Tag: dopamine

Oleh Hornykiewicz, Who Discovered Parkinson’s Treatment, Dies at 93

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Oleh Hornykiewicz in his Vienna office in 2009 He helped identify low dopamine levels as a cause of Parkinson’s disease, a finding that led to an effective treatment.

Oleh Hornykiewicz, a Polish-born pharmacologist whose breakthrough research on Parkinson’s disease has spared millions of patients the tremors and other physical impairments it can cause, died on May 27 in Vienna. He was 93.

His death was confirmed by his longtime colleague, Professor Stephen J. Kish of the University of Toronto, where Professor Hornykiewicz (pronounced whor-nee-KEE-eh-vitch) taught from 1967 until his retirement in 1992.

Professor Hornykiewicz was among several scientists who were considered instrumental in first identifying a deficiency of the neurotransmitter dopamine as a cause of Parkinson’s disease, and then in perfecting its treatment with L-dopa, an amino acid found in fava beans.

The Nobel laureate Dr. Arvid Carlsson and his colleagues had earlier shown that dopamine played a role in motor function. Drawing on that research, Professor Hornykiewicz and his assistant, Herbert Ehringer, discovered in 1960 that the brains of patients who had died of Parkinson’s had very low levels of dopamine.

He persuaded another one of his collaborators, the neurologist Walther Birkmayer, to inject Parkinson’s patients with L-dopa, the precursor of dopamine, which could cross the barrier between blood vessels and the brain and be converted into dopamine by enzymes in the body, thus replenishing those depleted levels. The treatment alleviated symptoms of the disease, and patients who had been bedridden started walking.

The initial results of this research were published in 1961 and presented at a meeting of the Medical Society of Vienna. The “L-dopa Miracle,” as it was called, inspired Dr. Oliver Sacks’s memoir “Awakenings” (1973) and the fictionalized movie of the same name in 1990.
As a therapy for Parkinson’s, L-dopa was further refined by other scientists, including George C. Cotzias and Melvin D. Yahr. But it was Professor Hornykiewicz, defying colleagues who had argued that post-mortem brain studies were worthless, who is credited with the critical breakthroughs.

His findings spurred the establishment of human brain tissue banks, research into dopamine and treatments of other diseases caused by low levels of neurotransmitters.

“Today, it is generally agreed that the initiation of the treatment of Parkinson’s disease with L-dopa represented one of the triumphs of pharmacology of our time,” Professor Hornykiewicz wrote in “The History of Neuroscience in Autobiography, Volume IV” (2004). “This provided, apart from the benefit to the patients, a stimulus for analogous studies of many other brain disorders, both neurological and psychiatric.”

He received several distinguished awards, including the Wolf Prize in Medicine in 1979 and the Ludwig Wittgenstein Prize of the Austrian Research Foundation in 1993.

In 2000, when Dr. Carlsson, of Sweden, and others were awarded the Nobel Prize in Physiology or Medicine for discovering dopamine and “allowing for the development of drugs for the disease,” as the Nobel committee wrote, more than 200 scientists signed a petition protesting that the prize had not also been awarded to Professor Hornykiewicz.

Oleh Hornykiewicz was born on Nov. 17, 1926, in the village of Sychow, near Lviv, in what was then southeastern Poland and is now western Ukraine. His was a fourth-generation family of Eastern Orthodox Catholic priests. His father, Theophil Hornykiewicz, ministered to the village’s several dozen parishioners and taught religion; his mother, Anna (Sas-Jaworsky) Hornykiewicz, managed the affairs of the village’s 300-year-old wooden church.

When the Soviet Union invaded in 1939, the family fled to Austria, his mother’s ancestral home, with whatever belongings they could carry. Oleh knew no German but learned it by reading Hitler’s “Mein Kampf,” which was readily available in Vienna. He suffered from tuberculosis and, when the war ended, decided to follow his eldest brother and become a doctor.

