“Noisy” Neurons May Repeatedly Disrupt Your Sleep

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You don’t remember it, but you woke up at least 100 times last night. These spontaneous arousals, lasting less than 15 seconds each, occur roughly every five minutes and don’t seem to affect how well-rested you feel. They are unrelated to waking up from a bad dream or your partner tossing and turning. Instead, they seem to be linked to some internal biological mechanism.

Frequently waking up throughout the night may have protected early humans from predators by increasing their awareness of their surroundings during sleep. “The likelihood someone would notice an animal is higher [if they] wake up more often,” says Ronny Bartsch, a senior lecturer in the Department of Physics at Bar-Ilan University in Israel. “When you wake up, you’re more prone to hear things. In deep sleep, you’re completely isolated.”

Sleep scientists, however, have been stumped as to what triggers these nocturnal disruptions. In a new Science Advances paper Bartsch proposes an innovative hypothesis that spontaneous arousals are due to random electrical activity in a specific set of neurons in the brain—aptly named the wake-promoting neurons.

Even when you are asleep your brain cells continuously buzz with a low level of electrical activity akin to white noise on the radio. Occasionally, this electrical clamor reaches a threshold that triggers the firing of neurons. The new paper suggests that when random firing occurs in the wake-promoting neurons, a person briefly jerks awake. But this is countered by a suite of sleep-promoting neurons that helps one quickly fall back to sleep.

Low-level electrical activity in neurons increases in colder temperatures whereas warmer temperatures flatten it. As a result, there should be fewer spontaneous arousals in hot weather. To test this theory, the researchers created computer models that mapped how neuronal noise should act at different temperatures and how the varying electrical activity could affect spontaneous arousals. They also measured sleep in zebra fish, which have similar day/night cycles to humans but are ectothermic, meaning their body temperature is controlled by the environment rather than by internal processes.

The researchers compared the fish’s sleep rates at four different water temperatures: 77, 82 (ideal for zebra fish), 84 and 93 degrees Fahrenheit. Across the board, the colder the water the more often the zebra fish woke up and the longer they stayed awake. The data from the zebra fish and the models of temperature, neuronal noise and arousal matched perfectly. “I think their theory is a perfectly good one and may even be correct,” says Clifford Saper, a neuroscientist at Harvard Medical School’s Division of Sleep Medicine and head of Neurology at Beth Israel Deaconess Medical Center who was not involved with the study. “But the experiment they did doesn’t test that hypothesis.”

The zebra fish experiment shows the fish wake up more frequently and stay awake for longer in colder temperatures but reveals nothing about these animals’ neuronal noise—or humans’, for that matter. Bartsch says that, so far, no studies have figured out how to measure neuronal noise in a sleeping animal.

The idea that warm temperatures cause fewer nocturnal disruptions also seemingly flies in the face of conventional wisdom that a colder bedroom leads to better sleep. But waking up because you are hot and uncomfortable is different from these brief spontaneous arousals. In fact, our bodies are pretty good at regulating their core brain and body temperatures, so the difference of a few degrees outside would not alter neuronal activity. In contrast, zebra fish’s temperature varies quite a bit. Saper says because of this zebra fish “are probably the last animal that I would use to try to make this point.”

Bartsch emphasizes the study is not trying to make a claim about thermoregulation in adults but he says it may have implications for newborn babies. “Because very young infants are more ectothermic than endothermic, their arousability could scale similarly to fish for different ambient temperatures.”

Infants are not as good at regulating their own temperature and so are more vulnerable to changes in the environment. (This is why premature babies have to be kept in incubators.) Consequently, the researchers think newborns may be more susceptible to heat-related fluctuations in neuronal noise.

The theory may have important implications for infant sleep. Although they may be disruptive to parents, spontaneous arousals could help save a baby’s life. Sudden infant death syndrome (SIDS) has been a leading cause of mortality in children between one month and one year of age and yet largely remains a mystery. One idea is that SIDS is caused by a stoppage in breathing, often through accidental suffocation. Waking up during the night can prompt babies to shift or cry out, helping to ensure that they do not have anything obstructing their airways and are still breathing. “We came up again with a theory that the babies with SIDS have low neuronal noise and therefore they have lower arousals,” says Hila Dvir, a physicist at Bar-Ilan. “Because they have low arousals, they are less protected from any hypoxic event—a shortage of oxygen.”

