How the brain copes with multi-tasking alters with age

The pattern of blood flow in the prefrontal cortex in the brains alters with age during multi-tasking, finds a new study in BioMed Central’s open access journal BMC Neuroscience. Increased blood volume, measured using oxygenated haemoglobin (Oxy-Hb) increased at the start of multitasking in all age groups. But to perform the same tasks, healthy older people had a higher and more sustained increase in Oxy-Hb than younger people.

Age related changes to the brain occur earliest in the prefrontal cortex, the area of the brain associated with memory, emotion, and higher decision making functions. It is changes to this area of the brain that are also associated with dementia, depression and other neuropsychiatric disorders. Some studies have shown that regular physical activity and cognitive training can prevent cognitive decline (use it or lose it!) but to establish what occurs in a healthy aging brain researchers from Japan and USA have compared brain activity during single and dual tasks for young (aged 21 to 25) and older (over 65) people.

Near infrared spectroscopy (NIRS) measurements of Oxy-Hb showed that blood flow to the prefrontal cortex was not affected by the physical task for either age group but was affected by the mental task. For both the young and the over 65s the start of the calculation task  coincided with an increase in blood volume which reduced to baseline once the task was completed.

The main difference between the groups was only seen when performing the physical and mental tasks at the same time - older people had a higher prefrontal cortex response which lasted longer than the younger group.

Hironori Ohsugi, from Seirei Christopher University, and one of the team who performed this research explained “From our observations during the dual task it seems that the older people turn their attention to the calculation at the expense of the physical task, while younger people are able to maintain concentration on both. Since our subjects were all healthy it seems that this requirement for increased activation of the prefrontal cortex is part of normal decrease in brain function associated with aging. Further study will show whether or not dual task training can be used to maintain a more youthful brain.”

(Image: Photos.com)

Is Athleticism Linked to Brain Size?

To find out, researchers at the University of California, Riverside performed laboratory experiments on house mice and found that mice that have been bred for dozens of generations to be more exercise-loving have larger midbrains than those that have not been selectively bred this way.

Theodore Garland’s lab measured the brain mass of these uniquely athletic house mice, bred for high voluntary wheel-running, and analyzed their high-resolution brain images. The researchers found that the volume of the midbrain — a small region of the brain that relays information for the visual, auditory, and motor systems — in the bred-for-athleticism mice was nearly 13 percent larger than the midbrain volume in the control or “regular” mice.

“To our knowledge, this is the first example in which selection for a particular mammalian behavior — high voluntary wheel running in house mice in our set of experiments — has been shown to result in a change in size of a specific brain region,” said Garland, a professor of biology and the principal investigator of the research project.

Study results appeared online Jan. 16 in The Journal of Experimental Biology

Individuals with a low risk for cocaine dependence have a differently shaped brain to those with addiction

People who take cocaine over many years without becoming addicted have a brain structure which is significantly different from those individuals who developed cocaine-dependence, researchers have discovered. New research from the University of Cambridge has found that recreational drug users who have not developed a dependence have an abnormally large frontal lobe, the section of the brain implicated in self-control. Their research was published in the journal Biological Psychiatry.

For the study, led by Dr Karen Ersche, individuals who use cocaine on a regular basis underwent a brain scan and completed a series of personality tests. The majority of the cocaine users were addicted to the drug but some were not (despite having used it for several years).

The scientists discovered that a region in the frontal lobes of the brain, known to be critically implicated in decision-making and self-control, was abnormally bigger in the recreational cocaine users. The Cambridge researchers suggest that this abnormal increase in grey matter volume, which they believe predates drug use, might reflect resilience to the effects of cocaine, and even possibly helps these recreational cocaine users to exert self-control and to make advantageous decisions which minimize the risk of them becoming addicted.

They found that this same region in the frontal lobes of the brain was significantly reduced in size in people with cocaine dependence, confirming earlier research that had found similar results. They believe that at least some of these changes are the result of drug use, which causes drug users to lose grey matter.

They also found that people who use illicit drugs like cocaine exhibit high levels of sensation-seeking personality traits, but only those developing dependence show personality traits of impulsivity and compulsivity.

Dr Ersche, of the Behavioural and Clinical Neuroscience Institute (BCNI) at the University of Cambridge, said: “These findings are important because they show that the use of cocaine does not inevitably lead to addiction in people with good self-control and no familial risk.

