given a placebo. Use of the probiotic milk – which the mothers drank beginning at week 36 in their pregnancy up through to three months after birth -- reduced the incidence of eczema by 40 percent in children up to age two, the researchers found. The study is a part of a larger research project at the university called the Prevention of Allergy Among Children in Trondheim, or PACT, an ongoing population-based intervention study in Norway focused on childhood allergy.
A new study on vitamin D levels and Parkinson's disease risk points to the need for further research on whether vitamin D supplements can protect against the movement disorder, according to an editorial in the July 2010 issue of Archives of Neurology.
The author of the editorial is Marian Evatt, MD, assistant professor of neurology at Emory University School of Medicine and director of the Atlanta Veterans Affairs Medical Center's Movement Disorders Clinic.
The study, also reported in Archives of Neurology, is the first to show that low vitamin D levels can help predict whether someone will later develop Parkinson's disease. Researchers at Finland's National Institute for Health and Welfare measured vitamin D levels from more than 3000 people, using blood samples taken between 1978 and 1980, and then followed those people to see whether they developed Parkinson's. People with the lowest levels of vitamin D were three times more likely to develop Parkinson's, compared to the group with the highest levels.
This report by itself does not prove a causal relationship where low vitamin D boosts Parkinson's risk. Other causal chains are possible. For example, it is possible some of the same genetic variants that cause differences in blood vitamin D level also separately cause changes in neuronal or immune system function and thereby change Parkinson's risk.
Vitamin D might provide protection by protecting dopaminergic neurons from toxins.
Research on animals suggests that vitamin D may protect neurons that produce dopamine from toxins. Besides vitamin D levels, factors such as genetics and exposure to pesticides also are associated with the risk for developing Parkinson's disease.
This report brings to mind a long studied link between multiple sclerosis and vitamin D. For example, a Canadian study found low vitamin D is linked to higher MS risk, MS is thought to be an auto-immune disorder, and vitamin D is thought to play a role modulating immune function. Curiously, a report in March 2010 found ultraviolet light might reduce the damage from MS independent of UV's stimulation of skin vitamin D synthesis. However, at least one study has found that vitamin D supplements appear to cut risk of MS relapse.
Choose your parents carefully. High rates of schizophrenia and bipolar among the offspring in Denmark.
Rates of schizophrenia were highest among offspring of two parents with schizophrenia. Of the 196 couples who both had schizophrenia, 27.3 percent of their 270 children were admitted to a psychiatric facility, increasing to 39.2 percent when schizophrenia-related disorders were included. This compared with a rate of 7 percent among 13,878 offspring of 8,006 couples in which one parent had schizophrenia and 0.86 percent in 2.2 million offspring of 1 million couples in which neither parent was admitted for schizophrenia.
Similarly, the risk of bipolar disorder was 24.9 percent in 146 offspring of 83 parent couples who were both admitted for bipolar disorder (increasing to 36 percent when unipolar depressive disorder was also included). This compared to a risk of 4.4 percent among 23,152 offspring of 11,995 couples with only one parent ever admitted for bipolar disorder and 0.48 percent in 2.2 million children of 1 million couples with neither parent ever admitted.
When one parent had bipolar disorder and the other had schizophrenia, offspring had a 15.6 percent risk of schizophrenia and an 11.7 percent risk of bipolar disorder.
Identification of all the genetic variants that cause schizophrenia and bipolar will open up the possibility of the mentally ill using in vitro fertilization, pre-implantation genetic diagnosis, and embryo selection to avoid passing along some of their genetic variants that cause mental illness. However, since some of those genetic variants might boost some forms of mental creativity we might collectively lose something. Perhaps genes that boost creativity without boosting mental illness will be found. Or perhaps some genetic variants stabilize personality in the presence of other genes that boost mental illness risks and creativity.
ST. PAUL, Minn. – New research shows people who regularly take ibuprofen may reduce their risk of developing Parkinson's disease, according to a study released today that will be presented at the American Academy of Neurology's 62nd Annual Meeting in Toronto April 10 to April 17, 2010.