Not everyone is convinced, though. “Over the years, people have come up with ideas to explain SIDS, like a single explanation for it, and they just keep hitting dead ends with it because it’s probably a complex, heterogeneous situation,” says Rafael Pelayo, a clinical professor at the Stanford Center for Sleep Sciences and Medicine “It is a cool idea that this neuronal noise is explaining the arousals. I just think they jumped a little bit when they got into SIDS. It has to be more complicated than that.”

https://www.scientificamerican.com/article/sound-awake-noisy-neurons-may-repeatedly-disrupt-your-sleep1/

Clock Nucleus and Aggression Centres Linked, Implication For Alzheimer’s Treatment

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A research team at University of Copenhagen including a researcher from the Faculty of Health and Medical Sciences has discovered a circuit in the brains of mice connecting circadian rhythm to aggressive behaviour. The discovery is particularly interesting to Alzheimer’s patients who experience increased aggression at night. The researchers have developed special protein tools capable of turning off the cells in the brain causing the behaviour.

Each year around 8,000 Danes are diagnosed with a form of dementia. Alzheimer’s disease is one of them. The disease manifests itself in memory difficulties in particular, but can also result in personality changes and mood swings.

When the sun sets 20 per cent of all Alzheimer’s patients experience increased bewilderment, anxiety, unease, disorientation, irritation and aggression. This phenomenon is called ‘sundowning’ or sundown syndrome. At worst, the condition can mean that the patient must be left in professional care, as it can be difficult for family members to handle. The cause of the condition is unknown, but previous research has suggested that it is connected to the circadian rhythm.

A research team including a researcher from the Department of Drug Design and Pharmacology at the University of Copenhagen is now able to confirm this connection. The researchers have identified and mapped a circuit between the part of the brain containing the circadian clock or circadian rhythm and a part of the brain controlling aggression.

’We have shown that the circadian clock in mice is closely linked to an aggression centre in the mouse brain by a cell circuit. The human brain has those same groups of cells that the circuit goes through. With this knowledge, we are now enabled to target this circuit pharmacologically and target cells that make people aggressive at the end of the day’, says Assistant Professor Timothy Lynagh from the Department of Drug Design and Pharmacology at the University of Copenhagen.

Turn off the Aggression
The inner clock or circadian rhythm is located in the part of the brain called suprachiasmatic nucleus. One of the parts of the brain that control aggressive behaviour is called the ventromedial hypothalamus. Researchers have previously observed a connection between the two parts of the brain, though none have had knowledge of the specific circuit connecting them.

Using electrophysiology and microscopy, the researchers measured the activity of the brain cells at main author Clifford Saper’s laboratory in Boston. They also turned off parts of the cell circuit in the brains of mice to map the circuit and to identify the cells connecting the two parts of the brain. To map circuits in the brain you need a protein tool that can turn off the various cells to determine their function. Assistant Professor Timothy Lynagh has designed precisely such a tool.

‘We take a receptor and mutate it, so that it is not sensitive to anything in the brain, but very sensitive to a particular drug. The tool works like an on/off switch. When you put the protein tool in the mouse brain, under normal circumstances, nothing will happen. But when you give the animal the drug, the cells that have the receptor on them will be turned off’, Timothy Lynagh explains.

Using this tool, the researchers can thus in theory turn off the cells that cause people suffering from sundown syndrome to become more aggressive at night.

May Be Used on Humans 20 Years into the Future
The tool can also be used in other contexts than sundown syndrome. In other studies, Tim Lynagh’s tool has been used to turn off cells in rats linked to anxiety and fear.

‘If you can start understanding which cells in the brain lead to which problems, you can then put this tool into any of those parts of the brain. The person who takes the drug will then have the cells causing the problem turned off’, Timothy Lynagh says.

Even though the study was conducted on mice, the tool and the knowledge the research has generated can potentially be used in the treatment of humans.

‘Because of the huge advances that are coming along with CRISPR, I would be tempted to say that based on a recent demonstration of gene therapy for brain disease, potentially, it could be used in the human brain in 20 years’ time. Of course it needs a lot more research’, he says.

Reference:
Todd, W. D., Fenselau, H., Wang, J. L., Zhang, R., Machado, N. L., Venner, A., … & Lowell, B. B. (2018). A hypothalamic circuit for the circadian control of aggression. Nature neuroscience, 1.

http://healthsciences.ku.dk/news/2018/05/researchers-discover-connection-between-circadian-rhythm-and-aggression/

Merck study failure may signal doom for a broad group of pivotal Alzheimer’s studies focused on the amyloid theory of treatment.

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by John Carroll

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The BACE theory in Alzheimer’s R&D is simple. Cut off the flow of amyloid beta to the brain and you can eliminate what is widely believed — though not proven — to be a cause of the disease. Do that, and you could bend the course of this devastating illness in millions of people with mild to moderate forms of the disease.

And Merck $MRK just spent a fortune to demonstrate that it may well be completely wrong.

