Posts Tagged ‘brain’

By Laura Counts

Can’t stop checking your phone, even when you’re not expecting any important messages? Blame your brain.

A new study by researchers at UC Berkeley’s Haas School of Business has found that information acts on the brain’s dopamine-producing reward system in the same way as money or food.

“To the brain, information is its own reward, above and beyond whether it’s useful,” says Assoc. Prof. Ming Hsu, a neuroeconomist whose research employs functional magnetic imaging (fMRI), psychological theory, economic modeling, and machine learning. “And just as our brains like empty calories from junk food, they can overvalue information that makes us feel good but may not be useful—what some may call idle curiosity.”

The paper, “Common neural code for reward and information value,” was published this month by the Proceedings of the National Academy of Sciences. Authored by Hsu and graduate student Kenji Kobayashi, now a post-doctoral researcher at the University of Pennsylvania, it demonstrates that the brain converts information into the same common scale as it does for money. It also lays the groundwork for unraveling the neuroscience behind how we consume information—and perhaps even digital addiction.

“We were able to demonstrate for the first time the existence of a common neural code for information and money, which opens the door to a number of exciting questions about how people consume, and sometimes over-consume, information,” Hsu says.

Rooted in the study of curiosity

The paper is rooted in the study of curiosity and what it looks like inside the brain. While economists have tended to view curiosity as a means to an end, valuable when it can help us get information to gain an edge in making decisions, psychologists have long seen curiosity as an innate motivation that can spur actions by itself. For example, sports fans might check the odds on a game even if they have no intention of ever betting.

Sometimes, we want to know something, just to know.

“Our study tried to answer two questions. First, can we reconcile the economic and psychological views of curiosity, or why do people seek information? Second, what does curiosity look like inside the brain?” Hsu says.

The neuroscience of curiosity

To understand more about the neuroscience of curiosity, the researchers scanned the brains of people while they played a gambling game. Each participant was presented with a series of lotteries and needed to decide how much they were willing to pay to find out more about the odds of winning. In some lotteries, the information was valuable—for example, when what seemed like a longshot was revealed to be a sure thing. In other cases, the information wasn’t worth much, such as when little was at stake.

For the most part, the study subjects made rational choices based on the economic value of the information (how much money it could help them win). But that didn’t explain all their choices: People tended to over-value information in general, and particularly in higher-valued lotteries. It appeared that the higher stakes increased people’s curiosity in the information, even when the information had no effect on their decisions whether to play.

The researchers determined that this behavior could only be explained by a model that captured both economic and psychological motives for seeking information. People acquired information based not only on its actual benefit, but also on the anticipation of its benefit, whether or not it had use.

Hsu says that’s akin to wanting to know whether we received a great job offer, even if we have no intention of taking it. “Anticipation serves to amplify how good or bad something seems, and the anticipation of a more pleasurable reward makes the information appear even more valuable,” he says.

Common neural code for information and money

How does the brain respond to information? Analyzing the fMRI scans, the researchers found that the information about the games’ odds activated the regions of the brain specifically known to be involved in valuation (the striatum and ventromedial prefrontal cortex or VMPFC), which are the same dopamine-producing reward areas activated by food, money, and many drugs. This was the case whether the information was useful, and changed the person’s original decision, or not.

Next, the researchers were able to determine that the brain uses the same neural code for information about the lottery odds as it does for money by using a machine learning technique (called support vector regression). That allowed them to look at the neural code for how the brain responds to varying amounts of money, and then ask if the same code can be used to predict how much a person will pay for information. It can.

In other words, just as we can convert such disparate things as a painting, a steak dinner, and a vacation into a dollar value, the brain converts curiosity about information into the same common code it uses for concrete rewards like money, Hsu says.

“We can look into the brain and tell how much someone wants a piece of information, and then translate that brain activity into monetary amounts,” he says.

Raising questions about digital addiction

While the research does not directly address overconsumption of digital information, the fact that information engages the brain’s reward system is a necessary condition for the addiction cycle, he says. And it explains why we find those alerts saying we’ve been tagged in a photo so irresistible.

“The way our brains respond to the anticipation of a pleasurable reward is an important reason why people are susceptible to clickbait,” he says. “Just like junk food, this might be a situation where previously adaptive mechanisms get exploited now that we have unprecedented access to novel curiosities.”

