NS/ Our thoughts alter our tactile perception
Neuroscience biweekly vol. 85, 10th May — 24th May
TL;DR
- If we sincerely believe that our index finger is five times bigger than it really is, our sense of touch improves. Researchers demonstrated that this is the case in an experiment in which the participants were put under professional hypnosis. When the participants signaled that they understood the opposite hypnotic suggestion that their index finger was five times smaller than it actually was, their sense of touch deteriorated accordingly. The study shows that our tactile perception is affected and can be altered by our mental processes.
- Pain is good. It’s the body’s way to keep an animal from harming itself or repeating a dangerous mistake. But sometimes the debilitating sensation can get in the way. So evolution has devised ways to tamp that response down under certain circumstances. Researchers identified the pathway in fruit flies that reduces the sensation of pain from heat. Remarkably, just a single neuron on each side of the animal’s brain controls the response. What’s more, the molecule responsible for suppressing this sensation in adult flies has the opposite role in fly larvae.
- Could changing your diet play a role in slowing or even preventing the development of dementia? We’re one step closer to finding out, thanks to a new UNLV study that bolsters the long-suspected link between gut health and Alzheimer’s disease.
- Researchers at UCLA Health and Harvard have identified 10 pesticides that significantly damaged neurons implicated in the development of Parkinson’s disease, providing new clues about environmental toxins’ role in the disease.
- Artificial intelligence could be a useful tool in mental health treatment, according to the results of a new pilot study led by University of Illinois Chicago researchers.
- Researchers have discovered new insights into how the human brain makes perceptual judgments of the external world. The study explored the computational mechanisms used by the human brain to perceive the size of objects in the world around us.
- While it has been long understood that limiting the amount of food eaten can promote healthy aging in a wide range of animals, including humans, a new study has revealed that the feeling of hunger itself may be enough to slow aging.
- Deep sleep, also known as non-REM slow-wave sleep, can act as a ‘cognitive reserve factor’ that may increase resilience against a protein in the brain called beta-amyloid that is linked to memory loss caused by dementia.
- Watching the clock while trying to fall asleep exacerbates insomnia and the use of sleep aids, according to research from Indiana University professors — and a small change could help people sleep better.
- After a stroke, physical activity can be pivotal to successful recovery. People who spend four hours a week exercising after their stroke achieve better functional recovery within six months than those who do not, a new study shows.
- And more!
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The latest news and research
Hypnotic suggestions cognitively penetrate tactile perception through top-down modulation of semantic contents
by Marius Markmann, Melanie Lenz, Oliver Höffken, Agnė Steponavičiūtė, Martin Brüne, Martin Tegenthoff, Hubert R. Dinse, Albert Newen in Scientific Reports
Do we always perceive the world in the same way? A hypnosis experiment proves that we certainly don’t.
If we sincerely believe that our index finger is five times bigger than it really is, our sense of touch improves. Researchers at Ruhr University Bochum demonstrated that this is the case in an experiment in which the participants were put under professional hypnosis. When the participants signaled that they understood the opposite hypnotic suggestion that their index finger was five times smaller than it actually was, their sense of touch deteriorated accordingly. The study shows that our tactile perception is affected and can be altered by our mental processes. The scientific community has been divided on this issue. Headed by PD Dr. Hubert Dinse, Professor Albert Newen and Professor Martin Tegenthoff, the researchers published their findings in the journal Scientific Reports.
The researchers measured the tactile perception of their 24 test participants using the two-point discrimination method. This involves the index finger lying relaxed on a device with two needles repeatedly touching the finger painlessly but perceptibly.
“If the needles are far enough apart, we can easily distinguish two points of contact,” explains Hubert Dinse from the Neurological Clinic of Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil. “But if the needles are very close together, we only feel the touch in one place.”
At a certain distance between the needles, the sensation changes from feeling two needles to feeling just one, although two are presented. This discrimination threshold is stable for each person given normal everyday consciousness.
“We wanted to find out whether it’s possible to change this sensation threshold by activating a verbally articulated thought in a person,” explains Albert Newen from the Philosophy Institute II at Ruhr University Bochum. The research team chose two thought cues: “Imagine your index finger is five times smaller” and “Imagine your index finger is five times bigger.”
To specifically activate these semantic contents, the researchers used hypnotic suggestion. During a controlled state of hypnosis induced by a professional hypnotist, the participant was asked to sincerely accept the first belief for a series of tests and then the second.