What I want to know: What's the effect of long term ibuprofen on all-cause mortality? Does the risk of stomach bleeding from taking ibuprofen outweigh the risk reduction from avoiding Parkinson's?
The research involved 136,474 people who did not have Parkinson's disease at the beginning of the research. Participants were asked about their use of non-steroid anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen and acetaminophen. After six years, 293 participants had developed Parkinson's disease.
The protective effect appears to be dose dependent.
The study found regular users of ibuprofen were 40 percent less likely to develop Parkinson's disease than people who didn't take ibuprofen. Also, people who took higher amounts of ibuprofen were less likely to develop Parkinson's disease than people who took smaller amounts of the drug. The results were the same regardless of age, smoking and caffeine intake.
The other studied NSAIDs did not deliver this benefit.
"Ibuprofen was the only NSAID linked to a lower risk of Parkinson's," said Xiang Gao, MD, with Harvard School of Public Health in Boston. "Other NSAIDs and analgesics, including aspirin and acetaminophen, did not appear to have any effect on lowering a person's risk of developing Parkinson's. More research is needed as to how and why ibuprofen appears to reduce the risk of Parkinson's disease, which affects up to one million people in the United States."
Since long term use of ibuprofen carries with it a risk of stomach bleeding (and the risk is greater above age 60) you shouldn't start taking it without a compelling reason that will convince you (and preferably your doctor too) that your benefits will outweigh your risks.
When many more genetic risk factors for Parkinson's become known it might become possible to narrow down to a much smaller population of people who are likely to cut their Parkinson's risk. Also, neurological or blood tests in middle age might some day help identify those at greater risk. Since most people do not get Parkinson's even in their old age most people won't experience a risk reduction from taking ibuprofen. The problem is that we do not know which people who take ibuprofen will benefit by either delaying or avoiding the development of Parkinson's.
Similarly, better genetic and other testing might identify those at most risk from bleeding when taking ibuprofen. The ideal group to take ibuprofen would be those at least risk of stomach bleeding who are also at higher risk for getting Parkinson's. Perhaps in another 5-10 years we'll have enough genetic testing capability to identify who ought to take ibuprofen.
A new study provides a novel theory for how delusions arise and why they persist. NYU Langone Medical Center researcher Orrin Devinsky, MD, performed an in-depth analysis of patients with certain delusions and brain disorders revealing a consistent pattern of injury to the frontal lobe and right hemisphere of the human brain. The cognitive deficits caused by these injuries to the right hemisphere, leads to the over compensation by the left hemisphere of the brain for the injury, resulting in delusions. The article entitled "Delusional misidentifications and duplications: Right brain lesions, left brain delusions" appears in the latest issue of the journal of Neurology.
"Problems caused by these brain injuries include impairment in monitoring of self, awareness of errors, and incorrectly identifying what is familiar and what is a work of fiction," said Dr. Devinsky, professor of Neurology, Psychiatry and Neurosurgery and Director of the NYU Epilepsy Center at NYU Langone Medical Center. "However, delusions result from the loss of these functions as well as the over activation of the left hemisphere and its language structures, that 'create a story', a story which cannot be edited and modified to account for reality. Delusions result from right hemisphere lesions, but it is the left hemisphere that is deluded."
Often bizarre in content and held with absolute certainty, delusions are pathologic beliefs that remain fixed despite clear evidence that they are incorrect. "Delusions are common problems in a variety of psychiatric and neurological disorders," said Dr. Devinsky. "Psychiatric disorders with delusions, for example- schizophrenia, have been proven to have functional and structural brain pathology. But now improved diagnostic techniques are allowing us to have increased identification of neurologic disorders among other patient populations with delusions."
In the study, the author finds that most neurologic patients with delusions usually have lesions in the right hemisphere and/or bifrontal areas. For example, the neurological disorders of Confabulation (incorrect or distorted statements made without conscious effort to deceive), Capgras (the ability to consciously recognize familiar faces but not emotionally connect with them) and Prosopagnosia (patients who may fail to recognize spouses or their own face but generate an unconscious response to familiar faces) result from right sided lesions.