How information is like snacks, money, and drugs—to your brain

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by ABBY OLENA

Animals learn by imitating behaviors, such as when a baby mimics her mother’s speaking voice or a young male zebra finch copies the mating song of an older male tutor, often his father. In a study published today in Science, researchers identified the neural circuit that a finch uses to learn the duration of the syllables of a song and then manipulated this pathway with optogenetics to create a false memory that juvenile birds used to develop their courtship song.

“In order to learn from observation, you have to create a memory of someone doing something right and then use this sensory information to guide your motor system to learn to perform the behavior. We really don’t know where and how these memories are formed,” says Dina Lipkind, a biologist at York College who did not participate in the study. The authors “addressed the first step of the process, which is how you form the memory that will later guide [you] towards performing this behavior.”

“Our original goals were actually much more modest,” says Todd Roberts, a neuroscientist at UT Southwestern Medical Center. Initially, Wenchan Zhao, a graduate student in his lab, set out to test whether or not disrupting neural activity while a young finch interacted with a tutor could block the bird’s ability to form a memory of the interchange. She used light to manipulate cells genetically engineered to be sensitive to illumination in a brain circuit previously implicated in song learning in juvenile birds.

Zhao turned the cells on by shining a light into the birds’ brains while they spent time with their tutors and, as a control experiment, when the birds were alone. Then she noticed that the songs that the so-called control birds developed were unusual—different from the songs of birds that had never met a tutor but also unlike the songs of those that interacted with an older bird.

Once Zhao and her colleagues picked up on the unusual songs, they decided to “test whether or not the activity in this circuit would be sufficient to implant memories,” says Roberts.

The researchers stimulated birds’ neural circuits with sessions of 50- or 300-millisecond optogenetic pulses over five days during the time at which they would typically be interacting with a tutor but without an adult male bird present. When these finches grew up, they sang adult courtship songs that corresponded to the duration of light they’d received. Those that got the short pulses sang songs with sounds that lasted about 50 milliseconds, while the ones that received the extended pulses held their notes longer. Some song features—including pitch and how noisy harmonic syllables were in the song—didn’t seem to be affected by optogenetic manipulation. Another measure, entropy, which approximates the amount of information carried in the communication, was not distinguishable in the songs of normally tutored birds and those that received 50-millisecond optogenetic pulses, but was higher in the songs of birds who’d received tutoring than in the songs of either isolated birds or those that received the 300-millisecond light pulses.

While the manipulation of the circuit affected the duration of the sounds in the finches’ songs, other elements of singing behavior—including the timeline of vocal development, how frequently the birds practiced, and in what social contexts they eventually used the songs—were similar to juveniles who’d learned from an adult bird.

The researchers then determined that when the birds received light stimulation at the same time as they interacted with a singing tutor, their adult songs were more like those of birds that had only received light stimulation, indicating that optogenetic stimulation can supplant tutoring.

When the team lesioned the circuit before young birds met their tutors, they didn’t make attempts to imitate the adult courtship songs. But if the juveniles were given a chance to interact with a tutor before the circuit was damaged, they had no problem learning the song. This finding points to an essential role for the pathway in forming the initial memory of the timing of vocalizations, but not in storing it long-term so that it can be referenced to guide song formation.

“What we were able to implant was information about the duration of syllables that the birds want to attempt to learn how to sing,” Roberts tells The Scientist. But there are many more characteristics birds have to attend to when they’re learning a song, including pitch and how to put the syllables in the correct order, he says. The next steps are to identify the circuits that are carrying other types of information and to investigate the mechanisms for encoding these memories and where in the brain they’re stored.

Sarah London, a neuroscientist at the University of Chicago who did not participate in the study, agrees that the strategies used here could serve as a template to tease apart where other characteristics of learned song come from. But more generally, this work in songbirds connects to the bigger picture of our understanding of learning and memory, she says.

Song learning “is a complicated behavior that requires multiple brain areas coordinating their functions over long stretches of development. The brain is changing anyway, and then on top of that the behavior’s changing in the brain,” she explains. Studying the development of songs in zebra finches can give insight into “how maturing neural circuits are influenced by the environment,” both the brain’s internal environment and the external, social environment, she adds. “This is a really unique opportunity, not just for song, not just for language, but for learning in a little larger context—of kids trying to understand and adopt behavioral patterns appropriate to their time and place.”

