Brain function of earthquake survivors gets acutely affected

Washington, Sep 1 (ANI): The earthquake that jolted Wenchuan, China, in 2008 has had an acute impact on the brain function of physically healthy survivors, and even poses a risk to their mental health, according a new research.

Working with collaborators from universities in China, the US and Liverpool, researchers at the Institute of Psychiatry focussed on the survivors of the earthquake that occurred on May 12 last year.

The researchers wanted to gain a better understanding of how functional brain systems adapt to severe emotional stress.

Previous animal studies have demonstrated the importance of limbic, paralimbic, striatal, and prefrontal structures of the brain in stress and fear responses.

Human studies, which have focused primarily on patients with clinically established posttraumatic stress disorders, have reported abnormalities in similar brain structures.

But not much is known about potential alterations of brain function in trauma survivors shortly after traumatic events such as an earthquake.

The epicentre of the devastating earthquake was in Wenchuan, in the Sichuan Province of China.

The tremor measured 8.0 on the Richter scale and severely affected many geographical regions including Yingxiu, Wenchuan, Dujiangyan, and Shifang, where 45 million people were directly affected.

The researchers found that a significant proportion of the survivors (around 20 per cent) are likely to develop stress-related disorders, such as acute stress disorder (ASD) and posttraumatic stress disorder (PTSD).

“Given the serious and persistent impact of these highly prevalent psychiatric disorders, it is vital to develop a better understanding of the alterations of cerebral function evident in the early stages of adaptation to trauma. Such knowledge may lead to a better understanding of posttraumatic responses and the development of more effective early interventions,” said Dr Andrea Mechelli from the Institute of Psychiatry at King’s College London.

The researchers used a method known as ‘resting-state fMRI’ to examine 44 healthy survivors and 32 controls shortly after the massive psychological trauma.

They found that significant alterations in brain function similar to those observed in posttraumatic stress disorders could be seen shortly after major traumatic experiences, highlighting the need for early evaluation and intervention for the survivors.

The results of the study show that individuals experiencing severe emotional trauma showed hyperactivity in certain areas of the brain, and decreased functional connectivity in others, shortly after the massively traumatic Wenchuan earthquake.

Particularly, the findings indicated that traumatic experiences affect not only regional function but also dynamic interactions within brain networks.

It is not clear if this pattern of brain alteration remains the same or evolves further over the following weeks or months after the traumatic experiences.

“A better understanding of the impact of traumatic events on brain function may help us identify those in need of early treatment and reduce the long-term psychological impact in trauma survivors of national disasters, military conflict, and other causes of severe emotional distress,” said Mechelli.

The results of the study have been published in PNAS online. (ANI)

Same neural networks in brain process familiar and newly learnt words

Washington, August 29 (ANI): A series of experiments conducted as part of the Academy of Finland’s Neuroscience Research Programme (NEURO) have shown that the brain uses the same neural networks to process both familiar and newly learnt words.

In one experiment, participants learnt the name and/or purpose of 150 ancient tools. They had never heard those words before.

Their brain function was measured by means of magnetoencelography during the naming of the tools, both before and after the learning period.

It was observed that their brains used the same neural networks to process both familiar and newly learned words.

Academy Professor Riitta Salmelin, HUT Low Temperature Laboratory, who is in charge of the research, revealed that the names of objects were processed in the left temporal and frontal lobe within half a second of showing the image of the tool to the subject.

“If the subject had only recently learned the name of the tool, the naming process induced an activation that was just as strong or stronger than the activation induced by the image of a familiar object,” the researcher said.

Salmelin added that the learning of the meaning of ancient tools did not cause corresponding clear differences in the function of the brain.

According to the researcher, it seems that the processing of meanings in the brain differs essentially from the processing of names.

On the other hand, said Salmelin, the performance results indicated that new definitions were learnt even faster than new names.

The research team are now working on a follow-up study to explore the retention of learned words.

“We are also conducting a separate series of experiments to find out how our brain learns phonetic structures and, on the other hand, how the brain learns to identify letter combinations that are typical of a certain language,” Salmelin said.

Another area of interest in the ongoing study is the role of grammar in language learning.