The subjects took part in a total of four experiments to determine the sensation threshold in each case: under normal everyday consciousness, under hypnosis without suggestion, and under two hypnotic conditions with the suggestions of a bigger or smaller index finger.
“Discrimination thresholds did not differ when measured during normal consciousness and hypnosis without suggestion. This supports our preliminary assumption that hypnosis alone doesn’t lead to changes,” says Martin Tegenthoff. “However, if the beliefs are induced as suggestions under hypnosis, we observe a systematic change in the tactile discrimination threshold.”
When a test person imagined that their index finger was five times bigger than it actually was, their discrimination threshold improved and they were able to feel two needles, even when they were closer together. When the suggestion was that their index finger was five times smaller, the discrimination threshold worsened. This means that it is the beliefs that change perception. The behavioral results were supported by parallel recordings of brain activity such as spontaneous EEG and sensory evoked potentials.
The scientific community is divided on the question of whether or not perceptual processes can be influenced by semantic content alone — experts refer to this as the question of cognitive penetrability of perception.
“Our study provides another building block supporting the idea that such top-down influences of beliefs on perception do indeed exist,” stresses Hubert Dinse. “The beliefs we hold do indeed change how we experience the world.”
Alleviation of thermal nociception depends on heat-sensitive neurons and a TRP channel in the brain
by Jiangqu Liu, Weiwei Liu, Dhananjay Thakur, John Mack, Aidin Spina, Craig Montell in Current Biology
Pain is good. It’s the body’s way to keep an animal from harming itself or repeating a dangerous mistake. But sometimes the debilitating sensation can get in the way. So evolution has devised ways to tamp that response down under certain circumstances.
Researchers at UC Santa Barbara identified the pathway in fruit flies that reduces the sensation of pain from heat. Remarkably, just a single neuron on each side of the animal’s brain controls the response. What’s more, the molecule responsible for suppressing this sensation in adult flies has the opposite role in fly larvae. The surprising results appear in Current Biology.
The brain of a fruit fly has about a million-fold fewer neurons than our own.
“Yet we didn’t anticipate that a single pair of neurons would have such an important role in pain suppression,” said senior author Craig Montell, Duggan professor and distinguished professor of molecular, cellular and developmental biology.
“We call them ‘Epione,’ or Epi neurons, for the Greek goddess of soothing pain,” said first author Jiangqu Liu, a postdoctoral fellow in the Montell lab.
The authors are quick to clarify a point. “Pain is an interpretation,” Montell said. “A hardy smack on the back from a teammate after a win might feel great, but not from a bully on the playground. Since we can’t ask fruit flies about their interpretation of hot temperatures, a more accurate term is ‘nociception,’ which refers to how the body senses a potentially harmful stimulus, and then relays the information to induce an avoidance response.”
Humans are well known to be able to suppress pain under some situations. However, scientists don’t know much about suppression of nociception in flies, which are workhorses for sensory research. Montell and his lab wanted to determine if flies have such a system, and if so, locate the neurons involved and understand the mechanism.
The researchers focused on nociception in response to heat. They first needed a way to measure how the animals responded to hot temperatures. They placed flies on a hot plate and measured the number that jumped off within 10 seconds. Nearly all the flies jumped between 38° and 44° Celsius (roughly 100° to 111° Fahrenheit). Now the team set out to see if they could identify neurons that suppress their aversion to high temperatures, and reduce the jump response.
The authors wondered whether the neurons involved in suppressing thermal pain might express a particular neuropeptide. Neuropeptides are a bit like neurotransmitters, except that neurotransmitters mediate between adjacent neurons, while neuropeptides can have a more systemic effect. As a result they impact many behaviors. Different sets of neurons tend to express different neuropeptides. Liu, Montell and their co-authors used the DNA segments that control the expression of 35 different neuropeptide genes to drive expression of a protein that activates neurons.
Out of the 35 different groups of neurons, one clearly reduced the flies’ tendency to jump from the hot plate. These neurons produce the neuropeptide AstC, which is related to a mammalian compound that contributes to pain suppression in humans.
The researchers then expressed the gene coding for a light-sensitive channel in this group of neurons. This enabled them to activate the neurons using light. As expected, stimulating these neurons reduced the flies’ tendency to jump off the hot plate.
The authors then used the section of DNA that controls expression of AstC to instead control a gene for green fluorescent protein. Now they could finally see which neurons were activating. That’s when they discovered that triggering just a single neuron on each side of the brain (the Epi neurons) suppressed the nociceptive response.