To be sure, Merck ran a clean study for verubecestat, the leading BACE drug in the clinic, and displayed the data on 1,958 patients for all to see today in the New England Journal of Medicine. Investigators carefully tracked amyloid beta flows in cerebrospinal cords and found that the drug did what it was intended to do, with a dramatic reduction of the toxic protein. 

It had no effect, with patients in the two dosage groups tracking in parallel decline on both cognition and function, the two classic measures for Alzheimer’s. 

The conclusion they reached is that the damage already present in the brains of patients with Alzheimer’s may be too extensive to treat with any BACE drug. And they also concede that the amyloid theory itself may be just flat wrong.

This suggests that once dementia is present, disease progression may be independent of Aβ production or, alternatively, that the amyloid hypothesis of Alzheimer’s disease may not be correct. Because Aβ deposition takes place years before clinical symptoms become apparent, it has been proposed that treatments targeting amyloid should be implemented early in the disease process, before the onset of clinical symptoms.

Soon after this study failed, Merck also threw in the towel on their second pivotal trial, noting it too was a flop. Those data are still being evaluated, but it underscores the belief that all of the BACE studies — including those at Eli Lilly $LLY, partnered with AstraZeneca $AZN, or Biogen $BIIB, allied with Eisai — are headed straight to failure.

Biogen is also rolling the dice on aducanumab, which the company has touted as a leading amyloid beta therapy. But with investigators in the field openly wondering whether the amyloid theory has lured a long lineup into a clinical disaster zone, it’s likely to face growing skepticism that it can develop a safe, effective therapy with just one drug.

This doesn’t by any means eliminate work in the area. True, Pfizer recently pulled out after spending hundreds of millions of dollars on their programs. But startups like Denali believe that new and better technology can give them better odds at success, while Celgene is jumping in with its own new pipeline. Others want to see if combination approaches using tau and amyloid beta together could work. 

Merck’s suggestion about going even earlier in the disease process has also prompted a range of studies in pre-symptomatic patients, while the FDA has signaled its interest in coming up with biomarkers to help speed new studies.

After more than 200 R&D projects ended in disaster, though, Alzheimer’s is looking like an increasingly daunting challenge, with no clear path forward that would inspire confidence among patients with the disease.

Merck study may signal doom for a broad group of pivotal Alzheimer’s studies

Horses remember if you smiled or frowned when they last saw you

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By Sam Wong

Why the long face? Horses can remember the facial expressions they see on human faces and respond differently if you smiled or frowned when they last saw you.

Leanne Proops, now at the University of Portsmouth, UK, and her colleagues at the University of Sussex showed in 2016 that horses respond differently to photographs of happy or angry human faces. Now they have studied whether horses can form lasting memories of people that depend on their facial expressions.

First, they showed horses a photo of one of two human models, displaying either a happy or angry face. Several hours later, the model visited the horse in person, this time with a neutral expression. As a control, some horses saw a different model in the second part to the one they saw in the photograph.

Crucially, the models didn’t know which photo the horse had seen earlier. In the early 20th century, a horse called Clever Hans amazed audiences by appearing to answer simple mathematical problems by tapping his hoof. It turned out he was responding to involuntary cues from his trainer. Proops’ study aimed to eliminate such cues.

Stop pulling faces!
Stop pulling faces!
Pal Teravagimov Photography / Getty
By Sam Wong

Why the long face? Horses can remember the facial expressions they see on human faces and respond differently if you smiled or frowned when they last saw you.

Leanne Proops, now at the University of Portsmouth, UK, and her colleagues at the University of Sussex showed in 2016 that horses respond differently to photographs of happy or angry human faces. Now they have studied whether horses can form lasting memories of people that depend on their facial expressions.

First, they showed horses a photo of one of two human models, displaying either a happy or angry face. Several hours later, the model visited the horse in person, this time with a neutral expression. As a control, some horses saw a different model in the second part to the one they saw in the photograph.

Crucially, the models didn’t know which photo the horse had seen earlier. In the early 20th century, a horse called Clever Hans amazed audiences by appearing to answer simple mathematical problems by tapping his hoof. It turned out he was responding to involuntary cues from his trainer. Proops’ study aimed to eliminate such cues.

The team found that the horses remembered the models’ previous facial expressions.

Horses prefer to look at negative and threatening sights with their left eye, and positive social stimuli with their right eye. In the study, when they saw a model they had seen frowning earlier, they spent more time looking with their left eye. They also exhibited more stress-related behaviours, like scratching and floor sniffing. In contrast, when they saw a model they had seen smiling earlier, they spent more time looking with their right eye.

Many other animals have shown an ability to remember human faces, including sheep and fish. Wild crows will hold a grudge for years against people who have treated them badly, and even teach other crows to mob their enemies.