The researchers say that they will try to explore how the brain learns to use the vocabulary and grammatical structure of an experimental miniature language. (ANI)

Why sleep deprivation affects some people more than others

Washington, June 25 (ANI): Conducting a new imaging research, scientists have explained why sleep deprivation affects some people more than others.

Researchers observed that people who are genetically vulnerable to sleep loss showed reduced brain activity after staying awake all night, while those who are genetically resilient showed expanded brain activity.

The findings help explain individual differences in the ability to compensate for lack of sleep.

“The extent to which individuals are affected by sleep deprivation varies, with some crashing out and others holding up well after a night without sleep,” said Dr. Michael Chee, at the Duke-National University of Singapore Graduate Medical School.

In the current study, the researchers, led by Dr. Pierre Maquet, at the University of Liege in Belgium selected study participants based on their genes.

Previous research showed that the PERIOD3 (PER3) gene predicts how people will respond to sleep deprivation. People carry either long or short variants of the gene.

Those with the short PER3 variant are resilient to sleep loss – they perform well on cognitive tasks after sleep deprivation.

However, those with the long PER3 variant are vulnerable – they show deficits in cognitive performance after sleep deprivation. Now the new study explains why.

The authors imaged study participants while they did a working memory task that requires attention and cognitive control – also called executive function.

They found that the resilient, short gene variant group compensated for sleep loss by “recruiting” extra brain structures.

Besides brain structures normally activated by the cognitive task, these participants showed increased activity in other frontal, temporal, and subcortical brain structures after a sleepless night.

On the other hand, after a sleepless night, vulnerable participants, the long PER3 group, showed reduced activity in brain structures normally activated by the task.

These participants also showed reduced brain activity in one brain structure – the right posterior inferior frontal gyrus – after a normal waking day.

The above data is consistent with previous research suggesting that people with the long gene variant perform better on executive tasks earlier, but not later, in the day.

“Our study uncovers some of the networks underlying individual differences in sleep loss vulnerability and shows for the first time how genetic differences in brain activity associate with cognitive performance and fatigue. The data also provide a basis for the development of measures to counteract individual cognitive deficits associated with sleep loss,” said study author Maquet.

The study is published in the latest issue of The Journal of Neuroscience. (ANI)

Mouse model may pave way for better anti-depressant treatments

Washington, May 28 (ANI): Using a new experimental mouse model of depression/anxiety, scientists have found that the anti-depressant effects of drugs like Prozac involve both neurogenesis-dependent and -independent mechanisms.

The finding could lead to development of better treatments for depression and anxiety.

The mouse model is the first to permit simultaneous examination of multiple effects of antidepressant treatment in the same animal.

Not much is known about the specific molecular influences of selective serotonin reuptake inhibitors (SSRIs) and other types of antidepressants commonly prescribed for treatment of depression and anxiety disorders.

“Recently, compelling work in rodents has suggested that SSRIs may stimulate changes in a brain region called the hippocampus as well as other brain structures. For example, anxiety/depression-like changes in behavior have been linked with a decrease in cell proliferation in the hippocampus, a change that is reversed by antidepressants,” said study author Dr. Denis J. David from the University of Paris-Sud.

Previous studies have already confirmed that long-term exposure to glucocorticoids induces anxiety and a depressive-like state in rodents. Elevated glucocorticoid levels have been linked with depression and anxiety in humans.

“We developed an anxiety/depression-like model based on elevation of glucocorticoid levels that offered an easy and reliable alternative to existing models,” said David.

Chronic anti-depressant treatment reversed the behavioural dysfunctions and inhibition of hippocampal neurogenesis observed in the experimental mice.

They observed that when hippocampal neurogenesis was prevented, the efficacy of Prozac was blocked in some but not all of the behavioural paradigms.

The researchers could identify candidate genes whose expression was decreased in a brain region called the hypothalamus and normalized by Prozac.

Mice deficient in one of these genes, beta-arrestin 2, displayed a reduced response to Prozac in multiple behavioural tasks.

This indicated that beta-arrestin signalling is necessary for the antidepressant effects of Prozac.

The finding suggested that both neurogenesis-dependent and – independent mechanisms underlie antidepressant actions.

The study has been published in the latest issue of the journal Neuron. (ANI)

Indian American helps develop software for early Alzhemier diagnosis

New York, May 25 (IANS) Analysis of the brain’s MRI studies, combined with a new software program, developed by a team led by an Indian American, may permit clinicians to track and diagnose Alzheimer’s disease at an early stage.