He received his medical degree from the University of Vienna in 1951 and began his academic and research career in its pharmacology department. He held a British Council Research Scholarship at the University of Oxford from 1956 to 1958. Beginning in 1967, he headed the psychopharmacology department at the Clarke Institute of Psychiatry in Toronto (now the Center for Addiction and Mental Health), where he established the Human Brain Laboratory in 1978.

He was named a full professor of pharmacology and psychiatry at the University of Toronto in 1973 and, in 1976, appointed to head the newly-founded Institute of Biochemical Pharmacology of the University of Vienna. He held both posts concurrently.

He is survived by his daughter, Maria Hentosz; three sons, Nicholas, Stephen and Joseph; six grandchildren; and one great-grandchild. His wife, Christina (Prus-Jablonowski) Hornykiewicz, had died.

“He was a pharmacologist, biochemist and neurologist who wanted to find out how the brain works and how dopamine was involved,” Professor Kish said. “And he wanted to be known also as a philosopher.”

Despite being snubbed by the Nobel committee, Professor Hornykiewicz was philosophical about what he had accomplished and the degree to which it had been credited.

“I am surprised to see that I have achieved everything I could have wished for,” he wrote in 2004. “The support and recognition I received for my work, I have accepted with gratitude, as a charming reminder to do more and better.”

Professor Kish, who heads the Human Brain Laboratory at the University of Toronto’s Centre for Addiction and Mental Health, said L-dopa, or Levodopa, as it is also called, is today “the mainstay treatment for Parkinson’s disease — no drug is more efficacious.”

“Hornykiewicz,” he added, “reminds us that before L-dopa, persons with Parkinson’s disease were bedridden, crowding chronic hospital wards, and the doctors were powerless to do anything. His discovery changed all that —- it was a miracle.”

https://bioreports.net/oleh-hornykiewicz-who-discovered-parkinsons-treatment-dies-at-93/

How information is like snacks, money, and drugs—to your brain

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By Laura Counts

Can’t stop checking your phone, even when you’re not expecting any important messages? Blame your brain.

A new study by researchers at UC Berkeley’s Haas School of Business has found that information acts on the brain’s dopamine-producing reward system in the same way as money or food.

“To the brain, information is its own reward, above and beyond whether it’s useful,” says Assoc. Prof. Ming Hsu, a neuroeconomist whose research employs functional magnetic imaging (fMRI), psychological theory, economic modeling, and machine learning. “And just as our brains like empty calories from junk food, they can overvalue information that makes us feel good but may not be useful—what some may call idle curiosity.”

The paper, “Common neural code for reward and information value,” was published this month by the Proceedings of the National Academy of Sciences. Authored by Hsu and graduate student Kenji Kobayashi, now a post-doctoral researcher at the University of Pennsylvania, it demonstrates that the brain converts information into the same common scale as it does for money. It also lays the groundwork for unraveling the neuroscience behind how we consume information—and perhaps even digital addiction.

“We were able to demonstrate for the first time the existence of a common neural code for information and money, which opens the door to a number of exciting questions about how people consume, and sometimes over-consume, information,” Hsu says.

Rooted in the study of curiosity

The paper is rooted in the study of curiosity and what it looks like inside the brain. While economists have tended to view curiosity as a means to an end, valuable when it can help us get information to gain an edge in making decisions, psychologists have long seen curiosity as an innate motivation that can spur actions by itself. For example, sports fans might check the odds on a game even if they have no intention of ever betting.

Sometimes, we want to know something, just to know.

“Our study tried to answer two questions. First, can we reconcile the economic and psychological views of curiosity, or why do people seek information? Second, what does curiosity look like inside the brain?” Hsu says.

The neuroscience of curiosity

To understand more about the neuroscience of curiosity, the researchers scanned the brains of people while they played a gambling game. Each participant was presented with a series of lotteries and needed to decide how much they were willing to pay to find out more about the odds of winning. In some lotteries, the information was valuable—for example, when what seemed like a longshot was revealed to be a sure thing. In other cases, the information wasn’t worth much, such as when little was at stake.

