Posts tagged neuroscience

Posts tagged neuroscience

Understanding parallels of human and animal parenting can benefit generations to come
Strong evidence now shows that human and animal parenting share many nervous system mechanisms. This is the conclusion of Yerkes National Primate Research Center researchers Larry Young, PhD, and James Rilling, PhD, in their review article about the biology of mammalian parenting, published in this week’s issue of Science. Better understanding this biology could lead to improved social development, benefitting generations of humans and animals to come.
In their article, Young and Rilling review the biological mechanisms governing a shift in mammals’ parental motivation that begins with aversion and transforms into irresistible attraction after giving birth. They say the same molecules that prepare the uterus for pregnancy, stimulate milk production and initiate labor also activate specific neural pathways to motivate parents to nurture, bond with and protect their offspring.
According to Young, “We have learned a tremendous amount about the specific hormonal and brain mechanisms regulating parental behavior and how parental nurturing influences the development of the offspring brain by using animal models, and many of these same mechanisms influence human parenting behavior as well.”
Young is division chief of Behavioral Neuroscience and Psychiatric Disorders at the Yerkes Research Center, director of the Center for Translational Social Neuroscience at Emory, a William P. Timmie professor in the Department of Psychiatry at Emory’s School of Medicine and author of The Chemistry Between Us: Love, Sex and the Science of Attraction, which also summarizes the parallels between brain mechanisms regulating sexual and parenting behaviors in animals and humans.
Rilling, who is a Yerkes researcher and an associate professor in Emory’s Department of Anthropology, adds, “The human brain has mechanisms in place to support parent-child bonding, and when functioning properly, these mechanisms facilitate the development of secure attachment and sound mental health that is transmitted across generations.”
The researchers divided their review into nine categories, including neural correlates of human parental care, two specific to parenting and oxytocin, two focused specifically on paternal caregiving by fathers and two related to the effect of parenting on social development. Examples within these categories include that the frustration inconsolable infant crying induces is a risk factor for infant abuse, highlighting the importance of emotion regulation for sensitive parenting; that oxytocin affects maternal motivation and paternal behaviors essential for nurturing, bonding and defending the offspring; that testosterone may interfere with parenting effort; and that variation in parental nurturing can affect brain development, thus affecting future social behaviors.
“With this comprehensive review, we can see nervous system correlations across species that result in positive and negative parental care,” says Young. “This information is critical to further studying social development in order to facilitate positive parental behaviors that will benefit generations to come,” he continues.
Bats bolster brain hypothesis, maybe technology, too
Amid a neuroscience debate about how people and animals focus on distinct objects within cluttered scenes, some of the newest and best evidence comes from the way bats “see” with their ears, according to a new paper in the Journal of Experimental Biology. In fact, the perception process in question could improve sonar and radar technology.
Bats demonstrate remarkable skill in tracking targets such as bugs through the trees in the dark of night. James Simmons, professor of neuroscience at Brown University, the review paper’s author, has long sought to explain how they do that.
It turns out that experiments in Simmons’ lab point to the “temporal binding hypothesis” as an explanation. The hypothesis proposes that people and animals focus on objects versus the background when a set of neurons in the brain attuned to features of an object all respond in synchrony, as if shouting in unison, “Yes, look at that!” When the neurons do not respond together to an object, the hypothesis predicts, an object is relegated to the perceptual background.
Because bats have an especially acute need to track prey through crowded scenes, albeit with echolocation rather than vision, they have evolved to become an ideal testbed for the hypothesis.
“Sometimes the most critical questions about systems in biology that relate to humans are best approached by using an animal species whose lifestyle requires that the system in question be exaggerated in some functional sense so its qualities are more obvious,” said Simmons, who plans to discuss the research at the 2014 Cold Spring Harbor Asia Conference the week of September 15 in Suzhou, China.
A focus of frequencies
Here’s how he’s determined over the years that temporal binding works in a bat. As the bat flies it emits two spectra of sound frequencies — one high and one low — into a wide cone of space ahead of it. Within the spectra are harmonic pairs of high and low frequencies, for example 33 kilohertz and 66 kilohertz. These harmonic pairs reflect off of objects and back to the bat’s ears, triggering a response from neurons in its brain. Objects that reflect these harmonic pairs in perfect synchrony are the ones that stand out clearly for the bat.
