Tag: brain

6 months of exercise may reverse mild cognitive impairment

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By Ana Sandoiu

New research finds that a 6-month regimen of aerobic exercise can reverse symptoms of mild cognitive impairment in older adults.

Mild cognitive impairment (MCI) is characterized by a mild loss of cognitive abilities, such as memory and reasoning skills.

A person with MCI may find it hard to remember things, make decisions, or focus on tasks.

While the loss of cognitive abilities is not serious enough to interfere with daily activities, MCI raises the risk of Alzheimer’s disease and other forms of dementia.

According to the Alzheimer’s Association, 15–20 percent of adults aged 65 and over in the United States have MCI.

New research suggests that there might be a way to reverse these age-related cognitive problems. James A. Blumenthal, Ph.D. — of Duke University Medical Center in Durham, NC — and colleagues examined the effects of regimented exercise in 160 people aged 65 on average.

They published their findings in the journal Neurology.

‘Transmissible’ Alzheimer’s theory gains traction

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A normal brain of a 70-year-old (left slice), compared with the brain of a 70-year-old with Alzheimer’s disease.Credit: Jessica Wilson/Science Photo Library

Neuroscientists have amassed more evidence for the hypothesis that sticky proteins that are a hallmark of neurodegenerative diseases can be transferred between people under particular conditions — and cause new damage in a recipient’s brain.

They stress that their research does not suggest that disorders such as Alzheimer’s disease are contagious, but it does raise concern that certain medical and surgical procedures pose a risk of transmitting such proteins between humans, which might lead to brain disease decades later.

“The risk may turn out to be minor — but it needs to be investigated urgently,” says John Collinge, a neurologist at University College London who led the research, which is published in Nature1 on 13 December.

The work follows up on a provocative study published by Collinge’s team in 20152. The researchers discovered extensive deposits of a protein called amyloid-beta during post-mortem studies of the brains of four people in the United Kingdom. They had been treated for short stature during childhood with growth-hormone preparations derived from the pituitary glands of thousands of donors after death.

The recipients had died in middle-age of a rare but deadly neurodegenerative condition called Creutzfeldt-Jakob disease (CJD), caused by the presence in some of the growth-hormone preparations of an infectious, misfolded protein — or prion — that causes CJD. But pathologists hadn’t expected to see the amyloid build up at such an early age. Collinge and his colleagues suggested that small amounts of amyloid-beta had also been transferred from the growth-hormone samples, and had caused, or ‘seeded’, the characteristic amyloid plaques.

Seeds of trouble
Amyloid plaques in blood vessels in the brain are a hallmark of a disease called cerebral amyloid angiopathy (CAA) and they cause local bleeding. In Alzheimer’s disease, however, amyloid plaques are usually accompanied by another protein called tau — and the researchers worry that this might also be transmitted in the same way. But this was not the case in the brains of the four affected CJD patients, which instead had the hallmarks of CAA.

The team has now more directly tested the hypothesis that these proteins could be transmitted between humans through contaminated biological preparations. Britain stopped the cadaver-derived growth hormone treatment in 1985 and replaced it with a treatment that uses synthetic growth hormone. But Collinge’s team was able to locate old batches of the growth-hormone preparation stored as powder for decades at room temperature in laboratories at Porton Down, a national public-health research complex in southern England.

When the researchers analysed the samples, their suspicions were confirmed: they found that some of the batches contained substantial levels of amyloid-beta and tau proteins.

Mouse tests
To test whether the amyloid-beta in these batches could cause the amyloid pathology, they injected samples directly into the brains of young mice genetically engineered to be susceptible to amyloid pathology. By mid-life, the mice had developed extensive amyloid plaques and CAA. Control mice that received either no treatment or treatment with synthetic growth hormone didn’t have amyloid build up.

The scientists are now checking in separate mouse experiments whether the same is true for the tau protein.

“It’s an important study, though the results are very expected,” says Mathias Jucker at the Hertie Institute for Clinical Brain Research in Tubingen, Germany. Jucker demonstrated in 2006 that amyloid-beta extracted from human brain could initiate CAA and plaques in the brains of mice3. Many other mouse studies have also since confirmed this.