Developed by a Massachusetts General Hospital (MGH) team, the software can accurately differentiate patients with milder versions of Alzheimer’s, from normal elderly individuals, based on anatomic differences in brain structures, affected by the disease.

“Traditionally Alzheimer’s has been diagnosed based on a combination of factors such as a neurologic exam, detailed medical history and written tests of cognitive functioning with neuroimaging…,” said Rahul Desikan of Boston University School of Medicine and co-author of the paper.

“Our findings show the feasibility and importance of using automated, MRI-based neuroatomic measures as a diagnostic marker for Alzheimer’s disease,” Desikan said, according to an MGH release.

Since drugs that may slow the progression of Alzheimer’s are in development, the ability to treat patients in the earliest stages of the disease may significantly delay progression to dementia.

These findings will appear in Brain and have been released online.

Now, software to analyse MR images and identify early Alzheimer’s disease

Washington, May 22 (ANI): Scientists at Massachusetts General Hospital (MGH) claim that they have developed a piece of software that can prove helpful in analysing MRI studies of the brain and allow diagnosis of Alzheimer’s disease and of mild cognitive impairment, a lesser form of dementia that precedes the development of Alzheimer’s by several years.

Writing about their work in the journal Brain, the researchers have revealed that their software program can accurately differentiate patients with mild cognitive impairment or Alzheimer’s disease from normal elderly individuals based on anatomic differences in brain structures known to be affected by the disease.

“Traditionally Alzheimer’s has been diagnosed based on a combination of factors – such as a neurologic exam, detailed medical history and written tests of cognitive functioning – with neuroimaging used primarily to rule out other diseases such as stroke or a brain tumor,” says Dr. Rahul Desikan, of the Martinos Center and Boston University School of Medicine, lead author of the Brain paper.

“Our findings show the feasibility and importance of using automated, MRI-based neuroanatomic measures as a diagnostic marker for Alzheimer’s disease,” he added.

The researchers point out that mild cognitive impairment occurs in about 20 percent of elderly individuals, and that 80 percent of them develop Alzheimer’s within five or six years.

Given that medications to slow the progression of Alzheimer’s are in development, they say that the ability to treat patients in the earliest stages of the disease may significantly delay progression to dementia.

With a view to finding out whether MR imaging could produce diagnostic markers for mild cognitive impairment and Alzheimer’s disease, the researchers used FreeSurfer – an openly available imaging software package developed at the Martinos Center and the University of California at San Diego – to examine a number of neuroanatomic regions across a range of normal individuals and patients with mild cognitive impairment and Alzheimer’s disease.

In the first phase of the study, they analysed MR images of 97 elderly individuals, some who had been determined to have mild cognitive impairment and others who were cognitively normal.

The researchers said that the analysis of those images led to the identification of three brain regions where structural differences distinguished the normal controls from participants with mild cognitive impairment with an accuracy of 91 percent.

Earlier pathological and imaging studies have found evidence of early Alzheimer’s disease in these three areas – the hippocampus, entorhinal cortex and the supramarginal gyrus.

The research group then analyzed imaging data from 216 individuals in the Alzheimer’s Disease Neuroimaging Database to validate the accuracy and assess the reliability of the first-phase observations.

They revealed that 94 of the individuals were normal, 58 who had mild cognitive impairment at the time of imaging and went on to develop dementia, and 65 who had probable Alzheimer’s based on their clinical symptoms.

These participants also had a series of neuropsychological tests, and samples of cerebrospinal fluid were available for many of them.

Automated MRI measures of the same three areas identified in the first phase – entorhinal cortex, hippocampus, and supramarginal gyrus – discriminated individuals with mild cognitive impairment from normal elderly controls with 95 percent accuracy, and patients with Alzheimer’s were discriminated from normal controls with 100 percent accuracy.

The MRI measures also were significantly correlated with clinical and cognitive tests of dementia, particularly memory decline, and with biomarkers of cellular pathology such as the Alzheimer’s-associated forms of the tau and amyloid proteins.

