Thursday, December 26, 2019

A brain link to overeating?


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Discovery creates the possibility scientists can someday develop treatments to curb impulsive eating

University of Georgia
Summary:
A team of researchers has now identified a specific circuit in the brain that alters food impulsivity.
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You're on a diet, but the aroma of popcorn in the movie theater lobby triggers a seemingly irresistible craving.


Within seconds, you've ordered a tub of the stuff and have eaten several handfuls.

Impulsivity, or responding without thinking about the consequences of an action, has been linked to excessive food intake, binge eating, weight gain and obesity, along with several psychiatric disorders including drug addiction and excessive gambling.

A team of researchers that includes a faculty member at the University of Georgia has now identified a specific circuit in the brain that alters food impulsivity, creating the possibility scientists can someday develop therapeutics to address overeating.

The team's findings were published recently in the journal Nature Communications.

"There's underlying physiology in your brain that is regulating your capacity to say no to (impulsive eating)," said Emily Noble, an assistant professor in the UGA College of Family and Consumer Sciences who served as lead author on the paper. "In experimental models, you can activate that circuitry and get a specific behavioral response."

Using a rat model, researchers focused on a subset of brain cells that produce a type of transmitter in the hypothalamus called melanin concentrating hormone (MCH).

While previous research has shown that elevating MCH levels in the brain can increase food intake, this study is the first to show that MCH also plays a role in impulsive behavior, Noble said.

"We found that when we activate the cells in the brain that produce MCH, animals become more impulsive in their behavior around food," Noble said.

To test impulsivity, researchers trained rats to press a lever to receive a "delicious, high-fat, high-sugar" pellet, Noble said. However, the rat had to wait 20 seconds between lever presses. If the rat pressed the lever too soon, it had to wait an additional 20 seconds.

Researchers then used advanced techniques to activate a specific MCH neural pathway from the hypothalamus to the hippocampus, a part of the brain involved with learning and memory function.

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Results indicated MCH doesn't affect how much the animals liked the food or how hard they were willing to work for the food. Rather, the circuit acted on the animals' inhibitory control, or their ability to stop themselves from trying to get the food."Activating this specific pathway of MCH neurons increased impulsive behavior without affecting normal eating for caloric need or motivation to consume delicious food," Noble said. "Understanding that this circuit, which selectively affects food impulsivity, exists opens the door to the possibility that one day we might be able to develop therapeutics for overeating that help people stick to a diet without reducing normal appetite or making delicious foods less delicious."


Wednesday, December 18, 2019

Early-life exposure to dogs may lessen risk of developing schizophrenia

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Early-life exposure to dogs may lessen risk of developing schizophrenia

Findings do not link similar contact with cats to either schizophrenia or bipolar disorder

Ever since humans domesticated the dog, the faithful, obedient and protective animal has provided its owner with companionship and emotional well-being. Now, a study from Johns Hopkins Medicine suggests that being around "man's best friend" from an early age may have a health benefit as well -- lessening the chance of developing schizophrenia as an adult.

Johns Hopkins Medicine


And while Fido may help prevent that condition, the jury is still out on whether or not there's any link, positive or negative, between being raised with Fluffy the cat and later developing either schizophrenia or bipolar disorder.