W. Zhao et al., “Inception of memories that guide vocal learning in the songbird,” Science, doi:10.1126/science.aaw4226, 2019.

https://www.the-scientist.com/news-opinion/researchers-implant-memories-in-zebra-finch-brains-66527?utm_campaign=TS_DAILY%20NEWSLETTER_2019&utm_source=hs_email&utm_medium=email&utm_content=77670023&_hsenc=p2ANqtz-87EBXf6eeNZge06b_5Aa8n7uTBGdQV0pm3iz03sqCnkbGRyfd6O5EXFMKR1hB7lhth1KN_lMxkB_08Kb9sVBXDAMT7gQ&_hsmi=77670023

Many people with Alzheimer’s disease take the drug donepezil (brand name Aricept) to help ease symptoms for a time. But those on the drug should be aware of a rare but potentially life-threatening side effect. The drug can cause muscles to break down, leading to a condition called rhabdomyolysis that can lead to kidney damage and even death.

The risk of hospitalization for rhabdomyolysis was more than double that for those taking Aricept compared to other Alzheimer’s drugs, a new study reports.

Still, the condition is very rare, and anyone taking Aricept should not stop taking it. But because rhabdomyolysis is potentially very serious, patients should be aware of the problem and seek medical care should symptoms arise.

The main symptom of rhabdomyolysis, or rhabdo as it is commonly called, is intense muscle pain or weakness that does not go away. Urine can also turn dark. Emergency treatment is needed to manage the condition and may require a week or longer stay in the hospital.

For the study, Canadian researchers analyzed data on 220,353 men and women over age 65 who had gotten a prescription between 2002 and 2017 for one of three Alzheimer’s drugs: donepezil, rivastigmine (Execlon) or galantamine (Razadyne).

There were 88 hospitalizations for rhabdo among 152,300 patients taking donepezil (0.06 percent prevalence), compared to 16 cases among the 68,053 patients taking one of the other drugs (0.02 percent prevalence).

The authors note that doctors should rule out rhabdo if someone on an Alzheimer’s drug comes to the hospital because of constant muscle pain. Still, the condition remains very rare (about 25,000 per year in the U.S. from all causes), and most of the cases in the current study were not life-threatening.

Other medications may also trigger the condition, including antipsychotic medications, which are also often prescribed to people with Alzheimer’s disease to allay symptoms like agitation and aggression. Cholesterol-lowering statin drugs have also been tied to an increased risk of rhabdo. It is possible that Aricept cannot trigger rhabdo alone. Further studies will be required to determine what other cofactors might act with Aricept to trigger rhabdo.

The condition more commonly arises after intense physical exertion, often in people who have not been training regularly. The condition can arise in military recruits undergoing basic training, and in people beginning high-intensity workouts at the gym.

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by Marc Flajolet, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

Jamie L. Fleet, Eric McArthur, Aakil Patel, et al: “Risk of rhabdomyolysis with donepezil compared with rivastigmine or galantamine: a population-based cohort study.” CMAJ – Canadian Medical Association Journal, Sept. 16, 2019


Microbes can produce so much alcohol that people become drunk—and sustain liver damage—without touching any booze.

by Ed Yong

The man’s troubles began in 2004, when, having moved from China to attend college in Australia, he got really drunk. That would hardly have been a noteworthy event, except that the man hadn’t consumed any alcohol—only fruit juice.

The bizarre incident soon turned into a pattern. About once a month, and out of the blue, he’d become severely inebriated without drinking any alcohol. Over time, the episodes became more severe and more frequent. He lost jobs because people suspected him of being a closet drinker. He was frequently hospitalized. In 2011, he returned to China and his mother cared for him while monitoring him with a Breathalyzer. His blood-alcohol levels, she found, would erratically and inexplicably soar to 10 times the legal limit for driving.

In June 2014, at the age of 27, he was admitted to the intensive-care unit of Chinese PLA General Hospital, in Beijing. At one point, so much alcohol was on his breath that he couldn’t sleep through the night. Another time, he threw up and blacked out after chugging some soda water. A CT scan showed that his liver was damaged, inflamed, and riddled with fatty deposits.

The man was diagnosed with a rare condition aptly known as auto-brewery syndrome, in which microbes in a person’s gut ferment carbohydrates into excessive amounts of alcohol. The earliest cases were documented in Japan in the 1950s, and a few dozen more have been reported since, in people all over the world, and even in children as young as 3. The microbial culprits are usually yeasts—the same fungi used to brew beer and wine—and the condition can often be treated with antifungal drugs.