“Our findings indicate that preventative strategies might be more effective if they were tailored more closely to those individuals at risk according to their personality profile and brain structure.”

The researchers will next explore the basis of the recreational users’ apparent resilience to drug dependence. Dr Ersche added: “Their high level of education, less troubled family background or the beginning of drug-taking only after puberty may all play a role.”

Mouse Research Links Adolescent Stress and Severe Adult Mental Illness

Working with mice, Johns Hopkins researchers have established a link between elevated levels of a stress hormone in adolescence - a critical time for brain development - and genetic changes that, in young adulthood, cause severe mental illness in those predisposed to it.

The findings, reported in the journal Science, could have wide-reaching implications in both the prevention and treatment of schizophrenia, severe depression and other mental illnesses.

"We have discovered a mechanism for how environmental factors, such as stress hormones, can affect the brain’s physiology and bring about mental illness," says study leader Akira Sawa, M.D., Ph.D., a professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine. "We’ve shown in mice that stress in adolescence can affect the expression of a gene that codes for a key neurotransmitter related to mental function and psychiatric illness. While many genes are believed to be involved in the development of mental illness, my gut feeling is environmental factors are critically important to the process."

Sawa, director of the Johns Hopkins Schizophrenia Center, and his team set out to simulate social isolation associated with the difficult years of adolescents in human teens. They found that isolating healthy mice from other mice for three weeks during the equivalent of rodent adolescence had no effect on their behavior. But, when mice known to have a genetic predisposition to characteristics of mental illness were similarly isolated, they exhibited behaviors associated with mental illness, such as hyperactivity. They also failed to swim when put in a pool, an indirect correlate of human depression. When the isolated mice with genetic risk factors for mental illness were returned to group housing with other mice, they continued to exhibit these abnormal behaviors, a finding that suggests the effects of isolation lasted into the equivalent of adulthood.

"Genetic risk factors in these experiments were necessary, but not sufficient, to cause behaviors associated with mental illness in mice," Sawa says. "Only the addition of the external stressor - in this case, excess cortisol related to social isolation - was enough to bring about dramatic behavior changes."

The investigators not only found that the “mentally ill” mice had elevated levels of cortisol, known as the stress hormone because it’s secreted in higher levels during the body’s fight-or-flight response. They also found that these mice had significantly lower levels of the neurotransmitter dopamine in a specific region of the brain involved in higher brain function, such as emotional control and cognition. Changes in dopamine in the brains of patients with schizophrenia, depression and mood disorders have been suggested in clinical studies, but the mechanism for the clinical impact remains elusive.

Light Exposure During Pregnancy Key to Normal Eye Development

New research in Nature concludes the eye – which depends on light to see – also needs light to develop normally during pregnancy.

Scientists say the unexpected finding offers a new basic understanding of fetal eye development and ocular diseases caused by vascular disorders – in particular one called retinopathy of prematurity that can blind premature infants. The research, led by scientists at Cincinnati Children’s Hospital Medical Center and the University of California, San Francisco (UCSF), appears online Jan. 16 ahead of print publication.

“This fundamentally changes our understanding of how the retina develops,” says study co-author Richard Lang, PhD, a researcher in the Division of Pediatric Ophthalmology at Cincinnati Children’s Hospital Medical Center. “We have identified a light-response pathway that controls the number of retinal neurons. This has downstream effects on developing vasculature in the eye and is important because several major eye diseases are vascular diseases.”

Lang is a principal investigator on the ongoing research along with project collaborator, David Copenhagen, PhD, a scientist in the departments of Ophthalmology and Physiology at UCSF. The scientists say their current study, conducted in mouse models, includes several unexpected findings.

"Several stages of mouse eye development occur after birth," says Copenhagen. "Because of this, we had always assumed that if light played a role in the development of the eye, it would also happen only after birth."

But researchers in the current study found that activation of the newly described light-response pathway must happen during pregnancy to activate the carefully choreographed program that produces a healthy eye. Specifically, they say it is important for a sufficient number of photons to enter the mother’s body by late gestation, or about 16 days into a mouse pregnancy.

Researchers were also surprised to learn that photons of light activate a protein called melanopsin directly in the fetus – not the mother – to help initiate normal development of blood vessels and retinal neurons in the eye.

One purpose of the light-response pathway is to suppress the number of blood vessels that form in the retina. These vessels are critical to retinal neurons, which require large amounts of oxygen to form and to function. When retinopathy of prematurity occurs in infants, retinal vessels grow almost unchecked. This continued expansion puts intense pressure on the developing eye and in extreme cases causes severe damage and blindness.