Once the team found the neurons responsible for suppressing thermal pain, they were curious whether Epi neurons were thermosensitive themselves, or were receiving a signal from some other neurons.
The researchers expressed a gene coding for a protein that would fluoresce when calcium ions flooded into Epi neurons. They found that calcium levels increased as the temperature rose, even when they used a chemical to block communication between neurons. These findings indicated that the Epi neurons were directly sensing the high temperature.
The researchers determined that a specific ion channel in the cell membrane of Epi neurons was responsible for detecting the heat. This channel, called “Painless,” is a member of the TRP family of channels. TRP channels have broad roles in sensation, including temperature sensation. In fact, Painless is also required for thermal nociception in fly larvae.
“So Painless can have opposite roles in the response to noxious heat,” Montell said. “In some neurons, the channel is required for the animal to escape from hot temperatures, while in Epi neurons, Painless is needed to suppress nociception. That is an interesting and surprising twist.”
“This is the first time, to my knowledge, that a TRP channel is found to sense noxious heat not to induce a nociceptive response, but to suppress it,” Montell added.
Genetic correlations between Alzheimer’s disease and gut microbiome genera
by Davis Cammann, Yimei Lu, Melika J. Cummings, Mark L. Zhang, Joan Manuel Cue, Jenifer Do, Jeffrey Ebersole, Xiangning Chen, Edwin C. Oh, Jeffrey L. Cummings, Jingchun Chen in Scientific Reports
Could changing your diet play a role in slowing or even preventing the development of dementia? We’re one step closer to finding out, thanks to a new UNLV study that bolsters the long-suspected link between gut health and Alzheimer’s disease.
The analysis — led by a team of researchers with the Nevada Institute of Personalized Medicine (NIPM) at UNLV and published this spring in the Nature journal Scientific Reports — examined data from dozens of past studies into the belly-brain connection. The results? There’s a strong link between particular kinds of gut bacteria and Alzheimer’s disease.
Between 500 and 1,000 species of bacteria exist in the human gut at any one time, and the amount and diversity of these microorganisms can be influenced by genetics and diet.
The UNLV team’s analysis found a significant correlation between 10 specific types of gut bacteria and the likelihood of developing Alzheimer’s disease. Six categories of bacteria — Adlercreutzia, Eubacterium nodatum group, Eisenbergiella, Eubacterium fissicatena group, Gordonibacter, and Prevotella9 — were identified as protective, and four types of bacteria — Collinsella, Bacteroides, Lachnospira, and Veillonella — were identified as a risk factor for Alzheimer’s disease.
Certain bacteria in humans’ guts can secrete acids and toxins that thin and seep through the intestinal lining, interact with the APOE (a gene identified as a major risk factor for Alzheimer’s disease), and trigger a neuroinflammatory response — affecting brain health and numerous immune functions, and potentially promoting development of the neurodegenerative disorder.
Researchers said their novel discovery of the distinct bacterial groups associated with Alzheimer’s disease provides new insights into the relationship between gut microbiota and the world’s most common form of dementia. The findings also advance scientists’ understanding of how an imbalance of that bacteria may play a role in the disorder’s development.
“Most of the microorganisms in our intestines are considered good bacteria that promote health, but an imbalance of those bacteria can be toxic to a person’s immune system and linked to various diseases, such as depression, heart disease, cancer, and Alzheimer’s disease,” said UNLV research professor Jingchun Chen. “The take-home message here is that your genes not only determine whether you have a risk for a disease, but they can also influence the abundance of bacteria in your gut.”
While their analysis established overarching categories of bacteria typically associated with Alzheimer’s disease, the UNLV team said further research is needed to drill down into the specific bacterial species that influence risk or protection.
The hope is to one day develop treatments that are customized for an individual patient and their genetic makeup, such as medications or lifestyle change. Studies have shown that changes in gut microbiome through probiotic use and dietary adjustments can positively impact the immune system, inflammation, and even brain function.
“With more research it would be possible to identify a genetic trajectory that could point to a gut microbiome that would be more or less prone to developing diseases such as Alzheimer’s,” said study lead author and UNLV graduate student Davis Cammann, “but we also have to remember that the gut biome is influenced by many factors including lifestyle and diet.”