For the most part, the study subjects made rational choices based on the economic value of the information (how much money it could help them win). But that didn’t explain all their choices: People tended to over-value information in general, and particularly in higher-valued lotteries. It appeared that the higher stakes increased people’s curiosity in the information, even when the information had no effect on their decisions whether to play.

The researchers determined that this behavior could only be explained by a model that captured both economic and psychological motives for seeking information. People acquired information based not only on its actual benefit, but also on the anticipation of its benefit, whether or not it had use.

Hsu says that’s akin to wanting to know whether we received a great job offer, even if we have no intention of taking it. “Anticipation serves to amplify how good or bad something seems, and the anticipation of a more pleasurable reward makes the information appear even more valuable,” he says.

Common neural code for information and money

How does the brain respond to information? Analyzing the fMRI scans, the researchers found that the information about the games’ odds activated the regions of the brain specifically known to be involved in valuation (the striatum and ventromedial prefrontal cortex or VMPFC), which are the same dopamine-producing reward areas activated by food, money, and many drugs. This was the case whether the information was useful, and changed the person’s original decision, or not.

Next, the researchers were able to determine that the brain uses the same neural code for information about the lottery odds as it does for money by using a machine learning technique (called support vector regression). That allowed them to look at the neural code for how the brain responds to varying amounts of money, and then ask if the same code can be used to predict how much a person will pay for information. It can.

In other words, just as we can convert such disparate things as a painting, a steak dinner, and a vacation into a dollar value, the brain converts curiosity about information into the same common code it uses for concrete rewards like money, Hsu says.

“We can look into the brain and tell how much someone wants a piece of information, and then translate that brain activity into monetary amounts,” he says.

Raising questions about digital addiction

While the research does not directly address overconsumption of digital information, the fact that information engages the brain’s reward system is a necessary condition for the addiction cycle, he says. And it explains why we find those alerts saying we’ve been tagged in a photo so irresistible.

“The way our brains respond to the anticipation of a pleasurable reward is an important reason why people are susceptible to clickbait,” he says. “Just like junk food, this might be a situation where previously adaptive mechanisms get exploited now that we have unprecedented access to novel curiosities.”

How information is like snacks, money, and drugs—to your brain

New tiny sensors track dopamine in the brain for more than a year, and could be useful for monitoring patients with Parkinson’s and other diseases.

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Mit-Dopamine-Tracking_0

By Anne Trafton

Dopamine, a signaling molecule used throughout the brain, plays a major role in regulating our mood, as well as controlling movement. Many disorders, including Parkinson’s disease, depression, and schizophrenia, are linked to dopamine deficiencies.

MIT neuroscientists have now devised a way to measure dopamine in the brain for more than a year, which they believe will help them to learn much more about its role in both healthy and diseased brains.

“Despite all that is known about dopamine as a crucial signaling molecule in the brain, implicated in neurologic and neuropsychiatric conditions as well as our abilty to learn, it has been impossible to monitor changes in the online release of dopamine over time periods long enough to relate these to clinical conditions,” says Ann Graybiel, an MIT Institute Professor, a member of MIT’s McGovern Institute for Brain Research, and one of the senior authors of the study.

Michael Cima, the David H. Koch Professor of Engineering in the Department of Materials Science and Engineering and a member of MIT’s Koch Institute for Integrative Cancer Research, and Rober Langer, the David H. Koch Institute Professor and a member of the Koch Institute, are also senior authors of the study. MIT postdoc Helen Schwerdt is the lead author of the paper, which appears in the Sept. 12 issue of Communications Biology.

Long-term sensing

Dopamine is one of many neurotransmitters that neurons in the brain use to communicate with each other. Traditional systems for measuring dopamine — carbon electrodes with a shaft diameter of about 100 microns — can only be used reliably for about a day because they produce scar tissue that interferes with the electrodes’ ability to interact with dopamine.

In 2015, the MIT team demonstrated that tiny microfabricated sensors could be used to measure dopamine levels in a part of the brain called the striatum, which contains dopamine-producing cells that are critical for habit formation and reward-reinforced learning.