Surgical implications
That the transmissibility of the amyloid-beta could be preserved after so many decades underlines the need for caution, says Jucker. The sticky amyloid clings tightly to materials used in surgical instruments, resisting standard decontamination methods4. But Jucker also notes that, because degenerative diseases take a long time to develop, the danger of any transfer may be most relevant in the case of childhood surgery where instruments have also been used on old people.

So far, epidemiologists have not been able to assess whether a history of surgery increases the risk of developing a neurodegenerative disease in later life — because medical databases tend not to include this type of data.

But epidemiologist Roy Anderson at Imperial College London says researchers are taking the possibility seriously. Major population cohort studies, such as the US Framingham Heart Study, are starting to collect information about participants’ past surgical procedures, along with other medical data.

The 2015 revelation prompted pathologists around the world to reexamine their own cases of people who had been treated with similar growth-hormone preparations — as well as people who had acquired CJD after brain surgery that had involved the use of contaminated donor brain membranes as repair patches. Many of the archived brain specimens, they discovered, were full of aberrant amyloid plaques5,6,7. One study showed that some batches of growth-hormone preparation used in France in the 1970s and 1980s were contaminated with amyloid-beta and tau — and that tau was also present in three of their 24 patients.8

Collinge says he applied unsuccessfully for a grant to develop decontamination techniques for surgical instruments after his 2015 paper came out. “We raised an important public-health question, and it is frustrating that it has not yet been addressed.” But he notes that an actual risk from neurosurgery has not yet been established.

https://www.nature.com/articles/d41586-018-07735-w?utm_source=fbk_nnc&utm_medium=social&utm_campaign=naturenews&sf204283628=1

Thank to Kebmodee for bringing this to the It’s Interesting community.

Chronic Bullying Could Actually Reshape The Brains of Teens

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by Carly Cassella

Sticks and stones may break your bones, but name-calling could actually change the structure of your brain.

A new study has found that persistent bullying in high school is not just psychologically traumatising, it could also cause real and lasting damage to the developing brain.

The findings are drawn from a long-term study on teenage brain development and mental health, which collected brain scans and mental health questionnaires from European teenagers between the ages of 14 and 19.

Following 682 young people in England, Ireland, France and Germany, the researchers tallied 36 in total who reported experiencing chronic bullying during these years.

When the researchers compared the bullied participants to those who had experienced less intense bullying, they noticed that their brains looked different.

Across the length of the study, in certain regions, the brains of the bullied participants appeared to have actually shrunk in size.

In particular, the pattern of shrinking was observed in two parts of the brain called the putamen and the caudate, a change oddly reminiscent of adults who have experienced early life stress, such as childhood maltreatment.

Sure enough, the researchers found that they could partly explain these changes using the relationship between extreme bullying and higher levels of general anxiety at age 19. And this was true even when controlling for other types of stress and co-morbid depressive symptoms.

The connection is further supported by previous functional MRI studies that found differences in the connectivity and activation of the caudate and putamen activation in those with anxiety.

“Although not classically considered relevant to anxiety, the importance of structural changes in the putamen and caudate to the development of anxiety most likely lies in their contribution to related behaviours such as reward sensitivity, motivation, conditioning, attention, and emotional processing,” explains lead author Erin Burke Quinlan from King’s College London.

In other words, the authors think all of this shrinking could be a mark of mental illness, or at least help explain why these 19-year-olds are experiencing such unusually high anxiety.

But while numerous past studies have already linked childhood and adolescent bullying to mental illness, this is the very first study to show that unrelenting victimisation could impact a teenager’s mental health by actually reshaping their brain.

The results are cause for worry. During adolescence, a young person’s brain is absolutely exploding with growth, expanding at an incredible place.

And even though it’s normal for the brain to prune back some of this overabundance, in the brains of those who experienced chronic bullying, the whole pruning process appears to have spiralled out of control.

The teenage years are an extremely important and formative period in a person’s life, and these sorts of significant changes do not bode well. The authors suspect that as these children age, they might even begin to experience greater shrinkage in the brain.

But an even longer long-term study will need to be done if we want to verify that hunch. In the meantime, the authors are recommending that every effort be made to limit bullying before it can cause damage to a teenager’s brain and their mental health.