A pesticide and iPSC dopaminergic neuron screen identifies and classifies Parkinson-relevant pesticides
by Kimberly C. Paul, Richard C. Krolewski, Edinson Lucumi Moreno, Jack Blank, Kristina M. Holton, Tim Ahfeldt, Melissa Furlong, Yu Yu, Myles Cockburn, Laura K. Thompson, Alexander Kreymerman, Elisabeth M. Ricci-Blair, Yu Jun Li, Heer B. Patel, Richard T. Lee, Jeff Bronstein, Lee L. Rubin, Vikram Khurana, Beate Ritz in Nature Communications
Researchers at UCLA Health and Harvard have identified 10 pesticides that significantly damaged neurons implicated in the development of Parkinson’s disease, providing new clues about environmental toxins’ role in the disease.
While environmental factors such as pesticide exposure have long been linked to Parkinson’s, it has been harder to pinpoint which pesticides may raise risk for the neurodegenerative disorder. Just in California, the nation’s largest agricultural producer and exporter, there are nearly 14,000 pesticide products with over 1,000 active ingredients registered for use.
Through a novel pairing of epidemiology and toxicity screening that leveraged California’s extensive pesticide use database, UCLA and Harvard researchers were able to identify 10 pesticides that were directly toxic to dopaminergic neurons. The neurons play a key role in voluntary movement, and the death of these neurons is a hallmark of Parkinson’s.
Further, the researchers found that co-exposure of pesticides that are typically used in combinations in cotton farming were more toxic than any single pesticide in that group.
For this study, published in Nature Communications, UCLA researchers examined exposure history going back decades for 288 pesticides among Central Valley patients with Parkinson’s disease who had participated in previous studies. The researchers were able to determine long-term exposure for each person and then, using what they labeled a pesticide-wide association analysis, tested each pesticide individually for association with Parkinson’s. From this untargeted screen, researchers identified 53 pesticides that appeared to be implicated in Parkinson’s — most of which had not been previously studied for a potential link and are still in use.
Those results were shared for lab analysis led by Richard Krolewski, MD, PhD, an instructor of neurology at Harvard and neurologist at Brigham and Women’s Hospital. He tested the toxicity for most of those pesticides in dopaminergic neurons that had been derived from Parkinson’s patients through what’s known as induced pluripotent stem cells, which are a type of “blank slate” cell that can be reprogrammed into neurons that closely resemble those lost in Parkinson’s disease.
The 10 pesticides identified as directly toxic to these neurons included: four insecticides (dicofol, endosulfan, naled, propargite), three herbicides (diquat, endothall, trifluralin), and three fungicides (copper sulfate [basic and pentahydrate] and folpet). Most of the pesticides are still in use today in the United States.
Aside from their toxicity in dopaminergic neurons, there is little that unifies these pesticides. They have a range of user types, are structurally distinct, and do not share a prior toxicity classification.
Researchers also tested the toxicity of multiple pesticides that are commonly applied in cotton fields around the same time, according to California’s pesticide database. Combinations involving trifluralin, one of the most commonly used herbicides in California, produced the most toxicity. Previous research in the Agricultural Health Study, a large research project involving pesticide applicators, had also implicated trifluralin in Parkinson’s.
Kimberly Paul, PhD, a lead author and assistant professor of neurology at UCLA, said the study demonstrated their approach could broadly screen for pesticides implicated in Parkinson’s and better understand the strength of these associations.
“We were able to implicate individual agents more than any other study has before, and it was done in a completely agnostic manner,” Paul said. “When you bring together this type of agnostic screening with a field-to-bench paradigm, you can pinpoint pesticides that look like they’re quite important in the disease.”
The researchers are next planning to study epigenetic and metabolomic features related to exposure using integrative omics to help describe which biologic pathways are disrupted among Parkinson’s patients who experienced pesticide exposure. More detailed mechanistic studies of the specific neuronal processes impacted by pesticides such as trifluralin and copper are also underway at the Harvard/Brigham and Women’s labs. The lab work is focused on distinct effects on dopamine neurons and cortical neurons, which are important for the movement and cognitive symptoms in Parkinson’s patients, respectively. The basic science is also expanding to studies of pesticides on non-neuronal cells in the brain — the glia — to better understand how pesticides influence the function of these critical cells.