But those drugs didn’t work on the Chinese patient. Baffled, a team of doctors, led by Jing Yuan from the Capital Institute of Pediatrics, analyzed the man’s stool samples and found that the alcohol in his body was being produced not by yeast, but by bacteria. During his first episode in the hospital, Klebsiella bacteria had bloomed so vigorously that it made up 19 percent of the microbes in his gut, and became 900 times more common than in healthy people.

Klebsiella pneumoniae is extremely common in both soils and human bodies. Though usually harmless, it’s also an opportunistic pathogen that can cause severe infections if given the chance. And while Klebsiella is not known for intoxicating its hosts, Yuan’s team found that the patient had two particular strains that can churn out alcohol. Many gut microbes do this, but at such low levels that their boozy by-products are easily removed by the liver. The Klebsiella strains in Yuan’s patient were exceptions: At one point, they produced so much of the stuff that it was as if the man had knocked back 15 shots of whiskey. “We were surprised that bacteria can produce so much alcohol,” Yuan says.

Auto-brewery syndrome is extreme, but it has similarities to other, milder and more prevalent conditions. For example, people with nonalcoholic fatty liver disease (NAFLD) build up fatty deposits in their liver in the style of heavy drinkers, despite touching little or no alcohol. This condition is very common, affecting 30 to 40 percent of American adults; the causes are still unclear and likely varied. Yuan wondered if Klebsiella might be involved, and when she analyzed 43 Chinese people with NAFLD, she found that 61 percent had the same high-alcohol strains as the man with auto-brewery syndrome. By contrast, just 6 percent of people with a healthy liver carry those strains.

To see if those strains were actually causing fatty livers, the team fed them to mice that had been raised in sterile conditions and lacked microbes of their own. Within two months, the rodents had signs of liver disease, inflammation, and scarring, comparable to mice that had been drinking alcohol itself. The same thing happened if the team transplanted the stool from an NAFLD patient into germ-free mice, but not if they first removed the alcohol-making Klebsiella using a virus—a phage—that specifically kills those strains. Although studies in mice should be treated with caution, Yuan nonetheless suggests that these strains could be an important cause of NAFLD, through the alcohol they produce.

Other researchers have suggested this before. In 2000, Anna Mae Diehl from Johns Hopkins University noticed that obese mice often have alcohol on their breath, which goes away after antibiotic treatment. “Intestinal production of ethanol may contribute to the genesis of obesity-related fatty liver,” she speculated. Two groups later showed that alcohol-producing microbes are more common in the guts of people with NAFLD than in those of their healthy peers.

While Yuan’s team pointed their fingers at Klebsiella, “it was found in only 60 percent of the human subjects they studied with NAFLD,” says Susan Baker at the State University of New York at Buffalo. “Others have identified other likely bacteria as possible culprits.” She cautions against focusing on any specific microbe, and instead considering the entire ecosystem of the body—bacteria, yeasts, viruses, gut cells, immune cells, liver, and all.

Yuan agrees. She notes that NAFLD is a complex and varied condition, and that even if Klebsiella does turn out to be a cause, it would be one of many. It also raises several questions: Why do some strains produce so much alcohol? Where do they come from? What makes them bloom so vigorously in people such as the unfortunate Chinese man who launched this study—genetics, diet, or something else? And perhaps most important, what can be done about them?

Phages might eventually help, as they did in Yuan’s mice. But for her patient with auto-brewery syndrome, simpler measures did the trick. He was treated with an antibiotic and put on a no-sugar, no-carbohydrate diet for three weeks. His intoxication symptoms eventually subsided, and two months later he was released from the hospital.

https://amp.theatlantic.com/amp/article/598414/


Nourianz is the first adenosine A2A receptor antagonist approved for use in Parkinson Disease

By Brian Park

The Food and Drug Administration (FDA) has approved Nourianz (istradefylline; Kyowa Kirin) tablets as adjunctive treatment to levodopa/carbidopa in adult patients with Parkinson disease (PD) experiencing “off” episodes.

Nourianz is an oral selective adenosine A2A receptor antagonist and non-dopaminergic pharmacologic option. Adenosine A2A receptors are found in the basal ganglia of the brain where degeneration or abnormality is noted in PD; the basal ganglia are involved in motor control.

The approval was based on data from four 12-week, randomized, placebo-controlled clinical trials that evaluated the efficacy and safety of Nourianz in 1143 patients with PD taking a stable dose of levodopa/carbidopa with or without other PD medications.