I expect advances in understanding of brain disorders to cause legal battles. If someone is deluded and a danger to self or others should that person be forcefully treated with, for example, stem cells that will do brain repair? If the alternative is institutionalization in a prison or mental hospital is treatment without consent a better choice?
Many drugs already can alter mental state. If patients in mental hospitals are forceably drugged then already a person's own judgment about what is core to their identity - their own thoughts - is effectively rejected and replaced by the judgment of managers and experts in mental hospitals. The ramifications of this power will become greater as the technology for permanently altering cognitive function becomes more powerful.
Findings from what is believed to be the largest comparison of blood samples collected from healthy individuals and people with schizophrenia suggest that infection with the common Toxoplasma gondii parasite, carried by cats and farm animals, may increase the risk of schizophrenia.
A report on the study, conducted among U.S. military personnel by researchers from Walter Reed Army Institute of Research and Johns Hopkins Children’s Center appears in the January issue of the American Journal of Psychiatry.
Researchers found that of the 180 study subjects diagnosed with schizophrenia, 7 percent had been infected with toxoplasma prior to their diagnosis, compared to 5 percent among the 532 healthy recruits. Thus, people exposed to toxoplasma had a 24 percent higher risk of developing schizophrenia. The difference, while seemingly small, is important, researchers say, because the ability to explain even a small portion of the 2 million cases of schizophrenia in the United States may offer clues to the disease and some possible treatments.
Recall that t. gondii infections are also suspected of causing personality changes. This explains the origins of Cat Woman.
People with body dysmorphic disorder (BDD) see their bodies as more disfigured and ugly than they really are. Some BDD sufferers disfigure themselves with pointless plastic surgery. Okay, so what's with them? BDD sufferers look at images with more activity in the analytical left side of their brains.
For the first time, functional magnetic resonance imaging (fMRI) was used to reveal how the patients’ brains processed visual input. The UCLA team outfitted 12 BDD patients with special goggles that enabled them to view digital photos of various faces as they underwent a brain scan.
Each volunteer viewed three types of images. The first type was an untouched photo. The second type was a photo altered to eliminate facial details that appear frequently, such as freckles, wrinkles and scars. This “low frequency” technique blurred the final image.
The third type of image essentially subtracted the blurred second image from the untouched photo. This “high frequency” technique resulted in a finely detailed line drawing.
Feusner’s team compared the BDD patients’ responses to 12 control subjects matched by age, gender, education and handedness. What the scientists observed surprised them.
“We saw a clear difference in how the right and left sides of the brain worked in people with BDD versus those without the disorder,” noted Feusner.
There are situations where being really analytical will get you into trouble.
BDD patients more often used their brain’s left side -- the analytic side attuned to complex detail -- even when processing the less intricate, low-frequency images. In contrast, the left sides of the control subjects’ brains activated only to interpret the more detailed high-frequency information. Their brains processed the untouched and low-frequency images on the right side, which is geared toward seeing things in their entirety.
“We don’t know why BDD patients analyze all faces as if they are high frequency,” said Feusner. “The findings suggest that BDD brains are programmed to extract details -- or fill them in where they don’t exist. It’s possible they are thinking of their own face even when they are looking at others.”
There's the capability to do analysis. Separately, there's what in your environment your mind tends to focus on to do analysis. If you focus on the wrong stimuli to process you can become pretty dysfunctional.
But will is this tendency to focus on analysis of facial and body shapes ever work to the benefit of some people? Do any painters or film makers do better jobs because their minds intensely analyze body shapes? Is the real problem with BDD the focus on one's own body rather than the bodies of other people? I suspect so.
Sustained inflammation response contributes the development of a variety of diseases. The bodies of depressed people respond to stresses with a larger inflammation response than non-depressed people experience.