Of course it’s more complicated than just that. Many things could reflect the same frequency pairs back at the same time. The real question is how a target object would stand out. The answer, Simmons writes, comes from the physics of the echolocation sound waves and how bat brains have evolved to process their signal. Those factors conspire to ensure that whatever the bat keeps front-and-center in its echolocation cone will stand out from surrounding interference.
The higher frequency sounds in the bat’s spectrum weaken in transit through the air more than lower frequency sounds. The bat also sends out the lower frequencies to a wider span of angles than the high frequencies. So for any given harmonic pair, the farther away or more peripheral a reflecting object is, the weaker the higher frequency reflection in the harmonic pair will be. In the brain, Simmons writes, the bat converts this difference in signal strength into a delay in time (about 15 microseconds per decibel) so that harmonic pairs with wide differences in signal strength end up being perceived as way out of synchrony in time. The temporal binding hypothesis predicts that the distant or peripheral objects with these out-of-synch signals will be perceived as the background while front-and-center objects that reflect back both harmonics with equal strength will rise above their desynchronized competitors.
With support from sources including the U.S. Navy, Simmons’s research group has experimentally verified this. In key experiments (some dating back 40 years) they have sat big brown bats at the base of a Y-shaped platform with a pair of objects – one a target with a food reward and the other a distractor – on the tines of the Y. When the objects are at different distances, the bat can tell them apart and accurately crawl to the target. When the objects are equidistant, the bat becomes confused. Crucially, when the experimenters artificially weaken the high-pitched harmonic from the distracting object, even when it remains equidistant, the bat’s acumen to find the target is restored.
In further experiments in 2010 and 2011, Simmons’ team showed that if they shifted the distractor object’s weakened high-frequency signal by the right amount of time (15 microseconds per decibel) they could restore the distractor’s ability to interfere with the target object by restoring the synchrony of the distractor’s harmonics. In other words, they used the specific predictions of the hypothesis and their understanding of how it works in bats to jam the bat’s echolocation ability.
If targeting and jamming sound like words associated with radar and sonar, that’s no coincidence. Simmons works with the U.S. Navy on applications of bat echolocation to navigation technology. He recently began a new research grant from the Office of Naval Research that involves bat sonar work in collaboration with researcher Jason Gaudette at the Naval Undersea Warfare Center in Newport, R.I.
Simmons said he believes the evidence he has gathered about the neuroscience of bats not only supports the temporal binding hypothesis, but also can inspire new technology.
“This is a better way to design a radar or sonar system if you need it to perform well in real-time for a small vehicle in complicated tasks,” he said.
Kessler stroke researchers and colleagues have identified an association between over-optimistic estimation of one’s own ability to take medications accurately, and memory loss among stroke survivors. Results indicate that assessing patients for their ability to estimate medication skills accurately may predict memory disorder. The article, “Stroke survivors over-estimate their medication self-administration ability (MSA), predicting memory loss,” was epublished ahead of print on May 28 by Brain Injury. The authors are AM Barrett, MD, and J Masmela of Kessler Foundation, Elizabeth E Galletta of Hunter College, Jun Zhang of St. Charles Hospital, Port Jefferson, NY, and Uri Adler, MD, of Kessler Institute for Rehabilitation.

Researchers compared 24 stroke survivors with 17 controls, using the Hopkins Medication Schedule to assess MSA, the Geriatric Depression Scale to assess mood, and the Hopkins Verbal Test and Mini-Mental State Examination to assess memory. Results showed that stroke survivors over-estimated their MSA in comparison to controls. Over-estimation of MSA correlated strongly with verbal memory deficit.
Strategies that enhance adherence to medication are a public health priority. “Few studies, however, have looked at cognitive factors that may interfere with MSA,” commented Dr. Barrett. “While some stroke survivors have obvious cognitive deficits, many people are not aware that stroke survivors can be intelligent and high functioning, but still have trouble with thinking that can cause errors in medication self-management. These individuals may not realize their own deficits, a condition called cognitive anosognosia. Screening stroke survivors for MSA may be a useful approach to identifying memory deficits that hinder rehabilitation and community participation and contribute to poor outcomes.”
Larger studies of left and right stroke survivors need to be conducted in the community and rehabilitation settings in order to determine the underlying mechanisms for both over-estimation and under-estimation of self-performance.