This study has been published in Molecular Psychiatry.

https://www.sciencealert.com/chronic-bullying-could-actually-reshape-the-brains-of-teens

Cannabinoid Exposure During Adolescence Disrupts Neural Regulation

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Cannabis exposure during adolescence may interfere with the brain’s maturation, at least in rats, according to research presented at the Society for Neuroscience meeting in San Diego this week. Scientists find that a synthetic cannabinoid can throw dopamine signaling out of whack and alter the development of the prefrontal cortex.

As states continue to legalize both medical and recreational marijuana, more and more teens are using the drug. According to the Scripps Research Institute’s Michael Taffe, who moderated a press conference today (November 6), 35 percent of high school seniors in the US have smoked pot in the past year, and 14 percent say they have smoked it every day for a month at some point in their lives.

This has cannabis researchers interested in how marijuana use affects teens’ developing brains. In one study described during the event with reporters, José Fuentealba Evans of the Pontificia Universidad Católica de Chile and his colleagues injected adolescent rats with a synthetic cannabinoid and found that such exposure had a “huge increase” in dopaminergic activity in the nigrostriatal pathway of the striatum compared with rats that received a placebo, he explains. This excitatory circuit plays a role in reward processing and addiction, for example, and such changes may encourage risky behavior.

In another study presented today, Jamie Roitman’s group at the University of Illinois at Chicago found that rats given this same drug had fewer inhibitory neurons in regions of the prefrontal cortex, as well as reduced levels of the perineuronal nets that help stabilize those circuits, compared with control animals. This part of the brain, which matures late in development as excitatory synapses are pruned and inhibitory synapses proliferate, controls the highly active motivational circuits, such as the nigrostriatal pathway, that mature earlier, Roitman explains.

“Adolescence is much more dopamine controlled, as you’re waiting for the prefrontal cortex to come online and execute planning and control over behavior,” she tells The Scientist. Thus, adolescents who use cannabis may be “at risk of changing the structure of the brain while it’s maturing.”

https://www.the-scientist.com/news-opinion/cannabinoid-exposure-during-adolescence-disrupts-neural-regulation-65047

See amputee Amanda Kitts manipulate objects using nervous impulses to control an early prototype of her advanced artificial limb.

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When Amanda Kitts’s car was hit head-on by a Ford F-350 truck in 2006, her arm was damaged beyond repair. “It looked like minced meat,” Kitts, now 50, recalls. She was immediately rushed to the hospital, where doctors amputated what remained of her mangled limb.

While still in the hospital, Kitts discovered that researchers at the Rehabilitation Institute of Chicago (now the Shirley Ryan AbilityLab) were investigating a new technique called targeted muscle reinnervation, which would enable people to control motorized prosthetics with their minds. The procedure, which involves surgically rewiring residual nerves from an amputated limb into a nearby muscle, allows movement-related electrical signals—sent from the brain to the innervated muscles—to move a prosthetic device.

Kitts immediately enrolled in the study and had the reinnervation surgery around a year after her accident. With her new prosthetic, Kitts regained a functional limb that she could use with her thoughts alone. But something important was missing. “I was able to move a prosthetic just by thinking about it, but I still couldn’t tell if I was holding or letting go of something,” Kitts says. “Sometimes my muscle might contract, and whatever I was holding would drop—so I found myself [often] looking at my arm when I was using it.”

What Kitts’s prosthetic limb failed to provide was a sense of kinesthesia—the awareness of where one’s body parts are and how they are moving. (Kinesthesia is a form of proprioception with a more specific focus on motion than on position.) Taken for granted by most people, kinesthesia is what allows us to unconsciously grab a coffee mug off a desk or to rapidly catch a falling object before it hits the ground. “It’s how we make such nice, elegant, coordinated movements, but you don’t necessarily think about it when it happens,” explains Paul Marasco, a neuroscientist at the Cleveland Clinic in Ohio. “There’s constant and rapid communication that goes on between the muscles and the brain.” The brain sends the intent to move the muscle, the muscle moves, and the awareness of that movement is fed back to the brain.

Prosthetic technology has advanced significantly in recent years, but proprioception is one thing that many of these modern devices still cannot reproduce, Marasco says. And it’s clear that this is something that people find important, he adds, because many individuals with upper-limb amputations still prefer old-school body-powered hook prosthetics. Despite being low tech—the devices work using a bicycle brake–like cable system that’s powered by the body’s own movements—they provide an inherent sense of proprioception.