ATLANTA--Individuals with major depression have an exaggerated inflammatory response to psychological stress compared to those who do not suffer from depression, according to a study by researchers at Emory University School of Medicine. Because an overactive inflammatory response may contribute to a number of medical disorders as well as to depression, the findings suggest that increased inflammatory responses to stress in depressed patients may be a link between depression and other diseases, including heart disease, as well as contributing to depression itself.
Results of the study, led by Andrew Miller, MD, and Christine Heim, PhD, of Emory's Department of Psychiatry and Behavioral Sciences, are published in the Sept. 1 issue of the American Journal of Psychiatry.
"Several examples of increased resting inflammation in depressed patients already exist in the literature, but this is the first time anyone has shown evidence to suggest that the inflammatory response to stress may be greater in depressed people," says Dr. Miller.
The study included 28 medically healthy male participants, half of whom were diagnosed with major depression and half of whom were not depressed. The participants were exposed to two moderately stressful situations during a 20-minute time period. Blood was collected every 15 minutes starting immediately before and then up to an hour and a half after the test to check for key indicators of inflammation. The researchers measured levels of a pro-inflammatory cytokine (a regulatory protein secreted by the immune system) called interleukin-6, and the activity of a pro-inflammatory signaling molecule in white blood cells called nuclear factor-kB.
While at rest (before the stress challenge), the depressed patients had increased inflammation relative to the control group. Both the depressed and the healthy groups showed an inflammatory response to the stress challenge, but people who were currently depressed exhibited the greatest increases of interleukin-6 and nuclear factor-kB.
Inflammation damages the body and basically accelerates aging.
"While inflammation is essential for us to fight bacterial and viral infections, too much inflammation can cause harm," says Dr. Miller. "There's always some collateral damage when the immune system gets fired up, and we now believe that too much inflammation, either at rest or during stress, may predispose people to become depressed or stay depressed." In addition, medical research over the last decade has shown that runaway inflammation may play a role in a number of disorders, including heart disease, cancer, and diabetes, all of which have been associated with depression.
If you are depressed and can not find an effective drug to treat your condition then consider diet and exercise as methods to decrease inflammation. Eat some fish for omega 3 fatty acids for starters. Eat lots of vegetables and fruits too.
If you are not depressed but know depressed people treat them kindly. They can not handle stress as well as you can.
Youth with bipolar disorder misread facial expressions as hostile and show heightened neural reactions when they focus on emotional aspects of neutral faces, researchers at the National Institutes of Health’s (NIH) National Institute of Mental Health (NIMH) have discovered. The study provides some of the first clues to the underlying workings of the episodes of mania and depression that disrupt friendships, school, and family life in up to one percent of children.
Brain scans showed that the left amygdala, a fear hub, and related structures, activated more in youth with the disorder than in healthy youth when asked to rate the hostility of an emotionally neutral face, as opposed to a non-emotional feature, such as nose width. The more patients misinterpreted the faces as hostile, the more their amygdala flared. Such a face-processing deficit could help account for the poor social skills, aggression, and irritability that characterizes the disorder in children, suggest Drs. Ellen Leibenluft, Brendan Rich, Daniel Pine, NIMH Mood and Anxiety Disorders Program, and colleagues, who report on their findings May 29, 2006 in the Proceedings of the National Academy of Sciences.
“Since children seem to have a more severe form of the disorder, they may provide a clearer window into the underlying illness process than adult onset cases,” explained Leibenluft. “Our results suggest that children with bipolar disorder see emotion where other people don’t. Our results also suggest that bipolar disorder likely stems from impaired development of specific brain circuits, as is thought to occur in schizophrenia and other mental illnesses.”
Magnetic Resonance Imaging (MRI) studies have shown that, unlike in adults with the illness, the amygdala is consistently smaller in bipolar children than in healthy age-mates. Also, the NIMH researchers had found earlier that bipolar children falter at identifying facial emotion and have difficulty regulating their attention when frustrated.