“Our results indicate that these automated MRI measures are one effective way of identifying individuals in the earliest stages of Alzheimer’s disease, but before this technology can be used clinically, several follow-up studies need to be done,” says Desikan. (ANI)

Intake of methamphetamine during pregnancy can lead to brain abnormalities in the children

Recent study has shown that intake of methamphetamine during pregnancy can lead to brain abnormalities in children. Methamphetamine is a highly addictive stimulant that is injected, snorted, smoked or swallowed by the people.

Research team led by Dr. Linda Chang of the University of Hawaii compared data collected from 29 3- and 4-year-olds whose mothers used methamphetamine during pregnancy with 37 children of the same ages whose mothers did not use the drug.

Research team used a new magnetic resonance imaging, or MRI, technique known as diffusion tensor imaging to look for abnormalities in tiny brain structures. Brain scans of the children revealed that there was a difference in the white matter structure, which carries messages across the brain, and maturation of brains of children with prenatal exposure to drug.

Dr. Linda Chang said: “Animal studies have shown if you give meth to an animal, their brain tissue becomes more densely packed.”

She said her team now plans to follow the children as they grow to see if these differences persist.

Prenatal meth exposure ’causes abnormal brain development in kids’

Washington, April 16 (ANI): Using a drug called methamphetamine during pregnancy can cause abnormal brain development in children, says a new study.

This study is the first of its kind to examine the effects of methamphetamine use during pregnancy.

“Methamphetamine use is an increasing problem among women of childbearing age, leading to an increasing number of children with prenatal meth exposure. But until now, the effects of prenatal meth exposure on the developing brain of a child were little known,” said study author Linda Chang, MD, with the John A. Burns School of Medicine, University of Hawaii at Manoa in Honolulu.

For the study, researchers conducted brain scans on 29 three and four-year-old children whose mothers used meth while pregnant and 37 unexposed children of the same ages.

The MRI scans used diffusion tensor imaging to help measure the diffusion of molecules in a child’s brain, which can indicate abnormal microscopic brain structures that might reflect abnormal brain development.

The scans revealed that children with prenatal meth exposure had differences in the white matter structure and maturation of their brains compared to unexposed children.

Researchers found that children with prenatal meth exposure had up to four percent lower diffusion of molecules in the white matter of their brains.

“Our findings suggest prenatal meth exposure accelerates brain development in an abnormal pattern. Such abnormal brain development may explain why some children with prenatal meth exposure reach developmental milestones later than others,” said Chang.

Previous studies have shown that prenatal meth exposure can lead to increased stress and lethargy and poorer quality of movement for infants.

“While we don’t know how prenatal meth exposure may lead to lower brain diffusion, less diffusion of molecules in white matter typically reflects more compact axonal fibers in the brain,” said Chang.

“This is consistent with our prior findings of smaller subcortical structures in children with prenatal meth exposure, which is the portion of the brain immediately below the cerebral cortex,” Chang added.

The study has been published in the April 15, 2009, online issue of Neurology, the medical journal of the American Academy of Neurology. (ANI)

Hormone replacement therapy ‘shrinks’ brain

Washington, Jan 13 (ANI): Hormone replacement therapy may lead to brain shrinkage in postmenopausal women, say researchers.

The study showed that volumes of brain lesions were not significantly increased among women prescribed hormone therapy, but that the total olumes of brain tissue in regions critical to memory were slightly smaller.

The research team found that women who had taken hormone therapy had slightly smaller brain volumes in two critical areas of the brain: the frontal lobe and the hippocampus.

Both areas are involved in thinking and memory skills, and loss of volume in the hippocampus is a risk factor for dementia.

“Our findings suggest one possible explanation for the increased risk for dementia in older women who had previously taken post-menopausal hormone therapy in the Women’s Health Initiative Memory Study,” said Susan Resnick, Ph.D., of the National Institute on Aging, which is part of NIH.

“Our findings suggest that hormone therapy in older post-menopausal women has a negative effect on brain structures important in maintaining normal memory functioning.

“However, this negative effect was most pronounced in women who already may have had some memory problems before using hormone therapy, suggesting that the therapy may have accelerated a neurodegenerative disease process that had already begun,” she added.

Researchers will next set out to determine whether the negative effects of hormone therapy on brain volumes continue over time through follow-up MRI studies of the women studied. (ANI)