(Source: kesslerfoundation.org)
New Penn Medicine research shows that neuropsychiatric symptoms such as depression, anxiety and fatigue are more common in newly diagnosed Parkinson’s disease (PD) patients compared to the general population. The study also found that initiation of dopamine replacement therapy, the most common treatment for PD, was associated with increasing frequency of impulse control disorders and excessive daytime sleepiness. The new findings, the first longitudinal study to come out of the Parkinson’s Progression Markers Initiative (PPMI), are published in the August 15, 2014, issue of Neurology®, the medical journal of the American Academy of Neurology.
The PPMI, a landmark, multicenter observational clinical study sponsored by The Michael J. Fox Foundation for Parkinson’s Research, uses a combination of advanced imaging, biologics sampling and behavioral assessments to identify biomarkers of Parkinson’s disease progression. The Penn study, which represents neuropsychiatric and cognitive data from baseline through the first 24 months of follow up, was conducted in collaboration with the Philadelphia VA Medical Center and the University Hospital Donostia in Spain.
The study examined 423 newly diagnosed, untreated Parkinson’s patients and 196 healthy controls at baseline and 281 people with PD at six months. Of these, 261 PD patients and 145 healthy controls were evaluated at 12 months, and 96 PD patients and 83 healthy controls evaluated at 24 months.
PD patients were permitted to begin dopamine therapy at any point after their baseline evaluation.
“We hypothesized that neuropsychiatric symptoms would be common and stable in severity soon after diagnosis and that the initiation of dopamine replacement therapy would modify their natural progression in some way,” says senior author, Daniel Weintraub, MD, associate professor of Psychiatry and Neurology at the Perelman School of Medicine at the University of Pennsylvania and a fellow in Penn’s Institute on Aging.
The Penn team showed that while there was no significant difference between PD patients and healthy controls in the frequency of impulse control disorders, a neuropsychiatric symptom that can lead to compulsive gambling, sexual behavior, eating or spending, 21 percent of newly diagnosed PD patients screened positive for such symptoms at baseline. That percentage did not increase significantly over the 24-month period.
However, six patients who had been on dopamine therapy for more than a year at the 24-month evaluation showed impulse control disorders or related behavior symptoms while no impulse control incident symptoms were reported in PD patients who had not commenced dopamine therapy. Dopamine therapy did help with fatigue, with 33 percent of patients improving their fatigue test score over 24 months compared with only 11 percent of patients not on dopamine therapy.
The investigators also found evidence that depression may be undertreated in early PD patients: Two-thirds of patients who screened positive for depression at any time point were not taking an antidepressant.
PPMI follows volunteers for five years, so investigators plan to expand upon these results, which Weintraub still considers preliminary. “We will more closely look at cognitive changes over time,” he says. “Two years is not a sufficient period of follow up to really look at meaningful cognitive decline.”
The perspective of time is what makes the PPMI such an important initiative, Weintraub points out, since many patients with the disease live for 10 to 20 years following their diagnosis. “It’s really a chance to assess the frequency and characteristics of psychiatric and cognitive symptoms in PD, compare it with healthy controls, and then also look at its evolution over time,” he says. “The hope is that we will be able to continue this work so that we can obtain long-term follow up data on these patients,” says Weintraub.
(Source: uphs.upenn.edu)
Do Gut Bacteria Rule Our Minds?
It sounds like science fiction, but it seems that bacteria within us — which outnumber our own cells about 100-fold — may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity.
In an article published this week in the journal BioEssays, researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way.
Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem — our digestive tracts — they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, PhD, co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF.
While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.
“Bacteria within the gut are manipulative,” said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer and corresponding author on the paper. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not.”
Fortunately, it’s a two-way street. We can influence the compatibility of these microscopic, single-celled houseguests by deliberating altering what we ingest, Maley said, with measurable changes in the microbiome within 24 hours of diet change.
“Our diets have a huge impact on microbial populations in the gut,” Maley said. “It’s a whole ecosystem, and it’s evolving on the time scale of minutes.”
There are even specialized bacteria that digest seaweed, found in humans in Japan, where seaweed is popular in the diet.
Research suggests that gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.
“Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good,” said Aktipis, who is currently in the Arizona State University Department of Psychology.
In mice, certain strains of bacteria increase anxious behavior. In humans, one clinical trial found that drinking a probiotic containing Lactobacillus casei improved mood in those who were feeling the lowest.
Maley, Aktipis and first author Joe Alcock, MD, from the Department of Emergency Medicine at the University of New Mexico, proposed further research to test the sway microbes hold over us. For example, would transplantation into the gut of the bacteria requiring a nutrient from seaweed lead the human host to eat more seaweed?