Because these probes are so small (about 10 microns in diameter), the researchers could implant up to 16 of them to measure dopamine levels in different parts of the striatum. In the new study, the researchers wanted to test whether they could use these sensors for long-term dopamine tracking.

“Our fundamental goal from the very beginning was to make the sensors work over a long period of time and produce accurate readings from day to day,” Schwerdt says. “This is necessary if you want to understand how these signals mediate specific diseases or conditions.”

To develop a sensor that can be accurate over long periods of time, the researchers had to make sure that it would not provoke an immune reaction, to avoid the scar tissue that interferes with the accuracy of the readings.

The MIT team found that their tiny sensors were nearly invisible to the immune system, even over extended periods of time. After the sensors were implanted, populations of microglia (immune cells that respond to short-term damage), and astrocytes, which respond over longer periods, were the same as those in brain tissue that did not have the probes inserted.

In this study, the researchers implanted three to five sensors per animal, about 5 millimeters deep, in the striatum. They took readings every few weeks, after stimulating dopamine release from the brainstem, which travels to the striatum. They found that the measurements remained consistent for up to 393 days.

“This is the first time that anyone’s shown that these sensors work for more than a few months. That gives us a lot of confidence that these kinds of sensors might be feasible for human use someday,” Schwerdt says.

Paul Glimcher, a professor of physiology and neuroscience at New York University, says the new sensors should enable more researchers to perform long-term studies of dopamine, which is essential for studying phenomena such as learning, which occurs over long time periods.

“This is a really solid engineering accomplishment that moves the field forward,” says Glimcher, who was not involved in the research. “This dramatically improves the technology in a way that makes it accessible to a lot of labs.”

Monitoring Parkinson’s

If developed for use in humans, these sensors could be useful for monitoring Parkinson’s patients who receive deep brain stimulation, the researchers say. This treatment involves implanting an electrode that delivers electrical impulses to a structure deep within the brain. Using a sensor to monitor dopamine levels could help doctors deliver the stimulation more selectively, only when it is needed.

The researchers are now looking into adapting the sensors to measure other neurotransmitters in the brain, and to measure electrical signals, which can also be disrupted in Parkinson’s and other diseases.

“Understanding those relationships between chemical and electrical activity will be really important to understanding all of the issues that you see in Parkinson’s,” Schwerdt says.

The research was funded by the National Institute of Biomedical Imaging and Bioengineering, the National Institute of Neurological Disorders and Stroke, the Army Research Office, the Saks Kavanaugh Foundation, the Nancy Lurie Marks Family Foundation, and Dr. Tenley Albright.

https://news.mit.edu/2018/brain-dopamine-tracking-sensors-0912

Eye tests may predict schizophrenia

On By A.P.In Neuropsychiatric Disease, Parkinson's disease, Psychosis, schizophreniaLeave a comment

Schizophrenia is associated with structural and functional alterations of the visual system, including specific structural changes in the eye. Tracking such changes may provide new measures of risk for, and progression of the disease, according to a literature review published online in the journal Schizophrenia Research: Cognition, authored by researchers at New York Eye and Ear Infirmary of Mount Sinai and Rutgers University.

Individuals with schizophrenia have trouble with social interactions and in recognizing what is real. Past research has suggested that, in schizophrenia, abnormalities in the way the brain processes visual information contribute to these problems by making it harder to track moving objects, perceive depth, draw contrast between light and dark or different colors, organize visual elements into shapes, and recognize facial expressions. Surprisingly though, there has been very little prior work investigating whether differences in the retina or other eye structures contribute to these disturbances.

“Our analysis of many studies suggests that measuring retinal changes may help doctors in the future to adjust schizophrenia treatment for each patient,” said study co-author Richard B. Rosen, MD, Director of Ophthalmology Research, New York Eye and Ear Infirmary of Mount Sinai, and Professor of Ophthalmology, Icahn School of Medicine at Mount Sinai. “More studies are needed to drive the understanding of the contribution of retinal and other ocular pathology to disturbances seen in these patients, and our results will help guide future research.”