Effects of a virtual voice-based coach delivering problem-solving treatment on emotional distress and brain function: a pilot RCT in depression and anxiety
by Thomas Kannampallil, Olusola A. Ajilore, Nan Lv, Joshua M. Smyth, Nancy E. Wittels, Corina R. Ronneberg, Vikas Kumar, Lan Xiao, Susanth Dosala, Amruta Barve, Aifeng Zhang, Kevin C. Tan, Kevin K. Cao, Charmi R. Patel, Ben S. Gerber, Jillian A. Johnson, Emily A. Kringle, Jun Ma in Translational Psychiatry
Artificial intelligence could be a useful tool in mental health treatment, according to the results of a new pilot study led by University of Illinois Chicago researchers.
The study, which was the first to test an AI voice-based virtual coach for behavioral therapy, found changes in patients’ brain activity along with improved depression and anxiety symptoms after using Lumen, an AI voice assistant that delivered a form of psychotherapy.
The UIC team says the results, which are published in the journal Translational Psychiatry, offer encouraging evidence that virtual therapy can play a role in filling the gaps in mental health care, where waitlists and disparities in access are often hurdles that patients, particularly from vulnerable communities, must overcome to receive treatment.
“We’ve had an incredible explosion of need, especially in the wake of COVID, with soaring rates of anxiety and depression and not enough practitioners,” said Dr. Olusola A. Ajilore, UIC professor of psychiatry and co-first author of the paper. “This kind of technology may serve as a bridge. It’s not meant to be a replacement for traditional therapy, but it may be an important stop-gap before somebody can seek treatment.”
Lumen, which operates as a skill in the Amazon Alexa application, was developed by Ajilore and study senior author Dr.Jun Ma, the Beth and George Vitoux Professor of Medicine at UIC, along with collaborators at Washington University in St. Louis and Pennsylvania State University, with the support of a $2 million grant from the National Institute of Mental Health.
The UIC researchers recruited over 60 patients for the clinical study exploring the application’s effect on mild-to-moderate depression and anxiety symptoms, and activity in brain areas previously shown to be associated with the benefits of problem-solving therapy.
Two-thirds of the patients used Lumen on a study-provided iPad for eight problem-solving therapy sessions, with the rest serving as a “waitlist” control receiving no intervention.
After the intervention, study participants using the Lumen app showed decreased scores for depression, anxiety and psychological distress compared with the control group. The Lumen group also showed improvements in problem-solving skills that correlated with increased activity in the dorsolateral prefrontal cortex, a brain area associated with cognitive control. Promising results for women and underrepresented populations also were found.
“It’s about changing the way people think about problems and how to address them, and not being emotionally overwhelmed,” Ma said. “It’s a pragmatic and patient-driven behavior therapy that’s well established, which makes it a good fit for delivery using voice-based technology.”
A larger trial comparing the use of Lumen with both a control group on a waitlist, and patients receiving human-coached problem-solving therapy is currently being conducted by the researcher. They stress that the virtual coach doesn’t need to perform better than a human therapist to fill a desperate need in the mental health system.
“The way we should think about digital mental health service is not for these apps to replace humans, but rather to recognize what a gap we have between supply and demand, and then find novel, effective and safe ways to deliver treatments to individuals who otherwise do not have access, to fill that gap,” Ma said.
Blurring the boundary between models and reality: Visual perception of scale assessed by performance
by Tim S. Meese, Daniel H. Baker, Robert J. Summers in PLOS ONE
Researchers from Aston University and the University of York have discovered new insights into how the human brain makes perceptual judgements of the external world.
The study explored the computational mechanisms used by the human brain to perceive the size of objects in the world around us.
The research, led by Professor Tim Meese, in the School of Optometry at Aston University and Dr Daniel Baker in the Department of Psychology at University of York, tells us more about how our visual system can exploit ‘defocus blur’ to infer perceptual scale, but that it does so crudely.
It is well known that to derive object size from retinal image size, our visual system needs to estimate the distance to the object. The retinal image contains many pictorial cues, such as linear perspective, which help the system derive the relative size of objects. However, to derive absolute size, the system needs to know about spatial scale.
By taking account of defocus blur, like the blurry parts of an image outside the depth of focus of a camera, the visual system can achieve this. The maths behind this has been well worked out by others, but the study asked the question: does human vision exploit this maths?
The research team presented participants with photographic pairs of full-scale railway scenes subject to various artificial blur treatments and small-scale models of railway scenes taken with long exposure and small aperture to diminish defocus blur. The task was to detect which photograph in each pair was the real full-scale scene.