The speed with which the microbiome can change may be encouraging to those who seek to improve health by altering microbial populations. This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Optimizing the balance of power among bacterial species in our gut might allow us to lead less obese and healthier lives, according to the authors.
“Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating,” the authors wrote.
The authors met and first discussed the ideas in the BioEssays paper at a summer school conference on evolutionary medicine two years ago. Aktipis, who is an evolutionary biologist and a psychologist, was drawn to the opportunity to investigate the complex interaction of the different fitness interests of microbes and their hosts and how those play out in our daily lives. Maley, a computer scientist and evolutionary biologist, had established a career studying how tumor cells arise from normal cells and evolve over time through natural selection within the body as cancer progresses.
In fact, the evolution of tumors and of bacterial communities are linked, points out Aktipis, who said some of the bacteria that normally live within us cause stomach cancer and perhaps other cancers.
“Targeting the microbiome could open up possibilities for preventing a variety of disease from obesity and diabetes to cancers of the gastro-intestinal tract. We are only beginning to scratch the surface of the importance of the microbiome for human health,” she said.
Depression is known to be a common symptom of Parkinson’s disease, but remains untreated for many patients, according to a new study by Northwestern Medicine investigators in collaboration with the National Parkinson’s Foundation (NPF).
In fact, depression is the most prevalent non-motor symptom of Parkinson’s, a chronic neurodegenerative disorder typically associated with movement dysfunction.
“We confirmed suspicion that depression is a very common symptom in Parkinson’s disease. Nearly a quarter of the people in the study reported symptoms consistent with depression,” said Danny Bega, MD, ’14 GME, instructor in the Ken and Ruth Davee Department of Neurology and first author of the study. “This is important because previous research has determined that depression is a major determinant of overall quality of life.”
Using the NPS’s patient database, the investigators looked at records of more than 7,000 people with Parkinson’s disease. Among those with high levels of depressive symptoms, only one-third had been prescribed antidepressants before the study began, and even fewer saw social workers or mental health professionals for counseling.
The investigators then focused their analysis on the remaining two-thirds of patients with depressive symptoms who were not receiving treatment at the start of the study. Throughout a year of observation, less than 10 percent of them received prescriptions for antidepressants or referrals to counseling. Physicians were most likely to identify depression and advocate treatment for patients with the severest depression scores.
The findings were published in the Journal of Parkinson’s Disease.
“The majority of these patients remained untreated,” said Dr. Bega. “Still, the physician recognition of depression in this population was actually better than previous reports had suggested.”
However, recognition may be lower for the general population of patients with Parkinson’s disease – the patients in this study visited medical centers deemed “Centers of Excellence” by the NPF.
“Physicians must be more vigilant about screening patients for depression as part of a routine assessment of Parkinson’s disease, and the effectiveness of different treatments for depression in this population need to be assessed,” said Dr. Bega.
(Source: feinberg.northwestern.edu)
Following another person’s gaze can reveal a wealth of information critical to social interactions and also to safety. Gaze following typically emerges in infancy, and new research looking at preterm infants suggests that it’s visual experience, not maturational age, that underlies this critical ability.
The research is published in Psychological Science, a journal of the Association for Psychological Science.

“To the best of our knowledge, this is the first study showing that some aspects of the early development of social cognition is influenced by experience, even when the human brain is highly immature,” says psychological scientist Marcela Peña of Pontificia Universidad Católica de Chile, lead researcher on the study. “Our results are important for modeling early cognitive development.”
Previous research on early cognitive development suggests that some cognitive functions develop only after the brain has matured sufficiently, while other cognitive functions develop in response to a rich social environment.
To disentangle the roles played by neural maturation and environmental exposure in relation to gaze following, Peña and colleagues decided to compare the gaze following abilities of preterm and full-term infants.
“Because preterm infants are exposed to face-to-face interactions earlier (in terms of postmenstrual age) than infants who are born at term, they may become sensitive to gaze direction sooner as well,” the researchers explain.
A total of 81 healthy infants participated in the study and they were split into four groups: Full-term 4-month-olds, full-term 7-month-olds, preterm 7-month-olds, and preterm 10-month-olds.
The preterm infants were born 2.5 to 3 months early – thus, full-term 4-month-olds and preterm 7-month-olds had an equivalent postmenstrual age of about 13 months, but the preterm 7-month-olds had an additional 2.5 to 3 months of visual experience as a result of having entered the world early.