Using functional MRI, the researchers measured brain activity in 22 bipolar youth and 21 healthy subjects while they rated faces. In addition to the amygdala, other parts of the emotion-regulating circuit — nucleus accumbens, putamen, and left prefrontal cortex — were also hyperactive in patients, compared to healthy peers, during the emotional tasks. Patients rated themselves as more afraid, and they rated the faces as more hostile, compared to healthy peers. The groups did not differ on nose width ratings, confirming that the differences were specific to perceiving emotional processes.
This has practical implications for governments: Political candidates for high office and diplomats could get tested under fMRI machines for their ability to correctly read the faces of others. It just would not do to have some President or Prime Minister imagining lots of hostile intent that is not there. Same holds true for police.
It would be helpful for each person to know what types of facial expression misreadings they are prone to.
This reminds me of a previous report that found when kids enter puberty they go through a period of decreased ability to read the emotions of others.
STANFORD, Calif. –A gene that regulates dopamine levels in the brain is involved in the development of schizophrenia in children at high risk for the disorder, say researchers at the Stanford University School of Medicine, Lucile Packard Children’s Hospital and the University of Geneva. The finding adds to mounting evidence of dopamine’s link to psychiatric and neurological disorders. It may also allow physicians to pinpoint a subset of these children for treatment before symptoms start.
“The hope is that we will one day be able to identify the highest-risk groups and intervene early to prevent a lifetime of problems and suffering,” said Allan L. Reiss, MD. “As we gain a much better understanding of these disorders, we can design treatments that are much more specific and effective.”
Gene therapy to restore COMT activity (see below) would probably be the ideal method for early intervention. More generally, as we discover the genetic contributors to more diseases we will need better gene therapy delivery techniques to make use of the discovered information.
30% of those with a deletion at a location on chromosome 22 will develop schizophrenia or a similar mental disorder.
Reiss and the study’s first author Doron Gothelf, MD, a child psychiatrist and postdoctoral scholar at Stanford, studied 24 children with a small deletion in one copy of chromosome 22. About 30 percent of children with this deletion, which occurs in about one in 4,000 births, will develop schizophrenia or a related psychotic disorder. These children also often have special facial features, cardiac defects and cleft anomalies that often make their speech hypernasal. Although these characteristics make it possible to identify them before psychiatric disorders develop, the disorder, called velocardiofacial syndrome, is under-diagnosed and under-recognized in this country despite its link to schizophrenia.
“We have strong evidence that this deletion is a major risk factor for the development of schizophrenia or related psychotic disorders,” said Reiss. “We asked, ‘What is it about this deletion that causes such an increase in risk?’”
The answer lay in the fact that one of the missing genes encodes a dopamine-degrading protein called COMT. Natural variations in the gene generate two versions of the protein: one with high activity, one with low.
Because most people have two copies of the gene, it doesn’t usually matter which versions of COMT they inherit; high-high, high-low and low-low all seem to provide enough COMT activity to get the job done (though some combinations confer a mild advantage for some cognitive tasks).
Note the point above about how some combinations of COMT variations confer a mild cognitive advantage. Quite possibly some of these COMT these variations which contribute to schizophrenia exist due to Darwinian natural selective pressure for higher cognitive ability. Some people get combinations of genes that boost their cognitive ability at the cost of higher risk of schizophrenia.
The researchers decided to see if excess levels of dopamine due to insufficient COMT activity perhaps acted as neurotoxins that brought on schizophrenia.
But children with the deletion have only the one copy that remains on their intact chromosome 22. Reiss and Gothelf, who is also an assistant professor at Tel Aviv University in Israel, surmised that a single copy of the low-activity COMT might not dispose of enough dopamine to produce optimal brain function. They set out to determine if the clinical course of the children with deletions who developed schizophrenia varied with the version of the COMT protein they had.
Since chromisomes come in pairs deletion on one chromosome 22 still leaves another copy of the gene on the other copy of chromosome 22. So the scientists investigated variations of COMT on that other copy of chromosome 22 for those who have deletions on one of their chromosome 22 copies.
The surmise of the researchers turned out to be correct. Of those children missing one copy of COMT the children who had the lower activity version of their only copy of COMT had worse symptoms than children who had a higher activity version of COMT.
