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Can Parkinson’s disease be prevented by exercise? - The Washington Post
But studies have found it actually doesn’t have to be every day or even for very long. A 2010 study of over 200,000 people found that men and women in their 30s who engaged in one to three hours per week of moderate to vigorous exercise had a significantly lower risk of getting Parkinson’s disease later in life (for men, by 17 percent and for women, by 39 percent). That risk declined even further with more hours exercised each week. For seven or more hours, for example, men had a 30 percent reduced risk and women had a 53 percent reduced risk.
High-intensity Exercise Can Reverse Neurodegeneration in Parkinson’s Disease < Yale School of Medicine
Following the six-month program, brain imaging showed a significant increase in both the neuromelanin and DAT signals in the substantia nigra. This suggests that high-intensity exercise not only slowed down the neurodegenerative process, but also helped the dopaminergic system grow healthier.
“Where we would have ordinarily expected to see a decline in the DAT and neuromelanin signals, we saw an increase,” says Bart de Laat, PhD, associate professor adjunct in psychiatry and the study’s first author. “We had hoped to see that the neurodegeneration would not progress as quickly or stop temporarily, but instead we saw an increase in nine out of 10 people. That was remarkable.”
The study highlights the importance of including an exercise regimen as part of one’s Parkinson’s treatment plan. “The medications we have available are only for symptomatic treatment. They do not change the disease course,” says Tinaz. “But exercise seems to go one step beyond and protect the brain at the neuronal level.”
High-intensity Exercise Can Reverse Neurodegeneration in Parkinson’s Disease < Yale School of Medicine
Prior research has shown that many forms of exercise are linked to improved symptoms of Parkinson’s disease. But there has been no evidence that hitting the gym could create changes at the brain level. Now, a small proof-of-concept study involving 10 patients showed that high-intensity aerobic exercise preserved dopamine-producing neurons, the brain cells that are most vulnerable to destruction in patients with the disease.
In fact, after six months of exercise, the neurons actually had grown healthier and produced stronger dopamine signals. Dopamine is a chemical that helps brain cells communicate with each other.
Differences in Dopamine Signals in Patients With History of Alcohol Use Disorder - Neuroscience News
“We’ve shown before that dopamine levels in humans seems to track information related to regret and relief,” Kishida said. Previous research suggests that learning from regret is impaired in patients with alcohol use disorder.
“In our study, dopamine measurements, at these really fast timescales, appear altered in patients with a history of alcohol use disorder. When their choice was the best it could have been, we see dopamine levels falling when we expected it to increase like we observed in patients without alcohol use disorder,” Kishida said.
Dopamine makes you feel happy, but we probably still have to rewrite the textbooks -- ScienceDaily
"ADHD drugs are a type of amphetamine that targets and blocks DAT. This means that not all dopamine returns to the cell for reuse, and we may have difficulty feeling rewarded. It is even worse with a substance such as cocaine which completely blocks DAT, preventing all dopamine from returning to the cell. This means that the nerve cells will continue to want more cocaine until there is no more dopamine left and you start to feel depressed," Claus Juul Løland explains.
Insulin in the brain influences dopamins levels -- ScienceDaily
Analysis of the study showed that the intranasal administration of insulin lowered dopamine levels and led to changes in the brain's network structure. "The study provides direct evidence of how and where in the brain signals triggered after eating -- such as insulin release and the reward system -- interact," said Professor Martin Heni, last author of the study, summarizing the results. "We were able to show that insulin is able to decrease dopamine levels in the striatum in normal-weight individuals. The insulin-dependent change in dopamine levels was also associated with functional connectivity changes in whoe-brain networks. Changes in this system may be an important driver of obesity and related diseases."