While sitting in his or her mother’s lap, the infants were presented with a sound and visual cue to grab their attention. As soon as they were looking at the screen, a video of a woman appeared and the woman made peek-a-boo like gestures. The woman then turned her head and directed her gaze toward one side of the screen; subsequently, a moving toy appeared on each side of the screen. Using an eyetracking system adapted for infants, the researchers were able to monitor which side of the screen infants looked to first. The researchers repeated this procedure with each infant 20 times.
The data showed that preterm 7-month-olds and preterm 10-month-olds behaved like full-term 7-month-olds, looking to the toy on the side of the screen indicated by the woman’s gaze. Full-term 4-month-olds, on the other hand, tended to look randomly to either side.
This pattern of results held even when the woman indicated direction with only her eyes, while her head continued to face forward.
Together, these findings suggest that exposure to visual experience outside the womb may matter most for early gaze following.
“Combined with previous results on vision and language cognition, our results support the idea that the early steps of human cognition develops in an asynchronous way,” says Peña. “Some systems are more or less sensitive to external stimulation, but others can be more influenced by biological maturation.”

(Image caption: This image shows an artificial connection that connects brain to spinal circuits. Credit: © Yukio Nishimura)
Bypass commands from the brain to legs through a computer
Gait disturbance in individuals with spinal cord injury is attributed to the interruption of neural pathways from brain to the spinal locomotor center, whereas neural circuits locate below and above the lesion maintain most of their functions. An artificial connection that bridges the lost pathway and connects brain to spinal circuits has potential to ameliorate the functional loss. A Japanese research group led by Shusaku Sasada, research fellow and Yukio Nishimura, associate professor of the National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences (NINS) has successfully made an artificial connection from the brain to the locomotion center in the spinal cord by bypassing with a computer interface. This allowed subjects to stimulate the spinal locomotion center using volitionally-controlled muscle activity and to control walking in legs. This result was published online in The Journal of Neuroscience on August 13, 2014.
Neural networks in the spinal cord, locomotion center are capable of producing rhythmic movements, such as swimming and walking, even when isolated from the brain. The brain controls spinal locomotion center by sending command to the spinal locomotion center to start, stop and change waking speed. In most cases of spinal cord injury, the loss of this link from the brain to the locomotion center causes problems with walking.
The research group came up with bypassing the functioning brain and locomotion center with the computer to compensate lost pathways as a way to enable individuals with spinal cord injury to regain walking ability.
Since the arm movement associate with leg movement when we walk they used muscle activity of arm to sarogate the brain activity. The computer interface allowed subjects to control magnetic stimulator that drive to the spinal locomotion center non-invassively using volitionally-controlled muscle activity and to control walking in legs. As a results of experiments in people who are neurologically intact, the subjects were asked to make own legs relaxed and passively controlled via computer interface that was controlled by arm muscle, walking behavior in legs was induced and subjects could control the step cycle volitionally as well. However without bypassing with the computer interface, the legs did not move even if the arms muscle was volitionally acivated.
"We hope that this technology would compensate for the interrupted pathways’ function by sending an intentionally encoded command to the preserved spinal locomotor center and regain volitionally-controlled walking in indviduals with paraplegia. However, the major challenge that this technology does not help them to dodge obstacles and to maintain posture. We are carefully working toward clinical application in near future", Nishimura said.
A new technique developed by Elisa Konofagou, professor of biomedical engineering and radiology at Columbia Engineering, has demonstrated for the first time that the size of molecules penetrating the blood-brain barrier (BBB) can be controlled using acoustic pressure—the pressure of an ultrasound beam—to let specific molecules through. The study was published in the July issue of the Journal of Cerebral Blood Flow & Metabolism.

“This is an important breakthrough in getting drugs delivered to specific parts of the brain precisely, non-invasively, and safely, and may help in the treatment of central nervous system diseases like Parkinson’s and Alzheimer’s,” says Konofagou, whose National Institutes of Health Research Project Grant (R01) funding was just renewed for another four years for an additional $2.22 million. The award is for research to determine the role of the microbubble in controlling both the efficacy and safety of drug safety through the BBB with a specific application for treating Parkinson’s disease.