However, the horses seem to form an opinion about people based only on their expression in a photograph. “That’s something we haven’t really seen in animals before,” says Proops.

“The horse family has the most expressive faces after the primates, so logically they pay attention to faces and expressions,” says Frans de Waal at Emory University in Atlanta. “Horses surrounded by people have ample opportunity to learn what our expressions mean.”

Journal reference: Current Biology, DOI: 10.1016/j.cub.2018.03.035

https://www.newscientist.com/article/2167423-horses-remember-if-you-smiled-or-frowned-when-they-last-saw-you/

Hidden Text Found on ‘Blank’ Dead Sea Scrolls

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By Laura Geggel

Previously hidden text on fragments of the Dead Sea Scrolls is now readable, revealing a possible undiscovered scroll and solving a debate about the sacred Temple Scroll. The discoveries came from a new infrared analysis of the artifacts, the Israel Antiquities Authority (IAA) announced yesterday (May 1).

The newfound writing came from the books of Deuteronomy and Leviticus, which are in the Hebrew Bible (also known as the Old Testament of the Christian Bible), and the Book of Jubilees, a text written at the same time as the Hebrew Bible that was never incorporated into the biblical books, the archaeologists said.

Researchers presented the newly revealed words at an international conference, called “The Dead Sea Scrolls at Seventy: Clear a Path in the Wilderness,” in Israel.

Local Bedouins and archaeologists discovered the Dead Sea Scrolls in the 1940s in caves near Qumran in the West Bank, located near the northern edge of the Dead Sea. Excavations in the following decades turned up tens of thousands of parchment and papyrus fragments that were dated to 2,000 years ago, the IAA said.

There were so many small and fragile fragments that archaeologists placed them in boxes to be studied at a later date. Now, that time has come: IAA researchers are digitizing the scrolls so that they can be studied and shared with the public without damaging the originals.

During one of these digital scans, Oren Ableman, a scroll researcher at the IAA’s Dead Sea Scrolls Unit and a doctoral student in the Department of Jewish History at the Hebrew University of Jerusalem, noticed something peculiar on a few dozen fragments that had been discovered in Cave 11 near Qumran.

These fragments looked blank to the naked eye. But, by using infrared imaging, Ableman discovered that they held Hebrew letters and words, he said in a statement. Ableman then deciphered the script and even connected the fragments to the manuscripts that they had likely been attached to before crumbling away.

Some of the more interesting fragments include the following:

1) A fragment from the Temple Scroll, a text that gives instructions for how to conduct services in the ideal temple. Scholars have debated whether there are two or three copies of the Temple Scroll from Cave 11. The discovery of the text on this fragment suggests that there are, indeed, three copies.

2) A fragment from the Great Psalms Scroll. This fragment contains part of the beginning of Psalm 147:1, and the end of the verse is preserved in a larger fragment from the same cave. The newfound fragment shows that the ancient Psalm is slightly shorter than the Hebrew text used nowadays.

3) Another fragment has letters written in paleo-Hebrew, an ancient Hebrew script. This fragment could not be attributed to any known manuscripts and could belong to an unknown manuscript.

https://www.livescience.com/62467-hidden-text-dead-sea-scrolls.html?utm_source=notification

Brain folds may indicate risk of schizophrenia

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By Bahar Gholipour

Schizophrenia may have a special fingerprint in the brain, even before its symptoms fully emerge. Now, a new method of analyzing this fingerprint — found within the folds of the brain — could help predict which young adults at high risk for schizophrenia will go on to develop the illness, a new study suggests.

The method, which was based on MRI scans of the brain, looked at the correlation between the amount of folding in different brain areas, which can reflect the strength of underlying connections between those areas. Using this method, the researchers could predict the outcome of 79 high-risk individuals with 80 percent accuracy, they reported yesterday (April 25) in the journal JAMA Psychiatry.

These findings need to be confirmed in larger future studies before the method can be used to in the clinic, the researchers said. And even then, a simple brain scan on its own won’t be enough to predict the future — it has to be used in conjunction with other symptoms for which a person is seeking help. But the goal is to find what clues from the brain’s structure could help clinicians better identify and treat patients before they experience full-blown schizophrenia and drop out of schools or lose their jobs due to a psychotic episode, said study investigator Dr. Lena Palaniyappan, an associate professor of psychiatry at Western University in Ontario, Canada.

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What the Folds of Your Brain Could Tell You About Schizophrenia Risk
A simplified representation of the folds in different brain regions.
Credit: University Psychiatric Clinics Basel
Schizophrenia may have a special fingerprint in the brain, even before its symptoms fully emerge. Now, a new method of analyzing this fingerprint — found within the folds of the brain — could help predict which young adults at high risk for schizophrenia will go on to develop the illness, a new study suggests.