The link between vision problems and schizophrenia is well established, with as many as 62 percent of adult patients with schizophrenia experience visual distortions involving form, motion, or color. One past study found that poorer visual acuity at four years of age predicted a diagnosis of schizophrenia in adulthood, and another that children who later develop schizophrenia have elevated rates of strabismus, or misalignment of the eyes, compared to the general population.

Dr. Rosen and Steven M. Silverstein, PhD, Director of the Division of Schizophrenia Research at Rutgers University Behavioral Health Care, were the lead authors of the analysis, which examined the results of approximately 170 existing studies and grouped the findings into multiple categories, including changes in the retina vs. other parts of the eye, and changes related to dopamine vs. other neurotransmitters, key brain chemicals associated with the disease.

The newly published review found multiple, replicated, indicators of eye abnormalities in schizophrenia. One of these involves widening of small blood vessels in the eyes of schizophrenia patients, and in young people at high risk for the disorder, perhaps caused by chronic low oxygen supply to the brain. This could explain several key vision changes and serve as a marker of disease risk and worsening. Also important in this regard was thinning of the retinal nerve fiber layer in schizophrenia, which is known to be related to the onset of hallucinations and visual acuity problems in patients with Parkinson’s disease. In addition, abnormal electrical responses by retinal cells exposed to light (as measured by electroretinography) suggest cellular-level differences in the eyes of schizophrenia patients, and may represents a third useful measure of disease progression, according to the authors.

In addition, the review highlighted the potentially detrimental effects of dopamine receptor-blocking medications on visual function in schizophrenia (secondary to their retinal effects), and the need for further research on effects of excessive retinal glutamate on visual disturbances in the disorder.

Interestingly, the analysis found that there are no reports of people with schizophrenia who were born blind, suggesting that congenital blindness may completely or partially protect against the development of schizophrenia. Because congenitally blind people tend to have cognitive abilities in certain domains (e.g., attention) that are superior to those of healthy individuals, understanding brain re-organization after blindness may have implications for designing cognitive remediation interventions for people with schizophrenia.

“The retina develops from the same tissue as the brain,” said Dr. Rosen. “Thus retinal changes may parallel or mirror the integrity of brain structure and function. When present in children, these changes may suggest an increased risk for schizophrenia in later life. Additional research is needed to clarify these relationships, with the goals of better predicting emergence of schizophrenia, and of predicting relapse and treatment response and people diagnosed with the condition.”

Dr. Silverstein points out that, to date, vision has been understudied in schizophrenia, and studies of the retina and other ocular structures in the disorder are in their infancy. However, he added, “because it is much faster and less expensive to obtain data on retinal structure and function, compared to brain structure and function, measures of retinal and ocular structure and function may have an important role in both future research studies and the routine clinical care of people with schizophrenia.”

http://www.eurekalert.org/pub_releases/2015-08/tmsh-rcm081715.php

Medication for Parkinson’s disease shown to lower morality and increase willingness to harm others

On By A.P.In Depression, morality, neurodegeneration, Neurology, Neuropsychiatric Disease, Parkinson's disease, Psychiatry, psychologist, psychology, psychopath, psychopathic personality, psychopathyLeave a comment


Healthy people who are given commonly prescribed mood-altering drugs see significant changes in the degree to which they are willing to tolerate harm against themselves and others, according to a study published Thursday. The research has implications for understanding human morality and decision-making.

A team of scientists from the University College London (UCL) and Oxford University found that healthy people who were given the serotonin-boosting antidepressant citalopram were willing to pay twice as much to prevent harm to themselves or others, compared to those given a placebo. By contrast, those who were given a dose of the dopamine-enhancing Parkinson’s drug levodopa made more selfish decisions, overcoming an existing tendency to prefer harming themselves over others.

The researchers said their findings, published in the journal Current Biology, provided clues to the neurological and chemical roots of common clinical disorders like psychopathy, which causes people to disregard the emotions of others.