As expected, about 29 percent, or seven, of the children with the deletion had developed a psychotic disorder by the second round of testing, compared with only one child in the control group. Of these seven, those with the low-activity version of COMT had experienced a significantly greater drop in their verbal IQ and expressive language skills and a markedly greater decrease in the volume of their prefrontal cortex than did their peers with the more highly active version of COMT. The psychotic symptoms of the low-activity subset were also significantly more severe.
In contrast, members of the control group experienced no significant differences in any of these categories, regardless of their COMT profiles.
What I want to know: are the COMT low activity and deletion mutations more examples of IQ "overclocking" mutations? The press release doesn't provide enough detail to tell. Which combinations of COMT variations resulted in the best cognitive performance? Also, are low activity versions of COMT or deletions of COMT more common among Ashkenazi Jews than among other populations?
By studying patients who developed abnormal hoarding behavior following brain injury, neurology researchers in the University of Iowa Roy J. and Lucille A Carver College of Medicine have identified an area in the prefrontal cortex that appears to control collecting behavior. The findings suggest that damage to the right mesial prefrontal cortex causes abnormal hoarding behavior by releasing the primitive hoarding urge from its normal restraints. The study was published online in the Nov. 17 Advance Access issue of the journal Brain.
Comparison of functional magnetic resonance imaging (fMRI) brain scans between collectors and normal people turned up the location where the collecting behavior comes from.
The UI team studied 86 people with focal brain lesions - very specific areas of brain damage – to see if damage to particular brain regions could account for abnormal collecting behavior. Other than the lesions, the patients' brains functioned normally and these patients performed normally on tests of intelligence, reasoning and memory.
A questionnaire completed by a close family member was used to identify problematic collecting and the behavior was classified as abnormal if the collection was extensive; the collected items were not "useful" or aesthetic; the collecting behavior began only after the brain injury occurred; and the patient was resistant to discarding the collected items.
The questionnaire very clearly split the patients into two groups – 13 patients who had abnormal collecting behavior and a majority (73 patients) who did not. Unlike normal collecting behavior such as stamp collecting, the abnormal collecting behavior of these patients significantly interfered with their normal daily life. Patients with abnormal collecting behavior filled their homes with vast quantities of useless items including junk mail and broken appliances. Despite showing no further interest in the collected items, patients resist attempts to discard the collection.
To determine if certain areas of damage were common to patients who had abnormal collecting behavior, the UI researchers used high-resolution, three-dimensional magnetic resonance imaging to map the lesions in each patient's brain and overlapped all the lesions onto a common reference brain.
"A pretty clear finding jumped out at us: damage to a part of the frontal lobes of the cortex, particularly on the right side, was shared by the individuals with abnormal behavior," Anderson said. "Our study shows that when this particular part of the prefrontal cortex is injured, the very primitive collecting urge loses its guidance.
So then are stamp collectors and baseball card collectors slightly brain damaged? My guess is that there is a continuum of urges to collect with some people having stronger natural urges that have to find some outlet.
It seems likely to me that just as there are people who have excessive urges to collect there are other people who lack mimimally sufficient urges to collect possessions to be able to keep enough possessions around them to take care of themselves. On average do wealthier people have stronger urges to collect possessions? Do people who buy things have stronger urges to collect objects than people who go and spend their money travelling and entertaining themselves? Seems plausible.
Li-Hai Tan Ph.D. (who apparently is both Director, Joint Laboratories for Language and Cognitive Neuroscience at the University of Hong Kong, China and working currently at the US National Institute of Mental Health) and colleagues found that dyslexia is caused by malfunctions in a different part of the brain in Chinese readers than in Western language readers.
There is no one cause for dyslexia: rather, the causes vary between languages. So conclude researchers who have found that Chinese children with reading difficulties have different brain anomalies to their Western counterparts1.
Instead of letter-to-sound conversion problems, Chinese dyslexics have difficulties extrapolating from a symbol's shape to its sound and meaning.