Most small—and all large—molecule drugs do not currently penetrate the blood-brain barrier that sits between the vascular bed and the brain tissue. “As a result,” Konofagou explains, “all central nervous system diseases remain undertreated at best. For example, we know that Parkinson’s disease would benefit by delivery of therapeutic molecules to the neurons so as to impede their slow death. But because of the virtually impermeable barrier, these drugs can only reach the brain through direct injection and that requires anesthesia and drilling the skull while also increasing the risk of infection and limiting the number of sites of injection. And transcranial injections rarely work—only about one in ten is successful.”
Focused ultrasound in conjunction with microbubbles—gas-filled bubbles coated by protein or lipid shells—continues to be the only technique that can permeate the BBB safely and non-invasively. When microbubbles are hit by an ultrasound beam, they start oscillating and, depending on the magnitude of the pressure, continue oscillating or collapse. While researchers have found that focused ultrasound in combination with microbubble cavitation can be successfully used in the delivery of therapeutic drugs across the BBB, almost all earlier studies have been limited to one specific-sized agent that is commercially available and widely used clinically as ultrasound contrast agents. Konofagou and her team were convinced there was a way to induce a size-controllable BBB opening, enabling a more effective method to improve localized brain drug delivery.
Konofagou targeted the hippocampus, the memory center of the brain, and administered different-sized sugar molecules (Dextran). She found that higher acoustic pressures led to larger molecules accumulating into the hippocampus as confirmed by fluorescence imaging. This demonstrated that the pressure of the ultrasound beam can be adjusted depending on the size of the drug that needs to be delivered to the brain: all molecules of variant sizes were able to penetrate the opened barrier but at distinct pressures, i.e., small molecules at lower pressures and larger molecules at higher pressures.
“Through this study, we’ve been able to show, for the first time, that we can control the BBB opening size through the use of acoustic pressure,” says Konofagou. “We’ve also learned much more about the physical mechanisms associated with the trans-BBB delivery of different-sized agents, and understanding the BBB mechanisms will help us to develop agent size-specific focused ultrasound treatment protocols.”
Konofagou and her Ultrasound Elasticity Imaging Laboratory team plan to continue to work on the treatment of Alzheimer’s and Parkinson’s in a range of models, and hope to test their technique in clinical trials within the next five years.
“It is frightening to think that in the 21st century we still have no idea how to treat most brain diseases,” Konofagou adds. “But we’re really excited because we now have a tool that could potentially change the current dire predictions that come with a neurological disorder diagnosis.”
(Source: engineering.columbia.edu)
People with schizophrenia struggle to turn goals into actions because brain structures governing desire and emotion are less active and fail to pass goal-directed messages to cortical regions affecting human decision-making, new research reveals.
Published in Biological Psychiatry, the finding by a University of Sydney research team is the first to illustrate the inability to initiate goal-directed behaviour common in people with schizophrenia.
The finding may explain why people with schizophrenia have difficulty achieving real-world goals such as making friends, completing education and finding employment.
"The apparent lack of motivation in schizophrenic patients isn’t because they lack goals or don’t enjoy rewards and pleasure," says the University of Sydney’s Dr Richard Morris, the study’s lead author.
"They enjoy as many experiences as other people, including food, movies and scenes of natural beauty.
"What appears to block them are specific brain deficits that prevent them from converting their desires and goals into choices and behaviour."
Using a control group research design, the researchers used a two-prong approach to reveal how and why schizophrenics fail to convert their preferences into congruent choices.
First, using a series of experiments involving choosing between different snack food rewards, experimenters revealed that:
Second, researchers used functional magnetic resonance imaging (fMRI) to measures brain activity while study subjects performed learning tasks involving snack foods.
This technique relies on the fact that cerebral blood flow and neuronal activity are coupled. When an area of the brain is in use, bloodflow to that region increases, thereby indicating neural activity. This neural activity can be presented graphically by colour-coding the strength of activation across the brain or in specific brain regions. The technique can localise neural activity to within millimetres.
Functional MRI results revealed the following:
"Pathology in the caudate and associated brain regions may prevent schizophrenic subjects from properly evaluating their desires then transmitting that information to guide their behavior," says Dr Morris.
"This means that desires and goals are intact in people with schizophrenia, however they have difficulty choosing the right course of action to achieve those goals.
"This failure to integrate desire with action means people with schizophrenia are stuck in limbo, wanting a normal life but unable to take the necessary steps to achieve it."
Schizophrenia affects one per cent of people worldwide, including in Australia.
However so-called “poor motivation” in schizophrenia is a major economic concern because it is not treated by current medicines, and often means patients fail to finish their education or hold a full-time job.
(Source: sydney.edu.au)