The method, which was based on MRI scans of the brain, looked at the correlation between the amount of folding in different brain areas, which can reflect the strength of underlying connections between those areas. Using this method, the researchers could predict the outcome of 79 high-risk individuals with 80 percent accuracy, they reported yesterday (April 25) in the journal JAMA Psychiatry.

These findings need to be confirmed in larger future studies before the method can be used to in the clinic, the researchers said. And even then, a simple brain scan on its own won’t be enough to predict the future — it has to be used in conjunction with other symptoms for which a person is seeking help. But the goal is to find what clues from the brain’s structure could help clinicians better identify and treat patients before they experience full-blown schizophrenia and drop out of schools or lose their jobs due to a psychotic episode, said study investigator Dr. Lena Palaniyappan, an associate professor of psychiatry at Western University in Ontario, Canada. [10 Things You Didn’t Know About the Brain]

Schizophrenia is a mental disorder characterized by psychotic episodes involving delusional thoughts and distorted perception. It is often preceded by subtle symptoms: A teenager who is withdrawn and suspicious, has anxiety, depression or sleep problems, and who experiences subtle changes in thinking and perception may be deemed by a doctor to be at high risk for developing schizophrenia in the next two or three years. But having these symptoms, which overlap with those of many other mental health conditions, doesn’t mean one will surely go on to develop schizophrenia — in fact, just about a third of individuals with these symptoms do.

“It’s really hard to know who is going to develop schizophrenia and who is not,” Palaniyappan told Live Science.

A wrinkle in the brain

Compared with other animals, the surface of the human brain is especially wrinkly — likely as a solution to fit a large brain inside a small skull. The patterns of folds in the brain’s surface, called the cortex, are determined before birth and change very little after the first or second year of life.

Previous studies of people with conditions such as schizophrenia and autism have detected local differences in folding patterns. For example, they have found a smoother surface in one brain region or a more wrinkled one in another, when comparing people with these conditions to the general population.

Palaniyappan and his colleagues examined all the brain regions and the relationship between their folding patterns. The idea is that the degree of folding would be similar between two brain areas if they are strongly interconnected. So, if an individual doesn’t show the same folding patterns as everyone else, it may suggest a problem in the wiring beneath the brain’s surface.

“Imagine two brain regions have a strong wire between them. If you cut the wire off, both of these regions would not be properly folded,” Palaniyappan said.

Sorting through scans

The team collected MRI brain scans from a group of people in Switzerland, who were on average 24 years old. The participants included 79 people with symptoms suggesting a high risk of schizophrenia and 44 healthy control subjects.

Then, the researchers followed the participants for four years and found 16 people in the high-risk group developed schizophrenia.

Looking back at the brain scans, the researchers found that 80 percent of the time, the relationship between folding patterns could correctly identify who developed schizophrenia and who didn’t. Those who did seemed to have a disorganized brain network — the folds of their cortical regions didn’t go hand in hand as much as the folds in the controls and in the high-risk people who didn’t develop the illness.

The earlier patients with schizophrenia receive psychotherapy or medication, the better they fare, according to a 2005 review of 30 studies published in the American Journal of Psychiatry. Early intervention may even change the course of the illness. One study published last year in Nature Neuropsychopharmacology, for instance, found a longer period of untreated symptoms was associated with weaker connectivity in the brain, especially in areas associated with responding to antipsychotic medications.

https://www.livescience.com/62414-brain-folds-schizophrenia.html

Midday naps improve teenagers’ grades

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Teenagers and sleep. It’s certainly a passionate subject for many American parents … and those in China. University of Delaware’s Xiaopeng Ji is investigating the relationship between midday-napping behaviors and neurocognitive function in early adolescents. In a study funded by the National Institutes of Health, the School of Nursing assistant professor and principal investigator Jianghong Liu (University of Pennsylvania) turned to the Chinese classroom. With participants from schools in Jintan, she measured midday napping, nighttime sleep duration and sleep quality, and performance on multiple neurocognitive tasks.

Ji is interested in the relationship between sleep and cognition. Because of the intensive learning and education demands, the adolescent population is key. Neurocognitive functioning is essential for learning, emotion and behavior control. Her findings suggest that an association between habitual midday napping and neurocognitive function, especially in China, where midday napping is a cultural practice.

“Daytime napping is quite controversial in the United States. In Western culture, the monophasic sleep pattern is considered a marker of brain maturation,” Ji said. “In China, time for napping is built into the post-lunch schedule for many adults in work settings and students at schools.”

Ji has studied the circadian rhythm of sleep (a person’s 24-hour cycle). A developmental change takes place in circadian rhythm during adolescence; teenagers’ rhythm shifts one to two hours later than the preadolescent period.