The research team led by Lang and Copenhagen conducted several experiments in laboratory mouse models that allowed them to identify the light-response pathway’s specific components and function.

Mice were reared in the dark and in a normal day-night cycle beginning at late gestation to observe the comparative effects on vascular development of the eye. The researchers verified the function of the light response pathway by mutating an opsin gene in mice called Opn4 that produces melanopsin, in essence preventing activation of the photo pigment.

Both mice reared under dark conditions from late gestation, and those with mutated Opn4, exhibited nearly identical promiscuous expansion of hyaloid vessels and abnormal retinal vascular growth. The unchecked vascular growth was driven by the protein vascular endothelial growth factor (Vegfa). When the light response pathway is properly engaged, it modulates Vegfa to help prevent promiscuous vascular growth, according to researchers.

The melanopsin protein is present in both mice and humans during pregnancy. Lang said the research team is continuing to study how the light-response pathway might influence the susceptibility of pre-term infants to retinopathy of prematurity and also be related to other diseases of the eye.

New research finds slower growth of preterm infants linked to altered brain development

Preterm infants who grow more slowly as they approached what would have been their due dates also have slower development in an area of the brain called the cerebral cortex, report Canadian researchers in a new study published in Science Translational Medicine.

The cerebral cortex is a two to four millimetre layer of cells that envelopes the top part of the brain and is involved in cognitive, behavioural, and motor processes.

Researchers analyzed MRI brain scans of 95 preterm infants born eight to 16 weeks too early at BC Women’s Hospital & Health Centre between 2006 and 2009. Infants were scanned soon after birth and a second time close to what would have been their due date, the ninth month of pregnancy. These MRI scans allowed researchers to measure the pattern of water movement inside the brain, which normally changes between scans as the brain matures. The researchers also assessed the babies’ weight, length, and head size. They found that preterm infants with slower growth had delayed development in the cerebral cortex compared to those infants who grew more quickly between scans.

“These results are an exciting first step because understanding the importance of growth in relation to the brain in these small babies may eventually lead to new discoveries that will help us optimize their brain development,” says Dr. Steven Miller, the study’s co‐lead. Dr. Miller is head of neurology at The Hospital for Sick Children (SickKids), the Bloorview Children’s Hospital Chair in Paediatric Neuroscience, professor in the department of Paediatrics at the University of Toronto, affiliate professor in the department of Pediatrics at the University of British Columbia (UBC), and affiliate investigator at the Child & Family Research Institute (CFRI) at BC Children’s Hospital. He led the study with Dr. Ruth Grunau, a professor in the UBC Department of Pediatrics and CFRI senior scientist.

“More research needs to be done to understand what is the optimal growth rate for the brain development of these babies,” says Jillian Vinall, the study’s first author and a UBC PhD student cosupervised by Dr. Grunau and Dr. Miller.

We’re especially grateful to the families for their generous and ongoing participation in this study,” says Dr. Miller. The researchers are following the babies through childhood to understand how preterm brain development is associated with their neurodevelopment outcomes.

Promising new finding for therapies to treat persistent seizures in epileptic patients

In a promising finding for epileptic patients suffering from persistent seizures known as status epilepticus, researchers reported today that new medication could help halt these devastating seizures. To do so, it would have to work directly to antagonize NMDA receptors, the predominant molecular device for controlling synaptic activity and memory function in the brain.

"Despite the development of new medications to prevent seizures, status epilepticus remains a life-threatening condition that can cause extensive brain damage in the patients that survive these persistent seizures," said David E. Naylor, MD, PhD, a lead researcher at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) and corresponding author of the new study. "Our research holds promise for the development of new therapies to treat this devastating condition because we have found a potential new target for medical intervention that should bolster the current standard therapies to treat the acute seizures. It may also prevent the long-term adverse effects of persistent seizure activity on the brain."

The research, reported online in the Neurology of Disease journal, used animal models to assess cellular activity in the brain during persistent seizures. It found that the seizure activity seemed to force the NMDA receptors from the interior to the surface of nerve cells causing their activity to increase by approximately 38%.