Home is the new coke
he study demonstrates that a signal for pleasure -- dopamine -- rises rapidly when mice are moved from a simple recording chamber to their home cage, but less so when they are returned to a cage not quite like the one they knew. Prior studies have shown that rodents will actively choose their home cage over a look-alike environment. Using a sensor for dopamine placed in the mouse brain's key reward center, FAU scientists are the first to demonstrate that home evokes a surge of dopamine that mimics the response to a dose of cocaine.
Scientists find neurochemicals have unexpectedly profound roles in the human brain: Dopamine, serotonin involved in sub-second perception, cognition -- ScienceDaily
"An enormous number of people throughout the world are taking pharmaceutical compounds to perturb the dopamine and serotonin transmitter systems to change their behavior and mental health," said P. Read Montague, senior author of the study and a professor and director of the Center for Human Neuroscience Research and the Human Neuroimaging Laboratory at the Fralin Biomedical Research Institute at Virginia Tech Carilion. "For the first time, moment-to-moment activity in these systems has been measured and determined to be involved in perception and cognitive capacities. These neurotransmitters are simultaneously acting and integrating activity across vastly different time and space scales than anyone expected."
Better understanding of the underlying actions of dopamine and serotonin during perception and decision-making could deliver important insight into psychiatric and neurological disorders, the researchers said.
"Every choice that someone executes involves taking in information, interpreting that information, and making decisions about what they perceived," said Kenneth Kishida, a corresponding author of the study and an assistant professor of physiology and pharmacology, and neurosurgery, at Wake Forest School of Medicine. "There's a whole host of psychiatric conditions and neurological disorders where that process is altered in the patients, and dopamine and serotonin are prime suspects."
In mice, alcohol dependence results in brain-wide remodeling of functional architecture -- ScienceDaily
"The neuroscience of addiction has made tremendous progress, but the focus has always been on a limited number of brain circuits and neurotransmitters, primarily dopaminergic neurons, the amygdala and the prefrontal cortex," said senior author Olivier George, PhD, associate professor in the Department of Psychiatry at UC San Diego School of Medicine.
"Research groups have been fighting for years about whether 'their' brain circuit is the key to addiction. Our results confirm these regions are important, but the fact that we see such a massive remodeling of the functional brain architecture was a real shock. It's like studying the solar system and then discovering that there is an entire universe behind it. It shows that if you really want to understand the neurobiological mechanisms leading to addiction, you can't just look at a handful of brain regions, you need to look at the entire brain, you need to take a step back and consider the whole organ."
George said the findings further undermine the idea that addiction is simply a psychological condition or consequence of lifestyle. "You would be surprised at how prevalent this view remains," he said. "The brain-wide remodeling of the functional architecture observed here is not 'normal.' It is not observed in a naïve animal. It is not observed in an animal that drinks recreationally. It is only observed in animals with a history of alcohol dependence and it is massive. Such a decrease in brain modularity has been observed in numerous brain disorders, including Alzheimer's disease, traumatic brain injury and seizure disorders."
Brain modularity is the theory that there are functionally specialized regions in the brain responsible for different, specific cognitive processes. For example, the frontal lobes of the human brain are involved in executive functions, such as reasoning and planning, while the fusiform face area located in the lower rear of the brain is involved in recognizing faces.
Reduced modularity, said George, likely interferes with "normal neuronal activity and information processing and contributes to cognitive impairment, emotional distress and intense craving observed in mice during abstinence from alcohol."
Due to the format of the testing, George said it was not clear if the reduced modularity was permanent. "So far, we only know that it lasts at least one week into abstinence. We have not tested longer durations of abstinence, but it's one of our goals."
Effect of D2 Antagonists in Smokers With Schizophrenia
Nicotine use in individuals with schizophrenia is extremely common, with recent estimates indicating that 80% of individuals with this condition smoke.[1] Greater smoking in this population has been linked to worse symptoms,[2] susceptibility to respiratory and cardiovascular diseases, and early mortality;[3] hence, reducing smoking in these patients is a key priority. Evidence suggests that patients taking first-generation antipsychotics, many of which produce potent dopamine (DA) D2 receptor antagonism, experience greater difficulty quitting with evidence-based cessation treatment.[4,5] Because these medications are foundational to the management of schizophrenia, an important question is whether DA D2 receptor antagonists modulate nicotine's reinforcing effects.