Most dyslexia research has focused on letter-based languages such as English or Italian. These studies suggest the condition is tied to the left temporoparietal region of the brain.
Functional Magnetic Resonanace Imaging (fMRI) on dyslexic Chinese children showed that in readers of Chinese characters the brain problem with dyslexia can be traced to the left middle frontal gyrus (LMFG).
The researchers used sophisticated imaging technology to study the brain activity of 16 Chinese dyslexic children as they performed various language-based tasks.
Their study suggests that for these children, the problem lies in another area of the brain - the left middle frontal gyrus (LMFG).
Do different languages cause humans to categorize the world in different ways? Do different symbol systems for written and spoken language take up different amounts of the brain's resources leaving differing amounts of the brain available to perform other tasks? It seems highly plausible, even probable, that the answer to these questions is "yes".
Different symbol encoding systems place different cognitive demands upon the brain. Also see my previous post Mandarin Language Uses More Of The Brain Than English.
ndividuals who suffer from severe depression have more nerve cells in the part of the brain that controls emotion, researchers at UT Southwestern Medical Center at Dallas have found.
Studies of postmortem brains of patients diagnosed with major depressive disorder (MDD) showed a 31 percent greater than average number of nerve cells in the portion of the thalamus involved with emotional regulation. Researchers also discovered that this portion of the thalamus is physically larger than normal in people with MDD. Located in the center of the brain, the thalamus is involved with many different brain functions, including relaying information from other parts of the brain to the cerebral cortex.
The findings, published in today's issue of The American Journal of Psychiatry, are the first to directly link a psychiatric disorder with an increase in total regional nerve cells, said Dr. Dwight German, professor of psychiatry at UT Southwestern.
"This supports the hypothesis that structural abnormalities in the brain are responsible for depression," he said. "Often people don't understand why mentally ill people behave in odd ways. They may think they have a weak will or were brought up in some unusual way.
"But if their brains are different, they're going to behave differently. Depression is an emotional disorder. So it makes sense that the part of the brain that is involved in emotional regulation is physically different."
I find it curious that an emotional disorder would seemingly need such a large change in the size of a part of the brain in order for the disorder to manifest. Small changes in enormous computer programs can lead to large malfunctions. Yet at least with major depression incredibly small changes are apparently not sufficient to cause it in most sufferers of depression.
Note, however, that sufferers of bipolar depression do not have an increase in the size of the mediodorsal and anteroventral/anteromedial areas of the thalamus. So then is there an abnormality in the size of some other part of the brain of bipolars waiting to be discovered?
Researchers from UT Southwestern, working with a team from Texas A&M University System Health Science Center, used special computer-imaging systems to meticulously count the number of nerve cells in the thalamus.
Results showed an increase of 37 percent and 26 percent, respectively, in the number of nerve cells in the mediodorsal and anteroventral/anteromedial areas of the thalamus in subjects with MDD when compared with similar cells in those with no psychiatric problems. The number of nerve cells in subjects with bipolar disorder and schizophrenia was normal.
Researchers also found that the size of the affected areas of the thalamus in subjects with MDD was 16 percent larger than those in the other groups.
"The thalamus is often referred to as the secretary of the cerebral cortex – the part of the brain that controls all kinds of important functions such as seeing, talking, moving, thinking and memory," Dr. German said. "Most everything that goes into the cortex has to go through the thalamus first.
"The thalamus also contains cells that are not involved with emotion. Our studies found these portions of the thalamus to be perfectly normal. But the ones that are involved in emotion are the ones that were abnormal."
Researchers also looked at the effect of antidepressant medications on the number of nerve cells and found no significant difference among any of the subject groups – whether they had taken antidepressants or not – reinforcing the belief that abnormalities in brain development are responsible for depression.
Does this report suggest any avenues for the development of therapeutic treatments? Could a drug be developed that would inhibit some of the neurons in the mediodorsal and anteroventral/anteromedial areas of the thalamus? Would such a drug reduce the symptoms of depression? It will be interesting to see what develops from this report.