The researchers compared how much pain subjects were willing to anonymously inflict on themselves or other people in exchange for money. Out of 175 subjects, 89 were given citalopram or a placebo and 86 were given levodopa or a placebo.

They were anonymously paired up into decision-makers and receivers, and all subjects were given shocks at their pain threshold. The decision-makers were then allowed to choose a different amount of money in exchange for a different amount of shocks, either to themselves or the receivers.

On average, people who were given a placebo were willing to pay about 35p per shock to prevent harm to themselves and 44p per shock to prevent harm to others. Those who were given citalopram became more averse to harm, paying an average of 60p to avoid harm to themselves and 73p per shock to avoid harm to others. This meant that citalopram users, on average, delivered 30 fewer shocks to themselves and 35 fewer shocks to others.

However, those who were given levodopa became more selfish, showing no difference in the amount they were willing to pay to prevent shocks to themselves or others. On average, they were willing to pay about 35p per shock to prevent harm to themselves or others, meaning that they delivered on average about 10 more shocks to others during the trial than those who took a placebo. They also showed less hesitation about shocking others than those given the placebo.

Similar research conducted by the same team in November found that subjects were willing to spare the stranger pain twice as often as they spared themselves, indicating that they preferred harming themselves over others for profit, a behavior known as “hyper-altruism.”

“Our findings have implications for potential lines of treatment for antisocial behavior, as they help us to understand how serotonin and dopamine affect people’s willingness to harm others for personal gain,” Molly Crockett of UCL, the study’s lead author, said in a press release. “We have shown that commonly-prescribed psychiatric drugs influence moral decisions in healthy people, raising important ethical questions about the use of such drugs.

“It is important to stress, however, that these drugs may have different effects in psychiatric patients compared to healthy people. More research is needed to determine whether these drugs affect moral decisions in people who take them for medical reasons.”

http://www.ibtimes.com/antidepressants-affect-morality-decision-making-new-study-finds-1995363

$5 Insanity’: 5 Crazy Facts About Flakka

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A new drug that gives people superhuman strength, but leads to violent delusions, is gaining attention.

The drug, which has the street name of Flakka, is a synthetic stimulant that is chemically similar to bath salts. Flakka is fast developing a reputation for what seem to be its nasty side effects, including a tendency to give people enormous rage and strength, along with intense hallucinations.”

Even though addicted, users tell us they are literally afraid of this drug,” said James Hall, an epidemiologist at the Center for Applied Research on Substance Use and Health Disparities at Nova Southeastern University in Florida. “As one user recently reported, it’s $5 insanity.”

From what it is to how it may work, here are five facts about Flakka.

1. What is it?

Flakka, which is also called gravel in some parts of the country, is the street name for a chemical called alpha-PVP, or alpha-pyrrolidinovalerophenone. The chemical is a synthetic cathinone, a category that includes the mild natural stimulant khat, which people in Somalia and the Middle East have chewed for centuries. Chemically, Flakka is a next-generation, more powerful version of bath salts. Flakka was banned by the Drug Enforcement Administration in early 2014.

2. What are its effects?

At low doses, Flakka is a stimulant with mild hallucinatory effects.

Like cocaine and methamphetamine, Flakka stimulates the release of feel-good brain chemicals such as dopamine and norepinephrine, Hall said. The drug also prevents neurons, or brain cells, from reabsorbing these brain chemicals, meaning the effects of the drug may linger in the system longer than people anticipate.

3. What are the dangers?

The danger comes from the drug’s incredible potency. A typical dose is just 0.003 ounces (0.1 grams), but “just a little bit more will trigger very severe adverse effects,” Hall told Live Science. “Even a mild overdose can cause heart-related problems, or agitation, or severe aggression and psychosis.”