To restore this sense for amputees who use the more modern prosthetics, Marasco and his colleagues decided to create a device based on what’s known as the kinesthetic illusion: the strange phenomenon in which vibrating a person’s muscle gives her the false sense of movement. A buzz to the triceps will make you think your arm is flexing, while stimulating the biceps will make you feel that it’s extending. The best illustration of this effect is the so-called Pinocchio illusion: holding your nose while someone applies a vibrating device to your bicep will confuse your brain into thinking your nose is growing.

“Your brain doesn’t like conflict,” Marasco explains. So if it thinks “my arm’s moving and I’m holding onto my nose, that must mean my nose is extending.”

To test the device, the team applied vibrations to the reinnervated muscles on six amputee participants’ chests or upper arms and asked them to indicate how they felt their hands were moving. Each amputee reported feeling various hand, wrist, and elbow motions, or “percepts,” in their missing limbs. Kitts, who had met Marasco while taking part in the studies he was involved in at the institute in Chicago, was one of the subjects in the experiment. “The first time I felt the sense of movement was remarkable,” she says.

In total, the experimenters documented 22 different percepts from their participants. “It’s hard to get this sense reliably, so I was encouraged to see the capability of several different subjects to get a reasonable sense of hand position from this illusion,” says Dustin Tyler, a biomedical engineer at Case Western Reserve University who was not involved in the work. He adds that while this is a new, noninvasive approach to proprioception, he and others are also working on devices that restore this sense by stimulating nerves directly with implanted devices.

Marasco and his colleagues then melded the vibration with the movement-controlled prostheses, so that when participants decided to move their artificial limbs, a vibrating stimulus was applied to the muscles to provide them with proprioceptive feedback. When the subjects conducted various movement-related tasks with this new system, their performance significantly improve.

“This was an extremely thorough set of experiments,” says Marcia O’Malley, a biomedical engineer at Rice University who did not take part in that study. “I think it is really promising.”

Although the mechanisms behind the illusion largely remain a mystery, Marasco says, the vibrations may be activating specific muscle receptors that provide the body with a sense of movement. Interestingly, he and his colleagues have found that the “sweet spot” vibration frequency for movement perception is nearly identical in humans and rats—about 90 Hz.

For Kitts, a system that provides proprioceptive feedback means being able to use her prosthetic without constantly watching it—and feeling it instead. “It’s whole new level of having a real part of your body,” she says.

https://www.the-scientist.com/notebook/vibrations-restore-sense-of-movement-in-prosthetics-64691

Eradicating Helicobacter Pylori Infections May Be A Key Treatment For Parkinson’s Disease

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Whiile human genetic mutations are involved in a small number of Parkinson’s disease (PD) cases, the vast majority of cases are of unknown environmental causes, prompting enormous interest in identifying environmental risk factors involved. The link between Helicobacter pylori (H. pylori) and gastric ulcers has been known for several decades, but new evidence suggests that this harmful bacterium may play a role in PD as well. A new review in the Journal of Parkinson’s Disease summarizes the current literature regarding the link between H. pylori and PD and explores the possible mechanisms behind the association.

In a comprehensive review of prior studies, investigators uncovered four key findings:

People with PD are 1.5-3-fold more likely to be infected with H. pylori than people without PD.
H. pylori-infected PD patients display worse motor functions than H. pylori-negative PD patients.
Eradication of H. pylori improved motor function in PD patients over PD patients whose H. pylori was not eradicated.
Eradication of H. pylori improved levodopa absorption in PD patients compared to PD patients whose H. pylori was not eradicated.
“This is an in-depth and comprehensive review that summarizes all the major papers in the medical literature on Parkinson’s disease and H. pylori, the common stomach bacterium that causes gastritis, ulcers and stomach cancer,” explained lead investigator David J. McGee, PhD, Associate Professor, Department of Microbiology and Immunology, LSU Health Sciences Center-Shreveport, Shreveport, LA, USA. “Our conclusion is that there is a strong enough link between the H. pylori and Parkinson’s disease that additional studies are warranted to determine the possible causal relationship.”

