Posts Tagged ‘brain’

By Yasemin Saplakoglu

The newest neuron has been named the “rosehip neuron,” thanks to its bushy appearance. The brain cell, with its unique gene expressions, distinctive shape and diverse connections with other neurons, has not been described before and, what’s more, it isn’t present in neuroscientists’ favorite subject: mice.

“It’s very bushy,” said Trygve Bakken, one of the lead authors of the paper and senior scientist at the Allen Institute for Brain Science in Seattle. Neurons have long branches called dendrites that receive signals from other neurons. In the rosehip cells, these dendrites are “very compact with lots of branch points, so it kind of looks a little bit like a rosehip,” Bakken told Live Science. (Rosehips are a type of fruit produced by rose plants.)

Also adding to the rosehip appearance are the large bulbs at the end of their axons that release neurotransmitters or chemical signals to other neurons, Bakken added.

The new finding is the result of a collaboration between Bakken and his team and researchers at the University of Szeged in Hungary. Both teams independently identified the distinctive-looking neurons and, when the teams learned they were looking at the same thing, they decided to work together, Bakken said.

The researchers at the Allen Institute documented the strange new neuron by examining the brain tissue of two deceased middle-age men. When the researchers looked at the genes of the rosehip neuron in this post-mortem tissue, they found that the neurons acted differently. “There are a number of genes that are turned on just in that cell and not in other[s],” Bakken said

Meanwhile, the team in Hungary further documented the rosehip neuron by studying the electrical activity and shapes of neurons in brain tissue that had been removed from people’s brains during surgery and kept alive in a solution.

A rare neuron

One reason rosehip neurons eluded neuroscientists for so long is likely because the cells are so rare in the brain, Bakken said. Another reason, he added, is because human brain tissue is difficult for scientists to obtain for study. Indeed, in the study, the researchers examined only one layer of the brain. It’s possible, however, that rosehip neurons could be found in other layers, too, Bakken said.

Specifically, the researchers found that the rosehip neurons make up about 10 percent of the first layer of the neocortex — the most recently evolved part of the cortex that’s involved in sight and hearing. They also found that rosehip neurons connect to neurons called pyramidal cells, a type of excitatory neuron that makes up two-thirds of all the neurons in the cortex, according to Cell.

The full extent of the rosehip neurons relationship to the pyramidal neurons is unclear, but the researchers did find that the rosehip neurons act as inhibitory neurons, or those that restrain the activity of other neurons. “They have the potential to sort of put the brakes on the excitability” of pyramidal neurons, Bakken said. But as to how this influences the brain’s behavior, “we don’t really know yet,” he added.

Absent in mice

All mammals have a cortex, and within it a neocortex, Bakken said. But there are about “a thousand times more cells in the human cortex compared to the mouse,” he said. In other words, it makes up a much bigger part of our brain than it does a mouse’s. So then, perhaps it’s not surprising that the team didn’t find any genetic hint of rosehip neurons in mice.

“Finding cell types that are uniquely human… helps our understanding of the physiological differences that under[lie] our higher cognitive abilities and may better inform upon treatment strategies for brain-related disorders,” said Blue B. Lake, an assistant project scientist in the bioengineering department at the University of California, San Diego who was not part of the study.

The absence of the rosehip neuron in mice brains might serve as a cautionary reminder that the results of some brain studies done on rats can’t be translated to humans, the researchers said.

“Mice have been a wonderful model organism for understanding how brains work in general and can help us understand how human brains work,” Bakken said. “But I think finding a part of that circuit that is not seen in a mouse that points to needing to study actual human tissue.”

There are enough parts of the brain conserved among mice, humans and other mammals that people can make “inferences about things we learn in the mouse and sort of, at least, hypothesize that something similar is likely to be happening in the human brain,” Bakken said. But, sometimes things present in human brains are “just not there” in mouse brains.

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The brain anatomy is consistently shaped by socioeconomic status from childhood to early adulthood, a study has found.

The brain anatomy is consistently shaped by socioeconomic status from childhood to early adulthood, a study has found. The findings, published in the journal JNeurosci, draws attention to the importance of preschool life as a period when associations between SES and brain organisation may first develop.

Researchers from the National Institute of Mental Health in the US analysed brain scans of the same individuals collected over time between five and 25 years of age. Comparing this data to parental education and occupation and each participants’ intelligence quotient (IQ) allowed the researchers to demonstrate positive associations between socioeconomic status (SES) and the size and surface area of brain regions involved in cognitive functions such as learning, language, and emotions.

This is the first study to associate greater childhood SES with larger volumes of two subcortical regions — the thalamus and striatum — thereby extending previous SES research that has focused on its relationship to the cortex.

Finally, the researchers identify brain regions underlying the relationship between SES and IQ. A better understanding of these relationships could clarify the processes by which SES becomes associated with a range of life outcomes, and ultimately inform efforts to minimise SES-related variation in health and achievement, they said.

https://www.timesnownews.com/health/article/socioeconomic-status-shapes-developing-brains-study/336480

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.


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.

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

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

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