Cycles of reward: New insight into ADHD treatment: Neural processes involved in ADHD -- ScienceDaily
Neurons release dopamine in different ways: phasic release is characterized by quick, high intensity spikes in the neurotransmitter, often in response to motivational stimuli like drugs or sugary treats. Tonic release, on the other hand, refers to slower, more regular firings of dopamine neurons, and is involved in muscle and joint movements.
Wickens and his collaborators initially thought that, since methylphenidate blocks the reuptake of dopamine by receptors in the brain, that the drug should increase the phasic dopamine signal. Rather, after analyzing their data, the researchers found the opposite: methylphenidate did not increase phasic dopamine. To explain this finding, Wickens suspects that the brain has a remarkably powerful feedback mechanism to keep the brain's dopamine levels in check, even when reuptake is blocked by methyphenidate.
"When you use methylphenidate in the intact brain there's a neural regulation mechanism to compensate for the direct effects of the drug," said Wickens. "Methylphenidate's therapeutic effects could be indirect consequences of this feedback loop."
The computer modeling suggests that methylphenidate primarily impacts the tonic dopamine signal. Shifts in tonic dopamine signaling may activate dopamine receptors in ways that improve the symptoms of ADHD.
"We know with flies, just like in mammals, there are neurons involved in positive reinforcement, there are neurons involved in negative reinforcement -- the valence neurons -- and then there are this third set," Tomchik says. "Nobody really knew what they did."
The fruit fly brain contains eight groups of neurons that produce dopamine. Three of them can be found in what's known as the fly brain's "mushroom body." Humans don't have an exact analogous brain section, but other brain regions perform similar functions. In Drosophila melanogaster, aka the fruit fly, the mushroom body is an area highly responsive to odors.
Past fly brain studies have shown that one of the dopamine-producing groups projecting into the mushroom body handles desire-inducing memories connected to odors. ("Mmmm, rotten bananas!") while another guides avoidant behavior related to negative experiences. ("Yikes, dangerous banana smell!")
To find out the role of the third group, referred to as PPL2, research associate and first author Tamara Boto, PhD, trained the flies with an experiment that involved exposing them to fruit-like odors while simultaneously giving them a mild electric shock.
Their conditioned response could be visualized under a microscope by adding a green fluorescent protein that releases light upon reacting to calcium. Calcium ions are released when neurons communicate. Stimulating the PPL2 neurons during the odor experiments changed the brightness of the fluorescence when presented with the odor, an indication that the structures involved in learning and memory had altered the degree of response.
"When we activated this PPL2 set of neurons, it would actually modulate the strength of that memory," Tomchik says. "So we see there are dopaminergic neurons that encode the aversive stimulus itself, and then there is this additional set that can turn the volume up or down on that memory."
Sensor created to detect dopamine, brain disorders, in seconds -- ScienceDaily
Current methods to detect dopamine are time consuming, require rigorous sample preparation, including blood-plasma separation, as well as specialized laboratory equipment. With this device, however, a few drops of blood on a palm-sized, rectangular chip is all that is needed.
"A neurotransmitter like dopamine is an important chemical to monitor for our overall well-being so we can help screen out neural disorders like Parkinson's disease, various brain cancers, and monitor mental health," said Debashis Chanda, an associate professor in UCF's NanoScience Technology Center and the study's principle investigator. "We need to monitor dopamine so that we can adjust our medical doses to help address those problems."
Plasma is separated from the blood within the chip. Cerium oxide nanoparticles, which coat the sensor surface, selectively capture dopamine at microscopic levels from the plasma. The capture of dopamine molecules subsequently changes how light is reflected from the sensor and creates an optical readout indicating the level of dopamine.