When the artificial blur was appropriately oriented with the ground plane (the horizontal plane representing the ground on which the viewer is standing) in the full-scale scenes, participants were fooled and believed the small models to be the full-scale scenes. Remarkably, this did not require the application of realistic gradients of blur. Simple uniform bands of blur at the top and bottom of the photographs achieved almost equivalent miniaturisation effects.
Tim Meese, professor of vision science at Aston University, said: “Our results indicate that human vision can exploit defocus blur to infer perceptual scale but that it does this crudely — more a heuristic than a metrical analysis. Overall, our findings provide new insights into the computational mechanisms used by the human brain in perceptual judgments about the relation between ourselves and the external world.”
Effects of hunger on neuronal histone modifications slow aging in Drosophila
by K. J. Weaver, R. A. Holt, E. Henry, Y. Lyu, S. D. Pletcher in Science
From low-carb to intermittent fasting, surgery to Ozempic — people turn to a seemingly never-ending array of diets, procedures and drugs to lose weight. While it has been long understood that limiting the amount of food eaten can promote healthy aging in a wide range of animals, including humans, a new study from University of Michigan has revealed that the feeling of hunger itself may be enough to slow aging.
Previous research has demonstrated that even the taste and smell of food can reverse the beneficial, life-extending effects of diet restriction, even without its consumption.
These intriguing findings drove first author Kristy Weaver, Ph.D., principal investigator Scott Pletcher, Ph.D., and their colleagues to examine whether changes in the brain that prompt the drive to seek food could be behind longer life.
“We’ve sort of divorced [the life extending effects of diet restriction] from all of the nutritional manipulations of the diet that researchers had worked on for many years to say they’re not required,” said Pletcher. “The perception of not enough food is sufficient.”
To do this, they induced hunger in flies in several ways. The first was to alter the amount of branched-chain amino acids, or BCAAs, in a test snack food and later allow the flies to freely feed on a buffet of yeast or sugar food. Flies fed the low-BCAA snack consumed more yeast than sugar in the buffet than did the flies fed the high-BCAA snack. This kind of preference for yeast over sugar is one indicator of need-based hunger.
The researchers noted that this behavior wasn’t due to the calorie content of the low-BCAA snack; in fact, these flies consumed more food and more total calories. When flies ate a low-BCAA diet for life, they also lived significantly longer than flies fed high-BCAA diets.
To look at hunger apart from dietary composition, they used a unique technique, activating neurons associated with the hunger drive in flies using exposure to red light, using a technique called optogenetics. These flies consumed twice as much food as did flies who were not exposed to the light stimulus. The red-light-activated flies also lived significantly longer than the flies used as a control.
“We think we’ve created a type of insatiable hunger in flies,” said Weaver. “And by doing so, the flies lived longer.”
What’s more, the team was able to map the molecular mechanics of hunger to changes in the epigenome of the neurons involved — and to identify that neurons responded to the presence or absence of a specific amino acid in the diet. These changes can affect how much specific genes are expressed in the brains of flies and, consequently, their feeding behavior and aging.
The authors note that caution should be used before applying the findings to people, but “there’s every reason to expect that the mechanisms discovered are likely to modulate hunger drives in other species.”
They next plan to examine how the drive to eat for pleasure, present in both flies and people, may also be linked to lifespan.
NREM sleep as a novel protective cognitive reserve factor in the face of Alzheimer’s disease pathology
by Zsófia Zavecz, Vyoma D. Shah, Olivia G. Murillo, Raphael Vallat, Bryce A. Mander, Joseph R. Winer, William J. Jagust, Matthew P. Walker in BMC Medicine
A deep slumber might help buffer against memory loss for older adults facing a heightened burden of Alzheimer’s disease, new research from the University of California, Berkeley, suggests.
Deep sleep, also known as non-REM slow-wave sleep, can act as a “cognitive reserve factor” that may increase resilience against a protein in the brain called beta-amyloid that is linked to memory loss caused by dementia. Disrupted sleep has previously been associated with a faster accumulation of beta-amyloid protein in the brain. However, the new research from a team at UC Berkeley reveals that superior amounts of deep, slow-wave sleep can act as a protective factor against memory decline in those with existing high amounts of Alzheimer’s disease pathology — a potentially significant advance that experts say could help alleviate some of dementia’s most devastating outcomes.
“With a certain level of brain pathology, you’re not destined for cognitive symptoms or memory issues,” said Zsófia Zavecz, a postdoctoral researcher at UC Berkeley’s Center for Human Sleep Science. “People should be aware that, despite having a certain level of pathology, there are certain lifestyle factors that will help moderate and decrease the effects.