Investigators also analyzed existing studies to try and find possible testable pathways between the bacterial infection and Parkinson’s to lay the groundwork for future research. They found four main possible explanations for the association:

Bacterial toxins produced by H. pylori may damage neurons.

The infection triggers a massive inflammatory response that causes damage to the brain.

H. pylori may disrupt the normal gut microbial flora.

The bacteria might interfere with the absorption properties of levodopa, the medication commonly used to treat the symptoms of Parkinson’s disease.

The onset of PD is often preceded by gastrointestinal dysfunction, suggesting that the condition might originate in the gut and spread to the brain along the brain-gut axis. In the review, investigators note that this has been documented in rats.

Screening PD patients for the presence of H. pylori and subsequent treatment if positive with anti-H. pylori triple drug therapy, may contribute to improved levodopa absorption and ultimately improvement of PD symptoms, potentially leading to a longer life span in patients with PD.

“Evidence for a strong association among H. pylori chronic infection, peptic ulceration and exacerbation of PD symptoms is accumulating,” concluded Dr. McGee.

“However, the hypotheses that H. pylori infection is a predisposing factor, disease progression modifier, or even a direct cause of PD remain largely unexplored. This gut pathology may be multifactorial, involving H. pylori, intestinal microflora, inflammation, misfolding of alpha-synuclein in the gut and brain, cholesterol and other metabolites, and potential neurotoxins from bacteria or dietary sources. Eradication of H. pylori or return of the gut microflora to the proper balance in PD patients may ameliorate gut symptoms, L-dopa malabsorption, and motor dysfunction.”

Eradicating Helicobacter pylori infections may be a key treatment for Parkinson’s disease

In 1960, about a half-million teens took a test. Now it could predict the risk of Alzheimer’s disease.

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High school students in 1960 take the Project Talent test, the largest survey of American teenagers ever done; it is now being used for research into dementia. (American Institutes for Research)

By Tara Bahrampour

In 1960, Joan Levin, 15, took a test that turned out to be the largest survey of American teenagers ever conducted. It took two-and-a-half days to administer and included 440,000 students from 1,353 public, private and parochial high schools across the country — including Parkville Senior High School in Parkville, Md., where she was a student.

“We knew at the time that they were going to follow up for a long time,” Levin said — but she thought that meant about 20 years.

Fifty-eight years later, the answers she and her peers gave are still being used by researchers — most recently in the fight against Alzheimer’s disease. A study released this month found that subjects who did well on test questions as teenagers had a lower incidence of Alzheimer’s and related dementias in their 60s and 70s than those who scored poorly.

Known as Project Talent, the test was funded by the U.S. government, which had been concerned, given the Soviet Union’s then-recent successful Sputnik launch, that Americans were falling behind in the space race.

Students answered questions about academics and general knowledge, as well as their home lives, health, aspirations and personality traits. The test was intended to identify students with aptitudes for science and engineering. Test-takers included future rock stars Janis Joplin, then a senior at Thomas Jefferson High School in Port Arthur, Tex., and Jim Morrison, then a junior at George Washington High School in Alexandria, Va.

In recent years, researchers have used Project Talent data for follow-up studies, including one published Sept. 7 in the Journal of the American Medical Association. Conducted by researchers at the Washington-based American Institutes for Research (AIR), the organization that originally administered the test, it compared results for more than 85,000 test-takers with their 2012-2013 Medicare claims and expenditures data, and found that warning signs for dementia may be discernible as early as adolescence.

The study looked at how students scored on 17 areas of cognitive ability such as language, abstract reasoning, math, clerical skills, and visual and spatial prowess, and found that people with lower scores as teenagers were more prone to getting Alzheimer’s and related dementias in their 60s and early 70s.

Specifically, those with lower mechanical reasoning and memory for words as teens had a higher likelihood of developing dementia in later life: Men in the lower-scoring half were 17 percent more likely, while women with lower scores were 16 percent more likely. Worse performance on other components of the test also increased the risk for later-life dementia.

An estimated 5.7 million Americans have Alzheimer’s disease, and in the absence of scientific breakthroughs to curb the disease, the Alzheimer’s Association projects that number could reach 14 million by 2050, with the cost of care topping $1 trillion per year.