“This phase delay is biologically driven in adolescents,” Ji said. “Think about that in a school schedule. Teenagers have to get up early for school. And, with this phase delay of going to bed later, they are at-risk for chronic sleep deprivation.”

Ji explained that these adolescents may experience impaired neurocognitive function, which makes paying attention in school even more difficult. Memory and reasoning ability also suffer.

A circadian dip occurs daily from 12 to 2 p.m. During that period, adolescents are more likely to fall asleep. In a U.S. school, a student does not have a formal opportunity to do so.

“Throughout childhood, U.S. kids experience decreases in napping tendencies. Kids are trained to remove their midday napping behavior,” said Ji. “Conversely in China, the school schedule allows children to maintain it.”

Researchers have taken a friend or foe mentality towards napping. Many consider a midday snooze as needed compensation for nighttime sleep deprivation; another faction believes daytime napping continually interferes with nighttime sleep. Many studies invite people to a lab setting — experimentally imposing the nap — and find the aforementioned cognitive benefits. But Ji said that’s difficult to correlate with habitual sleep at home.

“The results from lab studies may be different from what the population is habitually doing at home — sleeping in their own bed,” Ji said.

Lots of research exists on adults, but that’s not the case for adolescents. This lack of literature motivated Ji to take on the task. And since the American school schedule was a barrier to finding more information, researchers used Chinese data in the University of Delaware and University of Pennsylvania collaborative study.

Key findings

Ji investigated two dimensions of nap behavior — frequency and duration. Routine nappers, who napped five to seven days in a week, had sustained attention, better nonverbal reasoning ability and spatial memory. How long to nap is also an important question? The sweet spot is between 30 to 60 minutes. A nap longer than one hour interferes with circadian rhythm. Participants who slept between 30 to 60 minutes produced better accuracy in attention tasks as well as faster speed. She recommends not to nap after 4 p.m., nor over-nap.

Researchers were surprised to find a positive relationship between midday napping and nighttime sleep, which is different than the literature. Habitual nappers (who napped more often) tended to have a better nighttime sleep.

“That’s different than the findings in the United States, where napping may serve as a function to replace sleep lost from the previous night. Consequently, that may interfere with the following night’s sleep,” Ji said. “In China, a midday nap is considered a healthy lifestyle. Routine nappers are more likely to experience healthy nighttime sleep. So routine nappers are essentially trained to sleep well and sleep more at night.”

Ji was clear that this study was observational. At this point, she cannot conclude causality. She hopes this line of research can inform future studies and public health policy.

http://www.udel.edu/udaily/2018/april/xiaopeng-ji-napping-neurocognitive-function/

Flat-Earther Convention

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Most believers in a flat Earth think the planet is a flat disk surrounded by an ice wall.

By Jeanna Bryner

More than 200 flat-Earth enthusiasts descended on West Midlands, England, this past weekend to “engage freely in deep and meaningful discussions,” according to the Flat Earth Convention UK.

The Earth’s glorious globular-ness was proved more than 2,000 years ago by the ancient Greeks, but there’s a small subset of people who think the planet is a disk despite enjoying the downward pull of gravity that could only result from living on a sphere.

At this conference, they were presenting their scientific evidence for such a disk. One of the more interesting pieces of evidence came from speaker Darren Nesbit, who referred to the “Pac-Man effect” as the reason why planes don’t fall off the edge of a flat Earth, according to the science news website Physics-Astronomy.org. When a plane or other object reaches the edge of the horizon, such as when Pac-Man reaches the end of the screen, that object will teleport from one side of the planet to the other, a la Pac-Man entering from the other side of the screen.

According to the group that put on the convention, the gathering also included some “alternative viewpoints.”

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Flat-Earthers Explain Why We Don’t Fall Off the Edge of Our Planet, and It Involves Pac-Man
Most believers in a flat Earth think the planet is a flat disk surrounded by an ice wall.
Credit: Getty
More than 200 flat-Earth enthusiasts descended on West Midlands, England, this past weekend to “engage freely in deep and meaningful discussions,” according to the Flat Earth Convention UK.

The Earth’s glorious globular-ness was proved more than 2,000 years ago by the ancient Greeks, but there’s a small subset of people who think the planet is a disk despite enjoying the downward pull of gravity that could only result from living on a sphere.

At this conference, they were presenting their scientific evidence for such a disk. One of the more interesting pieces of evidence came from speaker Darren Nesbit, who referred to the “Pac-Man effect” as the reason why planes don’t fall off the edge of a flat Earth, according to the science news website Physics-Astronomy.org. When a plane or other object reaches the edge of the horizon, such as when Pac-Man reaches the end of the screen, that object will teleport from one side of the planet to the other, a la Pac-Man entering from the other side of the screen. [7 Ways to Prove the Earth Is Round]

According to the group that put on the convention, the gathering also included some “alternative viewpoints.” (You think?)