"The increased presence of the NMDA receptors on the cell surface during these seizures may explain the successful use of NMDA antagonists – medication that inhibits the activity of the NMDA receptors in the brain – in the latter stages of a seizure, long after other medications have stopped working," said Dr. Naylor. "We concluded that medications that suppress the activity of the NMDA receptors, in conjunction with other medications, may be successful in stopping persistent seizures. Further research is, of course, needed."

Scanning the Brain: Scientists Examine the Impact of fMRI Over the Past 20 Years

Understanding the human brain is one of the greatest scientific quests of all time, but the available methods have been very limited until recently. The development of functional magnetic resonance imaging (fMRI) — a tool used to gauge real-time brain activity by measuring changes in blood flow — opened up an exciting new landscape for exploration.

Now, twenty years after the first fMRI study was published, a group of distinguished psychological scientists reflect on the contributions fMRI has made to our understanding of human thought. Their reflections are published as part of a special section of the January 2013 issue of Perspectives on Psychological Science, a journal of the Association for Psychological Science.

In the last two decades, many researchers have used fMRI to try to answer various questions about the brain and mind. But some are not convinced of its usefulness.

“Despite the many new methods and results derived from fMRI research, some have argued that fMRI has done very little to advance knowledge about cognition and, in particular, has done little to advance theories about cognitive processes,” write Mara Mather, Nancy Kanwisher, and John Cacioppo, editors of the special section.

The aim of the special section is to tackle the question of how fMRI results have (or have not) changed the way we think about human psychology and the brain, resulting in a collection of 12 provocative articles.

Some of the authors argue that fMRI has fundamentally changed that way that researchers think about the aging mind. According to researchers Tor Wager and Lauren Atlas, fMRI may also provide a more direct way of measuring pain.

Others discuss the contributions fMRI has made to the longstanding debate about whether cognitive operations are modular or distributed across domains. And some emphasize the reciprocal relationship between fMRI and cognitive theories, highlighting how each informs the others.

As appealing as fMRI images might be, researchers Martha Farah and Cayce Hook find little support for the claim that fMRI data has a “seductive allure” that makes it more persuasive than other types of data.

In their concluding commentary, Mather, Cacioppo, and Kanwisher argue that fMRI does provide unique insights to our understanding of cognition. But, as powerful as it is, the researchers acknowledge that there are some questions fMRI will never answer.

“The best approach to answering questions about cognition,” say Mather, Cacioppo, and Kanwisher, “is a synergistic combination of behavioral and neuroimaging methods, richly complemented by the wide array of other methods in cognitive neuroscience.”

(Image courtesy of Glasgow University)

New Technique Helps Stroke Victims Communicate

Stroke victims affected with loss of speech caused by Broca’s aphasia have been shown to speak fluidly through the use of a process called “speech entrainment” developed by researchers at the University of South Carolina’s Arnold School of Public Health.

Aphasia, a severe communication problem caused by damage to the brain’s left hemisphere and characterized by halting speech, occurs in about one-third of people who have a stroke and affects personal and professional relationships. Using the speech entrainment technique, which involves mimicking other, patients showed significant improvement in their ability to speak.

The results of the study are published in a recent issue of the neurology journal Brain.

"This is the first time that we have seen people with Broca’s aphasia speak in fluent sentences,” said Julius Fridriksson, the study’s lead researcher and a professor with the Department of Communication Sciences and Disorders at the Arnold School. “It is a small study that gives us an understanding of how the brain functions after a stroke, and it offers hope for thousands of people who suffer strokes each year."

In Fridriksson’s study, 13 patients completed three separate behavioral tasks that were used to understand the effects of speech entrainment on speech production. During the “speech entrainment–audio visual" portion of the study, participants attempted to mimic a speaker in real-time whose mouth was made visible on the 3.5-inch screen of an iPod Touch and whose speech was heard via headphones.

The “speech entrainment–audio only” condition involved real-time mimicking speech presented via headphones with the screen of the iPod blank. During a spontaneous speech condition, patients spoke about a given topic without external aid.

Each patient also completed a three-week training phase where they practiced speech every day with the aid of speech entrainment. Overall, the training resulted in improved spontaneous speech production, something that is relatively rare in this population. Ultimately the patients were able to produce a short script about their stroke to tell to other people.

Neuroimaging results from the patient subjects have also given Fridriksson and his research team a greater understanding of the mechanism involved in speech entrainment.

"Preliminary results suggest that training with speech entrainment improves speech production in Broca’s aphasia, providing a potential therapeutic method for a disorder that has been shown to be particularly resistant to treatment," Fridriksson said.