The 1960 test could have the potential to be like the groundbreaking Framingham study, a decades-long study of men in Massachusetts that led to reductions in heart disease in the 1970s, ’80s and ’90s, said Susan Lapham, director of Project Talent and a co-author of the JAMA study.

“If Project Talent can be for dementia what the Framingham study was for heart disease, it will make a difference in public health,” she said. “It indicates that we should be designing interventions for kids in high school and maybe even earlier to maybe keep their brains active from a young age.”

This might include testing children, identifying those with lower scores and “getting them into a program to make sure they’re not missing out and maybe putting themselves at risk,” she said.

For years, little was done with the Project Talent data because the participants could not be found. A proposal in the 1980s to try to find them failed because, in that pre-Internet age, the task seemed too daunting.

In 2009, as the students’ 50th high school reunions were coming up, researchers decided to use the gatherings as an occasion to contact many of them. (About a quarter have died.) They were then able to use the test data to study things such as the effects of diabetes and personality type on later-life health.

But when contacted, the participants were most interested in dementia, Lapham said. “They wanted that to be studied more than any other topic,” she said. “They said, ‘The thing I fear most is dementia.’ ”

While students were supposed to have received their results soon after taking the test, some students said they did not remember getting them.

Receiving her results recently was interesting in hindsight, said Levin, a retired human-resources director who is now 73 and living in Cockeysville, Md. Most of her scores were over 75 percent, with very high marks in vocabulary, abstract reasoning and verbal memory, and lower marks in table reading and clerical tasks.

Low scores do not mean a person will get dementia; the correlation is merely associated with a higher risk. But even if her scores had been lower, Levin said she would want to know. “I’m kind of a planner, and I look ahead,” she said. “I’d want my daughter and her family to maybe have an idea of what to expect.”

Karen Altpeter, 75, of Prescott, Wis., said she would also probably want to know about her risk, because her mother and grandmother had Alzheimer’s. She liked the idea that the answers she had given as a teen could help science.

“If there’s any opportunity I can have to make a difference just by taking a test and answering some questions, I’ll do it,” she said. “I want the opportunity to make things better for people.”

Earlier studies had suggested a relationship between cognitive abilities in youth and dementia in later life, including one that followed 800 nuns earlier in the 20th century and found that the complexity of sentences they used in writing personal essays at 21 correlated with their dementia risk in old age.

But that study included only women and no minorities. Project Talent’s subjects reflected the nation’s demographic mix in 1960.

Today, however, the country is more diverse. The number of minorities 65 and older is projected to grow faster than the general population, and by 2060 there will be about 3.2 million Hispanics and 2.2 million African Americans with Alzheimer’s disease and related dementias, according to a study by the Centers for Disease Control and Prevention published this week. African Americans and Hispanics have a higher prevalence of Alzheimer’s and related diseases than non-Hispanic whites.

A follow-up study underway of a smaller sample of the Project Talent pool — 22,500 people — will be weighted to reflect today’s population mix and will dig more deeply into age-related brain and cognitive changes over time.

It will examine the long-term impact of school quality and school segregation on brain health, and the impact of adolescent socioeconomic disadvantage on cognitive and psychosocial resilience, with a special focus on the experiences of participants of color.

That study includes an on-paper survey of demographics, family and marriage history, residential history, educational attainment and health status; an online survey of health, mental health and quality of life; and a detailed cognitive assessment by phone of things such as memory for words and counting backward.

Researchers will also evaluate school quality to determine whether there are racial or ethnic differences in the benefits of attending higher quality schools, and explore more deeply why some people develop dementia and some do not.

The follow-up, slated to be completed next year, is funded by the National Institute on Aging, part of the National Institutes of Health, and conducted by AIR in conjunction with researchers from Columbia University Medical Center and the University of Southern California.

Cliff Jacobs, 75, of Arlington, Va., who took the Project Talent test as a high school junior in Tenafly, N.J., doesn’t remember hearing about any results. Then, a few months ago, researchers conducting the follow-up study contacted him, tested his cognitive abilities and asked about his life history.

“They delved into my issues growing up — did my parents smoke, and was I exposed to any secondhand smoke? Yeah, my parents both smoked, and I didn’t even think it was something to consider,” he said.

A retired geoscientist for the National Science Foundation, Jacobs said he would be interested in learning if he is at risk for dementia.