“One of those factors is sleep and, specifically, deep sleep.”
The research, published Wednesday in the journal BMC Medicine, is the latest in a large body of work aimed at finding a cure for Alzheimer’s disease and preventing it altogether.
As the most prevalent form of dementia, Alzheimer’s disease destroys memory pathways and, in advanced forms, interferes with a person’s ability to perform basic daily tasks. Roughly one in nine people over age 65 have the progressive disease — a proportion that is expected to grow rapidly as the baby boomer generation ages.
In recent years, scientists have probed the ways that deposits of beta-amyloid associate with Alzheimer’s disease and how such deposits also affect memory more generally. In addition to sleep being a foundational part of memory retention, the team at UC Berkeley previously discovered that the declining amount of a person’s deep sleep could act as a “crystal ball” to forecast a faster rate of future beta-amyloid buildup in the brain, after which dementia is more likely set in.
Years of education, physical activity and social engagement are widely believed to shore up a person’s resilience to severe brain pathology — essentially keeping the mind sharp, despite the decreased brain health. These are called cognitive reserve factors. However, most of them, such as past years of education or the size of one’s social network, cannot be easily changed or modified retroactively.
That idea of cognitive reserve became a compelling target for sleep researchers, said Matthew Walker, a UC Berkeley professor of neuroscience and psychology and senior author of the study.
“If we believe that sleep is so critical for memory,” Walker said, “could sleep be one of those missing pieces in the explanatory puzzle that would tell us exactly why two people with the same amounts of vicious, severe amyloid pathology have very different memory?”
“If the findings supported the hypothesis, it would be thrilling, because sleep is something we can change,” he added. “It is a modifiable factor.”
To test that question, the researchers recruited 62 older adults from the Berkeley Aging Cohort Study. Participants, who were healthy adults and not diagnosed with dementia, slept in a lab while researchers monitored their sleep waves with an electroencephalography (EEG) machine. Researchers also used a positron emission tomography (PET) scan to measure the amount of beta-amyloid deposits in the participants’ brains. Half of the participants had high amounts of amyloid deposits; the other half did not.
After they slept, the participants completed a memory task involving matching names to faces.
Those with high amounts of beta-amyloid deposits in their brain who also experienced higher levels of deep sleep performed better on the memory test than those with the same amount of deposits but who slept worse. This compensatory boost was limited to the group with amyloid deposits. In the group without pathology, deep sleep had no additional supportive effect on memory, which was understandable as there was no demand for resilience factors in otherwise intact cognitive function.
In other words, deep sleep bent the arrow of cognition upward, blunting the otherwise detrimental effects of beta-amyloid pathology on memory.
In their analysis, the researchers went on to control for other cognitive reserve factors, including education and physical activity, and still sleep demonstrated a marked benefit. This suggests that sleep, independent of these other factors, contributes to salvaging memory function in the face of brain pathology. These new discoveries, they said, indicate the importance of non-REM slow-wave sleep in counteracting some of the memory-impairing effects of beta-amyloid deposits.
Walker likened deep sleep to a rescue effort.
“Think of deep sleep almost like a life raft that keeps memory afloat, rather than memory getting dragged down by the weight of Alzheimer’s disease pathology,” Walker said. “It now seems that deep NREM sleep may be a new, missing piece in the explanatory puzzle of cognitive reserve. This is especially exciting because we can do something about it. There are ways we can improve sleep, even in older adults.”
Chief among those areas for improvement? Stick to a regular sleep schedule, stay mentally and physically active during the day, create a cool and dark sleep environment and minimize things like coffee late in the day and screen time before bed. A warm shower before turning in for the night has also been shown to increase the quality of deep, slow-wave sleep, Zavecz said.
With a small sample size of healthy participants, the study is simply an early step in understanding the precise ways sleep may forestall memory loss and the advance of Alzheimer’s, Zavecz said.
Still, it opens the door for potential longer-term experiments examining sleep-enhancement treatments that could have far-reaching implications.
“One of the advantages of this result is the application to a huge population right above the age of 65,” Zavecz said. “By sleeping better and doing your best to practice good sleep hygiene, which is easy to research online, you can gain the benefit of this compensatory function against this type of Alzheimer’s pathology.”