Because of the drug’s addictive properties, users may take the drug again shortly after taking their first dose, but that can lead to an overdose, Hall said. Then, users report, “they can’t think,” and will experience what’s known as the excited delirium syndrome: Their bodies overheat, often reaching 105 degrees Fahrenheit, they will strip off their clothes and become violent and delusional, he said. The drug also triggers the adrenaline-fueled fight-or-flight response, leading to the extreme strength described in news reports.

“Police are generally called, but it might take four or five or six officers to restrain the individual,” Hall said.

At that point, emergency responders will try to counteract the effects of the drug in the person’s system by injecting a sedative such as the benzodiazepine Ativan, and if they can’t, the person can die, Hall said.

In the last several months, 10 people have died from Flakka overdoses, he said. (Users of PCP, Ecstasy, cocaine and methamphetamine can also experience the excited delirium syndrome.)

4. How is it sold?

According to Hall’s research, alpha-PVP is often purchased online in bulk from locations such as China, typically at $1,500 per kilogram. Doses typically sell on the street for $4 or $5, and because each dose is so tiny, that means dealers can net about $50,000 from their initial investment, as long as they have the networks to distribute the drug.

5. Why are we only hearing about it now?

Evidence suggests the illegal drug has only recently come on the scene. Crime lab reports from seized drugs reveal that seizures of alpha-PVP have soared, from 699 samples testing positive for the drug in 2010, to 16,500 in 2013, according to the Drug Enforcement Administration’s National Forensic Laboratory Information System.

About 22 percent of the drug seizures that tested positive for alpha-PVP came from South Florida, according to the data.

http://www.livescience.com/50502-what-is-flakka.html

New research may help explain why curiosity promotes better memory

On By A.P.In aged brain, ageing, aging, brain, dopamine, hippocampus, Human Behavior, learning, LiveScience, Medicine, memory, mental concentration, MRI, Neurology, Neuron, Neuropsychiatric Disease, Neuroscience, neuroscientistLeave a comment

Everyone knows it’s easier to learn about a topic you’re curious about. Now, a new study reveals what’s going on in the brain during that process, revealing that such curiosity may give a person a memory boost.

When participants in the study were feeling curious, they were better at remembering information even about unrelated topics, and brain scans showed activity in areas linked to reward and memory.

The results, detailed October 2 in the journal Neuron, hint at ways to improve learning and memory in both healthy people and those with neurological disorders, the researchers said.

“Curiosity may put the brain in a state that allows it to learn and retain any kind of information, like a vortex that sucks in what you are motivated to learn, and also everything around it,” Matthias Gruber, a memory researcher at the University of California, Davis, said in a statement. “These findings suggest ways to enhance learning in the classroom and other settings.”

Gruber and his colleagues put people in a magnetic resonance imaging (MRI) scanner and showed them a series of trivia questions, asking them to rate their curiosity about the answers to those questions. Later, the participants were shown selected trivia questions, then a picture of a neutral face during a 14-second delay, followed by the answer. Afterward, the participants were given a surprise memory test of the faces, and then a memory test of the trivia answers.

Not surprisingly, the study researchers found that people remembered more information about the trivia when they were curious about the trivia answers. But unexpectedly, when the participants were curious, they were also better at remembering the faces, an entirely unrelated task. Participants who were curious were also more likley than others to remember both the trivia information and unrelated faces a day later, the researchers found.

The brain scans showed that, compared with when their curiosity wasn’t piqued, when people were curious, they showed more activation of brain circuits in the nucleus accumbens, an area involved in reward. These same circuits, mediated by the neurochemical messenger dopamine, are involved in forms of external motivation, such as food, sex or drug addiction.

Finally, being curious while learning seemed to produce a spike of activity in the hippocampus, an area involved in forming new memories, and strengthened the link between memory and reward brain circuits.

The study’s findings not only highlight the importance of curiosity for learning in healthy people, but could also give insight into neurological conditions. For example, as people age, their dopamine circuits tend to deteriorate, so understanding how curiosity affects these circuits could help scientists develop treatments for patients with memory disorders, the researchers said.

http://www.livescience.com/48121-curiosity-boosts-memory-learning.html