“The statistical correlation is not one that will necessarily apply to you, but they can give you some probabilities,” he said. “I guess basic human nature would be, ‘Yeah, you’d probably want to know.’ ”

Try these 12 sample questions from the test.


Can’t see the Quiz? Click Here.

1

In the Bible story, Samson knew he would lose his strength if

his hair were cut.

he fell in love.

he left Jerusalem.

he spoke with a Philistine.

he went to war.

2

Chartreuse is a mixture of

green and blue.

yellow and orange.

yellow and green.

orange and brown.

red and orange.

3

The above is usually called a

fly.

spoon.

spinner.

plug.

streamer.

4

High pointed arches are used chiefly in

Roman architecture.

Greek architecture.

Gothic architecture.

Renaissance architecture.

modern architecture.

5

If a camper sees a garter snake, he should

leave it alone.

pin its head down with a forked stick.

hit it with a rock.

climb the nearest tree.

stand still until it leaves.

6

Tartar sauce is most often served with

tossed salad.

ice cream.

fish.

barbecued beef.

chow mein.

7

Suppose that after the post office is closed, someone finds he urgently needs stamps. He should probably try getting them

in a drug store.

from a stamp collector.

by phoning the postmaster’s home.

in a department store.

in a gas station.

8

In a suspension bridge, the road bed is supported by

pontoons.

pilings.

arches.

cables.

cantilevers.

9

Which of these guns has the largest bore?

12 ga.

.22 cal.

.44 cal.

16 ga.

20 ga.

10

A boy takes a girl to a movie and they find a pair of seats on a side aisle. Usually the girl should take the seat

on the left.

on the right.

nearest the aisle.

furthest from the aisle.

nearest the center of the theater.

11

About when did Leonardo de Vinci live?

1st century

5th century

10th century

15th century

20th century

12

Locks were built into the Panama Canal because

the Atlantic Ocean is higher than the Pacific.

the Pacific Ocean is higher than the Atlantic.

Panama is above sea level.

the canal is narrow.

the canal is wide.

The Gut of Mice Communicates with the Brain Through the Vagus Nerve, forming a possible basis for a 6th Sense

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by SUKANYA CHARUCHANDRA

Previous research has shown that the gut-brain connection, which refers to signaling between the digestive and the central nervous systems, is based on the transport of hormones, but a study published today (September 21) in Science suggests there may be a more direct link—the vagus nerve.

This research presents “a new set of pathways that use gut cells to rapidly communicate with . . . the brain stem,” Daniel Drucker, who studies gut disorders at the Lunenfeld-Tanenbaum Research Institute in Toronto, Canada, and was not involved with the project, tells Science.

Building on an earlier study in which the team found that gut cells had synapses, the researchers injected a rabies virus, expressing green fluorescence, into the stomachs of mice and watched it travel speedily from the intestines to the rodents’ brainstems.

When they grew sensory gut cells together with neurons from the vagus nerve, the neurons moved across the dish to form synapses with the gut cells and began electrically coupling with them. Adding sugar to the dish sped up the rate of signaling between the gut and brain cells, a finding that suggests glutamate, a neurotransmitter involved in sensing taste, may be key to the process. Blocking glutamate secretion in gut cells brought these signals to a grinding halt.

“We think these findings are going to be the biological basis of a new sense,” coauthor Diego Bohórquez, an assistant professor of medicine at Duke University School of Medicine, says in a statement. “One that serves as the entry point for how the brain knows when the stomach is full of food and calories. It brings legitimacy to idea of the ‘gut feeling’ as a sixth sense.”

https://www.the-scientist.com/news-opinion/the-gut-of-mice-communicates-with-the-brain-through-the-vagus-nerve-64846?utm_campaign=TS_DAILY%20NEWSLETTER_2018&utm_source=hs_email&utm_medium=email&utm_content=66141129&_hsenc=p2ANqtz–EaFM3BB6i_l04LL2zbvjlEHCWVwrSrks2D9Aksml-wGa9f88gfOwPhtiPCXEMJRqzu6WG53_vzEvHht0oAGylLgMANQ&_hsmi=66141129

A protein in skeletal muscles helps mice recover from sleep deprivation.