Gut Bacteria Linked to Depression Identified – Neuroscience News
Mireia Valles-Colomer (VIB-KU Leuven): ‘Many neuroactive compounds are produced in the human gut. We wanted to see which gut microbes could participate in producing, degrading, or modifying these molecules. Our toolbox not only allows to identify the different bacteria that could play a role in mental health conditions, but also the mechanisms potentially involved in this interaction with the host. For example, we found that the ability of microorganisms to produce DOPAC, a metabolite of the human neurotransmitter dopamine, was associated with better mental quality of life.’
Dopamine modulates reward experiences elicited by music -- ScienceDaily
Researchers pharmacologically manipulated the dopaminergic transmission of twenty-seven participants while they were listening to music and showed for the first time a causal link between dopamine and musical pleasure and motivation. While the dopamine precursor levodopa increased the hedonic experience and motivational responses, such as willingness to purchase a song, the dopamine antagonist risperidone led to a reduction of both. These results critically shed new light on the neurobiology and neurochemistry underpinning reward responses, contributing to an open debate on human pleasures.
Dopamine's different roles in different circuits
“Our work delineates for the first time the precise brain circuitry in which learning about rewarding and aversive outcomes occurs,” Lammel said. “Having separate neuronal correlates for appetitive and aversive behavior in our brain may explain why we are striving for ever-greater rewards while simultaneously minimizing threats and dangers. Such balanced behavior of approach-and-avoidance learning is surely helpful for surviving competition in a constantly changing environment.”
The newly discovered role for dopamine aligns with an increasing recognition that the neurotransmitter has quite different roles in different areas of the brain, exemplified by its function in voluntary movement, which is affected in Parkinson’s disease. The results also explain earlier conflicting experiments, some of which showed that dopamine increases in response to aversive stimuli, while others did not.
What if the Placebo Effect Isn’t a Trick? - The New York Times
The discovery of this genetic correlation to placebo response set Hall off on a continuing effort to identify the biochemical ensemble she calls the placebome — the term reflecting her belief that it will one day take its place among the other important “-omes” of medical science, from the genome to the microbiome. The rs4680 gene snippet is one of a group that governs the production of COMT, and COMT is one of a number of enzymes that determine levels of catecholamines, a group of brain chemicals that includes dopamine and epinephrine. (Low COMT tends to mean higher levels of dopamine, and vice versa.) Hall points out that the catecholamines are associated with stress, as well as with reward and good feeling, which bolsters the possibility that the placebome plays an important role in illness and health, especially in the chronic, stress-related conditions that are most susceptible to placebo effects.
Dopamine Drives Early Addiction to Heroin - Neuroscience News
To prove that increased dopamine directly causes drug reinforcement, the team looked at the effects of silencing dopamine in mice with a well-established heroin addiction and were consistently self-administering the drug using a lever. They found that when they silenced the dopamine neurons, the mice were much less likely to self-administer heroin. Crucially, when they did this early in the addiction phase, the mice were less likely to develop the habit of self-administering heroin. This showed that activation of dopamine neurons in the nucleus accumbens is required for the early positive reinforcing effects of opioid drugs.
Just a few drinks can change how memories are formed -- ScienceDaily
One of the downstream dominos in the signaling pathway affected by alcohol is a gene called dopamine-2-like receptor, which makes a protein on neurons that recognizes dopamine, the "feel-good" neurotransmitter.
"The dopamine-2-like receptor is known to be involved in encoding whether a memory is pleasing or aversive," Petruccelli said. And alcohol hijacks this conserved memory pathway to form cravings.
In the case of the alcohol reward pathway studied, the signaling cascade didn't turn the dopamine receptor gene on or off, or increase or decrease the amount of protein made, Kaun said. Instead, it had a subtler effect -- it changed the version of the protein made by a single amino acid "letter" in an important area.