“In conjunction with a select number of well-known flat-earth speakers, we have also provided some alternative viewpoints. We truly hope that new friendships are forged, ideas and experiments are brain stormed and future actions are set in motion,” they state on their website.

Among the nine speakers were Nesbit, a musician who became interested in flat-Earth beliefs in 2014; Dave Marsh, a manager with England’s National Health Service; and Gary John, an independent flat-Earther who put on the convention.

Marsh was one of four speakers who are associated with the flat-Earth research group called FEcore. His research focuses on the moon, “as he believes it is the key to unlocking the globe earth deception,” according to the convention website: https://www.flatearthconventionuk.co.uk/home.html

He studies the speed of the moon across the night sky. (Flat-Earthers believe the moon and sun orbit around Earth’s North Pole.) “My research destroys big bang cosmology,” he said, according to Physics-Astronomy.org. “It supports the idea that gravity doesn’t exist and the only true force in nature is electromagnetism.”

Another speaker, Martin Kenny, purports to have broader views of a flat Earth than other believers. “It is my innerstanding that there are other lands, dimensions and civilizations yet to be discovered across and within the plane of our Earth. The whole earth consists of 4 concentric rings of land, each ring having its own sun and moon, which would be our wandering stars,” he says on the convention website.

Flat-Earthers like Kenny agree that the planet is a flat plane, though they have varied ideas for the disk’s particular layout. Many seem to think the Earth is a disk surrounded by an ice wall and that those who show evidence to the contrary — including NASA, with its many satellite pics beamed down of our blue marble — are fakes. These conspiracy theorists believe NASA and others are trying to keep this secret from the public.

As for how many people buy into this clearly mistaken belief, that is unknown. However, the oldest flat-Earth organization, the Flat Earth Society, claims to have 555 registered members as of August 2016. According to the society’s website, the group was founded by an English inventor named Samuel Birley Rowbotham in the 1800s.

In addition to the Q&A’s with the nine speakers at the three-day convention, there was apparently a talk entitled “Heliocentric v Geocentric experts Debate.” The convention’s site doesn’t indicate who was debating these two views, one proved ages ago, and the other suggesting Earth is fixed in space with the universe revolving around it.

This isn’t the first flat-Earth convening. In November 2017, the Flat Earth International Conference was held in Raleigh, North Carolina. That convention hosted some big-name (in flat-Earth circles, at least) speakers, such as founder of the Flat Earth Clues series on YouTube, Mark Sargent, who thinks we are all locked inside a “Truman Show”-like dome structure. The next FEIC is scheduled for Nov. 15 -16 in Denver.

https://www.livescience.com/62454-flat-earthers-explain-pac-man-effect.html?utm_source=notification

Personal subjective reports of memory ability may be a reliable early marker of Alzheimer’s disease.

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Psychological sciences doctoral student Marci Horn (left) conducts a name-face memory test as part of a study at the Center for Vital Longevity.

New research from the Center for Vital Longevity (CVL) at The University of Texas at Dallas suggests that subjective complaints about poor memory performance, especially in people over 60, could be a useful early marker for the onset of mild cognitive decline, which sometimes foreshadows Alzheimer’s disease.

Subjective memory is a person’s unscientific self-evaluation of how good his or her memory is, and whether, in that person’s opinion, there has been any worsening of memory through age. While some changes may be undetectable to others and are often too subtle to register on cognitive tests, the person subjectively believes that memory is slipping.

Published recently in Psychology and Aging, the research from Dr. Karen Rodrigue’s lab at CVL examined subjective memory complaints in nearly 200 healthy adults, ages 20 to 94. Previous studies suggest that subjective memory complaints are not necessarily indicative of cognitive decline, and may stem from underlying conditions such as anxiety and depression, which have been shown to impede memory.

The current study measured mood and screened out depressed individuals. Researchers also measured participants for known risk factors for memory loss and Alzheimer’s, such as higher levels of beta-amyloid in the brain and the presence of a gene variant called ApoE4. These factors were taken into account to examine whether subjective memory alone was a reliable correlate of actual memory ability.

The study focused on associative memory — for example, remembering word pairs and name-face pairs. This type of memory is particularly sensitive to age-related decline, and the most common complaint of aging individuals.

The study found that a person’s intuitive or intrinsic assessment of his or her own memory was actually a reliable predictor of performance on the laboratory memory assessment. This result was particularly true for individuals with genetic risk for memory loss.