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mice-x

by SUKANYA CHARUCHANDRA

The protein Bmal1, which helps regulate the body’s internal clock, is found in especially high levels in the brain and in skeletal muscles. Mice completely deficient in Bmal1 were known to suffer from sleep impairments, but the specifics at play weren’t clear. At the University of California, Los Angeles, Ketema Paul and colleagues looked to these mice for clues about the role Bmal1 plays in sleep regulation.

MUSCLE PLAY
When Paul’s team restored levels of the Bmal1 protein in the mice’s brains, their ability to rebound from a night of bad sleep remained poor. However, turning on production in skeletal muscles alone enabled mice to sleep longer and more deeply to recover after sleep loss.

SWEET DREAMS
For decades, scientists have thought sleep was controlled purely by the brain. But the new study indicates the ability to catch up on one’s sleep after a bout of sleeplessness is locked away in skeletal muscles, not the brain—at least for mice. “I think it’s a real paradigm shift for how we think about sleep,” says John Hogenesch, a chronobiologist at Cincinnati Children’s Hospital Medical Center who discovered the Bmal1 gene but was not involved in this study.

TARGET LOCKED
Paul’s group also found that having too much of the Bmal1 protein in their muscles not only made mice vigilant but also invulnerable to the effects of sleep loss, so that they remained alert even when sleep-deprived and slept fewer hours to regain lost sleep. “To me, that presents a potential target where you could treat sleep disorders,” says Paul, noting that an inability to recover from sleep loss can make us more susceptible to diseases.

The paper
J.C. Ehlen et al., “Bmal1 function in skeletal muscle regulates sleep,” eLife, 6:e26557, 2017.

https://www.the-scientist.com/the-literature/muscles-hold-a-key-to-sleep-recovery-64685?utm_campaign=TS_DAILY%20NEWSLETTER_2018&utm_source=hs_email&utm_medium=email&utm_content=66141129&_hsenc=p2ANqtz–EaFM3BB6i_l04LL2zbvjlEHCWVwrSrks2D9Aksml-wGa9f88gfOwPhtiPCXEMJRqzu6WG53_vzEvHht0oAGylLgMANQ&_hsmi=66141129

Researchers have discovered a gene that has evolved through natural selection to impact both psychiatric disorders and personality, and may help to maintain human diversity.

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How and why human-unique characteristics such as highly social behavior, languages and complex culture have evolved is a long-standing question. A research team led by Tohoku University in Japan has revealed the evolution of a gene related to such human-unique psychiatric traits.

PhD candidate Daiki Sato and Professor Masakado Kawata have discovered SLC18A1 (VMAT1), which encodes vesicular monoamine transporter 1, as one of the genes evolved through natural selection in the human lineage. VMAT1 is mainly involved in the transport of neurochemicals, such as serotonin and dopamine in the body, and its malfunction leads to various psychiatric disorders. VMAT1 has variants consisting of two different amino acids, threonine (136Thr) and isoleucine (136Ile), at site 136.

Several studies have shown that these variants are associated with psychiatric disorders, including schizophrenia, bipolar disorder, anxiety, and neuroticism (a personality trait). It has been known that individuals with 136Thr tend to be more anxious and more depressed and have higher neuroticism scores. They showed that other mammals have 136Asn at this site but 136Thr had been favored over 136Asn during human evolution. Moreover, the 136Ile variant had originated nearly at the Out-of-Africa migration, and then, both 136Thr and 136Ile variants have been positively maintained by natural selection in non-African populations.

The study by Sato and Kawata indicates that natural selection has possibly shaped our psychiatric traits and maintained its diversity. The results provide two important implications for human psychiatric evolution. First, through positive selection, the evolution from Asn to Thr at site 136 on SLC18A1 was favored by natural selection during the evolution from ancestral primates to humans, although individuals with 136Thr are more anxious and have more depressed minds.

Second, they showed that the two variants of 136Thr and 136Ile have been maintained by natural selection using several population genetic methods. Any form of natural selection that maintains genetic diversity within populations is called “balancing selection”. Individual differences in psychiatric traits can be observed in any human population, and some personality traits are also found in non-human primates. This suggests the possibility that a part of genetic diversity associated with personality traits and/or psychiatric disorders are maintained by balancing selection, although such selective pressure is often weak and difficult to detect.

The Evolution of Psychiatric Disorders and Personality Traits