"We don't know what the biological consequences of that small change are, but one of the important findings from this study is that scientists need to look not only at which genes are being turned on and off, but which forms of each gene are getting turned on and off," Kaun said. "We think these results are highly likely to translate to other forms of addiction, but nobody has investigated that."
New target of alcohol in the brain -- ScienceDaily
"The KCNK13 channel is absolutely required for alcohol to stimulate the release of dopamine by these neurons," said Mark Brodie, professor of physiology and biophysics in the UIC College of Medicine and lead author of the study. "Without the channel, alcohol can't stimulate the release of dopamine, and so drinking is likely less rewarding. We think that the KCNK13 channel presents an extremely exciting new target for drugs that could potentially help people with alcohol use disorder to stop drinking."
Dads' Nicotine Use May Cause Cognitive Problems for Children and Grandchildren - Neuroscience News
Analysis of spermatozoa from the original nicotine-exposed males indicated that promoter regions of multiple genes had been epigenetically modified, including the dopamine D2 gene, critical for brain development and learning, suggesting that these modifications likely contributed to the cognitive deficits in the descendants.
Connection Between Dopamine and Behavior Related to Pain and Fear - Neuroscience News
The researchers subjected the animals to small electric shocks, but also taught the animals how to escape the shocks by pressing a small lever. Using optogenetics, they controlled the amount of dopamine released by neurons in the nucleus accumbens. Animals with high levels of dopamine in this brain region learned to avoid a shock more quickly and more often than animals that had a lower level of dopamine in this region.
The researchers also examined the role that endocannabinoids play in this process. Endocannabinoids, brain chemicals that resemble the active ingredients in marijuana, play key roles in many brain processes. Here, Dr. Cheer and his colleagues found that endocannabinoids essentially open the gate that allows the dopamine neurons to fire. When the researchers reduced the level of endocannabinoids, the animals were much less likely to move to avoid shocks.
Exercise Can Help Beat Cocaine Addiction - Neuroscience News
Using animal models, Thanos found that regular aerobic exercise (one hour on a treadmill, five times a week) decreased stress-induced cocaine-seeking behavior. Exercise also altered behavioral and physiological responses to stress.
Individuals who are addicted to cocaine have altered neural, behavioral and physiological responses to stress. Recent research by Thanos demonstrated how exercise can alter the brain’s mesolimbic dopamine pathway, which is linked to the rewarding and reinforcing properties of drugs such as cocaine.
In addition, exercise has been shown to reduce stress hormones and elevate mood, which could assist in alleviating anxiety and negative emotions associated with withdrawal.
Reward and unease are closely linked in the brain -- ScienceDaily
One of the key components of the reward system is the signal substance dopamine, which acts as a chemical messenger between nerve cells. Dopamine stimulates motivation and causes animals and humans to exert themselves to achieve anything that is experienced as rewarding. When the researchers examined the dopamine-based signalling in the brain, they saw that the dopamine level in normal mice fell in the reward centre of the brain when the animals experienced something unpleasant. In contrast, it increased slightly in the mice that lacked melanocortin 4 receptors.
"It seems that this receptor in some way prevents danger signals from activating the reward system. If the receptor is missing, the danger signals will gain access to the reward system and activate it. This means that mice that lack the receptor will seek out things that are associated with danger or discomfort," says David Engblom.
Why folks coming off stimulants have panic attacks
After conditioning rats to associate a specific sound (think of it as their Jaws music) with an aversive experience (a mild footshock), the team then began the extinction process. As expected, when the sound was played many times without the footshock, rats stopped behaving as if they were afraid of the sound. However, when VTA dopamine neurons were silenced just after playing the sound -- exactly when the rats expected their feet to be shocked -- they could not unlearn the fear response. This showed that without VTA dopamine activity at that specific time, the mental link between the sound and the shock could not be removed.