"Serious psychiatric disorders have been associated with alterations in the immune system linked to environmental exposures in early life, and since household pets are often among the first things with which children have close contact, it was logical for us to explore the possibilities of a connection between the two," says Robert Yolken, M.D., chair of the Stanley Division of Pediatric Neurovirology and professor of neurovirology in pediatrics at the Johns Hopkins Children's Center, and lead author of a research paper recently posted online in the journal PLOS One.
In the study, Yolken and colleagues at Sheppard Pratt Health System in Baltimore investigated the relationship between exposure to a household pet cat or dog during the first 12 years of life and a later diagnosis of schizophrenia or bipolar disorder. For schizophrenia, the researchers were surprised to see a statistically significant decrease in the risk of a person developing the disorder if exposed to a dog early in life. Across the entire age range studied, there was no significant link between dogs and bipolar disorder, or between cats and either psychiatric disorder.
The researchers caution that more studies are needed to confirm these findings, to search for the factors behind any strongly supported links, and to more precisely define the actual risks of developing psychiatric disorders from exposing infants and children under age 13 to pet cats and dogs.
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According to the American Pet Products Association's most recent National Pet Owners Survey, there are 94 million pet cats and 90 million pet dogs in the United States. Previous studies have identified early life exposures to pet cats and dogs as environmental factors that may alter the immune system through various means, including allergic responses, contact with zoonotic (animal) bacteria and viruses, changes in a home's microbiome, and pet-induced stress reduction effects on human brain chemistry.
Some investigators, Yolken notes, suspect that this "immune modulation" may alter the risk of developing psychiatric disorders to which a person is genetically or otherwise predisposed.
In their current study, Yolken and colleagues looked at a population of 1,371 men and women between the ages of 18 and 65 that consisted of 396 people with schizophrenia, 381 with bipolar disorder and 594 controls. Information documented about each person included age, gender, race/ethnicity, place of birth and highest level of parental education (as a measure of socioeconomic status). Patients with schizophrenia and bipolar disorder were recruited from inpatient, day hospital and rehabilitation programs of Sheppard Pratt Health System. Control group members were recruited from the Baltimore area and were screened to rule out any current or past psychiatric disorders.
All study participants were asked if they had a household pet cat or dog or both during their first 12 years of life. Those who reported that a pet cat or dog was in their house when they were born were considered to be exposed to that animal since birth.
The relationship between the age of first household pet exposure and psychiatric diagnosis was defined using a statistical model that produces a hazard ratio -- a measure over time of how often specific events (in this case, exposure to a household pet and development of a psychiatric disorder) happen in a study group compared to their frequency in a control group. A hazard ratio of 1 suggests no difference between groups, while a ratio greater than 1 indicates an increased likelihood of developing schizophrenia or bipolar disorder. Likewise, a ratio less than 1 shows a decreased chance.
Analyses were conducted for four age ranges: birth to 3, 4 to 5, 6 to 8 and 9 to 12.
Surprisingly, Yolken says, the findings suggests that people who are exposed to a pet dog before their 13th birthday are significantly less likely -- as much as 24% -- to be diagnosed later with schizophrenia.
"The largest apparent protective effect was found for children who had a household pet dog at birth or were first exposed after birth but before age 3," he says.
Yolken adds that if it is assumed that the hazard ratio is an accurate reflection of relative risk, then some 840,000 cases of schizophrenia (24% of the 3.5 million people diagnosed with the disorder in the United States) might be prevented by pet dog exposure or other factors associated with pet dog exposure.
"There are several plausible explanations for this possible 'protective' effect from contact with dogs -- perhaps something in the canine microbiome that gets passed to humans and bolsters the immune system against or subdues a genetic predisposition to schizophrenia," Yolken says.
For bipolar disorder, the study results suggest there is no risk association, either positive or negative, with being around dogs as an infant or young child.
Overall for all ages examined, early exposure to pet cats was neutral as the study could not link felines with either an increased or decreased risk of developing schizophrenia or bipolar disorder.
"However, we did find a slightly increased risk of developing both disorders for those who were first in contact with cats between the ages of 9 and 12," Yolken says. "This indicates that the time of exposure may be critical to whether or not it alters the risk."
One example of a suspected pet-borne trigger for schizophrenia is the disease toxoplasmosis, a condition in which cats are the primary hosts of a parasite transmitted to humans via the animals' feces. Pregnant women have been advised for years not to change cat litter boxes to eliminate the risk of the illness passing through the placenta to their fetuses and causing a miscarriage, stillbirth, or potentially, psychiatric disorders in a child born with the infection.
In a 2003 review paper, Yolken and colleague E. Fuller Torrey, M.D., associate director of research at the Stanley Medical Research Institute in Bethesda, Maryland, provided evidence from multiple epidemiological studies conducted since 1953 that showed there also is a statistical connection between a person exposed to the parasite that causes toxoplasmosis and an increased risk of developing schizophrenia. The researchers found that a large number of people in those studies who were diagnosed with serious psychiatric disorders, including schizophrenia, also had high levels of antibodies to the toxoplasmosis parasite.
Because of this finding and others like it, most research has focused on investigating a potential link between early exposure to cats and psychiatric disorder development. Yolken says the most recent study is among the first to consider contact with dogs as well.
"A better understanding of the mechanisms underlying the associations between pet exposure and psychiatric disorders would allow us to develop appropriate prevention and treatment strategies," Yolken says.
Working with Yolken on the research team are the following members from Sheppard Pratt Health System: Cassie Stallings, Andrea Origoni, Emily Katsafanas, Kevin Sweeney, Amalia Squire, and Faith Dickerson, Ph.D., M.P.H.
The study was largely supported by grants from the Stanley Medical Research Institute.