Use of Sleep Aids in Insomnia
by Spencer C. Dawson, Barry Krakow, Patricia L. Haynes, Darlynn M. Rojo-Wissar, Natalia D. McIver, Victor A. Ulibarri in The Primary Care Companion For CNS Disorders
Watching the clock while trying to fall asleep exacerbates insomnia and the use of sleep aids, according to research from an Indiana University professor — and a small change could help people sleep better.
The research, led by Spencer Dawson, clinical assistant professor and associate director of clinical training in the College of Arts and Sciences’ Department of Psychological and Brain Sciences, focuses on a sample of nearly 5,000 patients presenting for care at a sleep clinic.
Insomnia affects between 4 and 22% of adults and is associated with long-term health problems including cardiovascular disease, diabetes and depression.
Participants completed questionnaires about the severity of their insomnia, their use of sleep medication and the time they spent monitoring their own behavior while trying to fall asleep. They were also asked to report any psychiatric diagnoses. Researchers conducted mediation analyses to determine how the factors influenced each other.
“We found time monitoring behavior mainly has an effect on sleep medication use because it exacerbates insomnia symptoms,” Dawson said. “People are concerned that they’re not getting enough sleep, then they start estimating how long it will take them to fall back asleep and when they have to be up. That is not the sort of activity that’s helpful in facilitating the ability to fall asleep — the more stressed out you are, the harder time you’re going to have falling asleep.”
As the frustration over sleeplessness grows, people are more likely to use sleep aids in an attempt to gain control over their sleep.
The results are published in The Primary Care Companion for CNS Disorders. Additional co-authors are Dr. Barry Krakow, professor of psychiatry and behavioral health in the Mercer University School of Medicine; Patricia Haynes, associate professor in the Mel and Enid Zuckerman School of Public Health at the University of Arizona and Darlynn Rojo-Wissar, a postdoctoral fellow at Alpert Medical School of Brown University.
Dawson said the research indicates a simple behavioral intervention could provide help for those struggling with insomnia. He gives the same advice to every new patient the first time they meet.
“One thing that people could do would be to turn around or cover up their clock, ditch the smart watch, get the phone away so they’re simply not checking the time,” Dawson said. “There’s not any place where watching the clock is particularly helpful.”
With 15 years of research and clinical experience in the sleep field, Dawson is interested in comparing individuals’ sleeping experiences with what is concurrently happening in their brains. He trains and supervises doctoral students in the Department of Psychological and Brain Science’s Clinical Science Program.
Physical Activity Trajectories and Functional Recovery After Acute Stroke Among Adults in Sweden
by Dongni Buvarp, Adam Viktorisson, Felix Axelsson, Elias Lehto, Linnea Lindgren, Erik Lundström, Katharina S. Sunnerhagen in JAMA Network Open
After a stroke, physical activity can be pivotal to successful recovery. People who spend four hours a week exercising after their stroke achieve better functional recovery within six months than those who do not, a University of Gothenburg study shows.
The study, now published in the scientific journal JAMA Network Open, is based on data concerning 1,500 stroke patients in 35 Swedish hospitals. The participants were grouped according to their poststroke patterns of physical activity.
The results show that increased or maintained physical activity, with four hours’ of exercise weekly, doubled the patients’ chances of recovering well by six months after a stroke. Men and people with normal cognition kept up an active life relatively more often, with better recovery as a result.
The researchers have previously succeeded in demonstrating a clear inverse association between physical activity and the severity of stroke symptoms at the actual onset of the condition. These new findings highlight the importance of maintaining a healthy, active lifestyle after a stroke.
The first and corresponding author of the study, Dongni Buvarp, is a researcher in clinical neuroscience at Sahlgrenska Academy, University of Gothenburg. Besides her research internship, she is a resident doctor at an initial stage of specialist training at Sahlgrenska University Hospital.
“Physical activity reprograms both the brain and the body favorably after a stroke. Exercise improves the body’s recovery at the cellular level, boosts muscle strength and well-being, and reduces the risk of falls, depression, and cardiovascular disease. Regardless of how severe the stroke has been, those affected can derive benefits from exercising more,” she says.
“Being physically active is hugely important, especially after a stroke. That’s a message that health professionals, stroke victims and their loved ones should all know. Women and people with impaired cognition seem to become less active after stroke. The study results indicate that these groups need more support to get going with physical activity,” Buvarp says.
One weakness of the study is that, with a few exceptions, the researchers were unable to study the participants’ degree of activity before the stroke. The patients included were treated in Sweden in the period from 2014 to 2019.
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