“Our findings show that subjective memory can be a reliable indicator of memory performance, even in cognitively healthy adults,” said psychological sciences doctoral student Marci Horn, the lead author of the study. “The same people who self-report memory problems may also have other risk factors associated with increased risk of Alzheimer’s disease.”

The researchers also found that men who had higher amyloid levels reported the most subjective memory complaints in the study. Previous studies had not uncovered a sex-specific relationship, nor did they account for the genetic and amyloid risk factors in these associations, the researchers said.

The strongest correlation of subjective memory complaints with actual cognitive performance was in study participants older than 60, when people are generally at greater risk for Alzheimer’s disease.

“It seems that awareness of memory changes may be a reliable indicator of one’s current memory ability, and may serve as another harbinger of future loss, as this relationship was strongest in those with known risk factors for Alzheimer’s disease, namely ApoE4 genotype and beta-amyloid burden in the brain,” said Rodrigue, the senior author of the study and assistant professor in the School of Behavioral and Brain Sciences (BBS). “We are following these individuals over time to further test this idea.”

Dr. Kristen Kennedy, an assistant professor in BBS, also was an author of the study. The research was funded in part by grants from the National Institutes of Health.

https://www.utdallas.edu/news/2018/4/30-32929_Subjective-Memory-May-Play-Role-in-Signaling-Cogni_story-wide.html?WT.mc_id=NewsHomePageCenterColumn

University of Michigan scientists develop a pill that may be superior to mammogram from detecting breast cancer

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As many as one in three women treated for breast cancer undergo unnecessary procedures, but a new method for diagnosing it could do a better job distinguishing between benign and aggressive tumors.

Researchers at the University of Michigan are developing a pill that makes tumors light up when exposed to infrared light, and they have demonstrated that the concept works in mice.

Mammography is an imprecise tool. About a third of breast cancer patients treated with surgery or chemotherapy have tumors that are benign or so slow-growing that they would never have become life-threatening, according to a study out of Denmark last year. In other women, dense breast tissue hides the presence of lumps and results in deaths from treatable cancers. All that, and mammograms are notoriously uncomfortable.

“We overspend $4 billion per year on the diagnosis and treatment of cancers that women would never die from,” said Greg Thurber, U-M assistant professor of chemical engineering and biomedical engineering, who led the team. “If we go to molecular imaging, we can see which tumors need to be treated.”

The move could also catch cancers that would have gone undetected. Thurber’s team uses a dye that responds to infrared light to tag a molecule commonly found on tumor cells, in the blood vessels that feed tumors and in inflamed tissue. By providing specific information on the types of molecules on the surface of the tumor cells, physicians can better distinguish a malignant cancer from a benign tumor.

Compared to visible light, infrared light penetrates the body easily—it can get to all depths of the breast without an X-ray’s tiny risk of disrupting DNA and seeding a new tumor. Using a dye delivered orally rather than directly into a vein also improves the safety of screening, as a few patients in 10,000 can have severe reactions to intravenous dyes. These small risks turn out to be significant when tens of millions of women are screened every year in the U.S. alone.

But it’s not easy to design a pill that can carry the dye to the tumor.

“To get a molecule absorbed into the bloodstream, it needs to be small and greasy. But an imaging agent needs to be larger and water-soluble. So you need exact opposite properties,” Thurber said.

Fortunately, they weren’t the only people looking for a molecule that could get from the digestive system to a tumor. The pharmaceutical company Merck was working on a new treatment for cancer and related diseases. They got as far as phase II clinical trials demonstrating its safety, but unfortunately, it wasn’t effective.

“It’s actually based on a failed drug,” Thurber said. “It binds to the target, but it doesn’t do anything, which makes it perfect for imaging.”

The targeting molecule has already been shown to make it through the stomach unscathed, and the liver also gives it a pass, so it can travel through the bloodstream. The team attached a molecule that fluoresces when it is struck with infrared light to this drug. Then, they gave the drug to mice that had breast cancer, and they saw the tumors light up.

The research is described in a study in the journal Molecular Pharmaceutics, titled, “Oral administration and detection of a near-infrared molecular imaging agent in an orthotopic mouse model for breast cancer screening.”

This work was done in collaboration with David Smith, the John G. Wagner Collegiate Professor of Pharmaceutical Sciences at the U-M College of Pharmacy. It was supported by the Foundation for Studying and Combating Cancer and the National Institutes of Health.
Bhatnagar, S., Verma, K. D., Hu, Y., Khera, E., Priluck, A., Smith, D., & Thurber, G. M. (2018). Oral Administration and Detection of a Near-Infrared Molecular Imaging Agent in an Orthotopic Mouse Model for Breast Cancer Screening. Molecular Pharmaceutics. doi:10.1021/acs.molpharmaceut.7b00994