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The study was largely supported by grants from the Stanley Medical Research Institute.


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Wednesday, December 4, 2019

For spinal cord injury, micro implants could restore standing and walking


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Micro implants could restore standing and walking

December 3, 2019
University of Alberta Faculty of Medicine & Dentistry
Researchers are focused on restoring lower-body function after severe spinal injuries using a tiny spinal implant. In new research, the team showcases a map to identify which parts of the spinal cord trigger the hip, knees, ankles and toes, and the areas that put movements together.
When Vivian Mushahwar first applied to grad school, she wrote about her idea to fix paralysis by rewiring the spinal cord.
It was only after she was accepted into a bioengineering program that the young electrical engineer learned her idea had actually prompted laughter.
"I figured, hey I can fix it, it's just wires," Mushahwar said. "Yeah, well, it's not just wires. So I had to learn the biology along the way."
It's taken Mushahwar a lot of work over two decades at the University of Alberta, but the Canada Research Chair in Functional Restoration is still fixated on the dream of helping people walk again. And thanks to an electrical spinal implant pioneered in her laboratory and work in mapping the spinal cord, that dream could become a reality in the next decade.
Because an injured spinal cord dies back, it's not simply a matter of reconnecting a cable. Three herculean feats are needed. You have to translate brain signals. You have to figure out and control the spinal cord. And you have got to get the two sides talking again.
People tend to think the brain does all the thinking, but Mushahwar says the spinal cord has built-in intelligence. A complex chain of motor and sensory networks regulate everything from breathing to bowels, while the brain stem's contribution is basically "go!" and "faster!" Your spinal cord isn't just moving muscles, it's giving you your natural gait.
Other researchers have tried different avenues to restore movement. By sending electrical impulses into leg muscles, it's possible to get people standing or walking again. But the effect is strictly mechanical and not particularly effective. Mushahwar's research has focused on restoring lower-body function after severe injuries using a tiny spinal implant. Hair-like electrical wires plunge deep into the spinal grey matter, sending electrical signals to trigger the networks that already know how to do the hard work.
In a new paper in Scientific Reports, the team showcases a map to identify which parts of the spinal cord trigger the hip, knees, ankles and toes, and the areas that put movements together. The work has shown that the spinal maps have been remarkably consistent across the animal spectrum, but further work is required before moving to human trials.
The implications of moving to a human clinical setting would be massive, but must follow further work that needs to be done in animals. Being able to control standing and walking would improve bone health, improve bowel and bladder function, and reduce pressure ulcers. It could help treat cardiovascular disease -- the main cause of death for spinal cord patients -- while bolstering mental health and quality of life. For those with less severe spinal injuries, an implant could be therapeutic, removing the need for months of gruelling physical therapy regimes that have limited success.
"We think that intraspinal stimulation itself will get people to start walking longer and longer, and maybe even faster," said Mushahwar. "That in itself becomes their therapy."
Progress can move at a remarkable pace, yet it's often maddeningly slow.
"There's been an explosion of knowledge in neuroscience over the last 20 years," Mushahwar said. "We're at the edge of merging the human and the machine."
Given the nature of incremental funding and research, a realistic timeline for this type of progress might be close to a decade.
Mushahwar is the director of the SMART Network, a collaboration of more than 100 U of A scientists and learners who intentionally break disciplinary silos to think of unique ways to tackle neural injuries and diseases. That has meant working with researchers like neuroscientist Kathryn Todd and biochemist Matthew Churchward, both in the psychiatry department, to create three-dimensional cell cultures that simulate the testing of electrodes.

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The next steps are fine-tuning the hardware -- miniaturizing an implantable stimulator -- and securing Health Canada and FDA approvals for clinical trials. Previous research has tackled the problem of translating brain signals and intent into commands to the intraspinal implant; however, the first generation of the intraspinal implants will require a patient to control walking and movement. Future implants could include a connection to the brain.
It's the same goal Mushahwar had decades ago. Except now it's no longer a laughable idea.
"Imagine the future," Mushahwar said. "A person just thinks and commands are transmitted to the spinal cord. People stand up and walk. This is the dream."