Results from all 4 studies have demonstrated a statistically significant decrease from baseline in daily “off” time in patients treated with Nourianz compared with placebo. Regarding safety, the most common treatment-emergent adverse reactions were dyskinesia, dizziness, constipation, nausea, hallucination, and insomnia.

“Istradefylline is an Adenosine A2A receptor antagonist, and is a novel non-dopaminergic pharmacologic approach to treating OFF episodes for people living with PD,” said Dr Stuart Isaacson, MD, Parkinson’s Disease and Movement Disorders Center of Boca Raton, Florida. “Based on data from four clinical studies, istradefylline taken as an adjunct to levodopa significantly improved OFF time and demonstrated a well-tolerated safety profile. Istradefylline represents an important new treatment option for patients with Parkinson’s disease who experience ‘OFF’ episodes.”

The FDA had accepted the resubmitted NDA for Nourianz in April 2019 after previously rejecting the submission in 2008 due to concerns over efficacy findings.

For more information visit kyowakirin.com.

FDA Approves New Adjunct Treatment for Parkinson Disease

by Nicole Fisher

Friday evening The Lancet Neurology published a new study concluding that a handheld portable device and blood test could help detect real-time brain injuries, even if a CT scan does not. Findings from the Transforming Research and Clinical Knowledge in Traumatic Brain Injury (TRACK-TBI) study suggest that technology might be able to fill a significant gap in emergency departments, sport fields and battle fields. Within as little as 15 minutes, patients who might have otherwise gone undiagnosed can be identified.

Although concussions and brain injuries are still greatly misunderstood, each year 4.8 million people in the U.S. visit the emergency room to be evaluated for a brain injury, and 82% of those have a head CT scan performed to test for TBI. Further, according to the Defense and Veterans Brain Injury Center, more than 380,000 military members have sustained TBIs over the past 20 years. But the most troubling part of brain injury statistics is that previous research found half of concussions go undetected and undiagnosed. That’s millions a year.

One of the main reasons is that current tools are not capable of detecting all brain injuries. Thus, even for those who do suspect an injury, cognitive and neurological questionnaires and CT scans simply cannot do the job well enough. And in situations like those following an accident or during combat, missing a diagnosis or waiting days for one could have significant consequences. But new blood-based biomarkers are emerging as an important tool to detect TBI.

Unfortunately, the field of neuroscience – and brain injuries in particular – have gotten a lot of attention over the last decade, but with much of the literature and many claims going unsubstantiated, or unable to be validated and replicated. But the authors of this article claim that the large, prospective cohort design and dynamic partnerships of TRACK-TBI are what make these results different, important, and exciting.

The TRACK-TBI study is one of the largest concussion studies of its kind, having evolved from the largest and most comprehensive natural history study of TBI ever conducted in the U.S. Led by the University of California San Francisco (UCSF), funding for the study comes from the National Institute of Neurological Disorders and Stroke (NINDS) and the U.S. Department of Defense (DOD), through U.S. Army Medical Research and Materiel Command (USAMRMC) and U.S. Army Medical Materiel Development Activity (USAMMDA), as well as funding from philanthropic and private partners, like Abbott.

According to Geoffrey T. Manley, M.D., Ph.D., the principal investigator of TRACK-TBI and a neurosurgeon and professor of neurosurgery at UCSF, “We all have a unified, common goal to advance technologies that provide objective information about what’s happening to the brain. The brain and brain injury are extremely complex. So, this work and the results are really about the power of partnership.”

In 2014, the DOD and Abbott partnered to begin working on developing a portable blood test that helps assess concussions right at a person’s side. And the military continues to use Abbott’s current i-STAT system, a handheld blood analyzer that carries out a range of clinical tests. Building on this, with its involvement in TRACK-TBI, Abbott now has more than 120 scientists devoted to researching and developing the concussion assessment test for the next generation of i-STAT™ Alinity™ system.

A critical part of the TRACK-TBI research initiative is to evaluate the effectiveness of blood-based biomarkers to detect brain injury.Consequently, the goal of this collaboration is to have a blood test based on robust, proven data that can easily be utilized in the military, on the field, and in hospitals around the world. To do this, Abbott provided its newest blood test to TRACK-TBI for analysis, while being blinded throughout the study to which samples represented which subjects.

The study results looked at the new handheld blood test, which specifically measures two types of proteins – GFAP and UCH-L1 – that are released from the brain and into the blood when the brain is injured. Or, as Beth McQuiston, M.D., R.D., neurologist and medical director in diagnostics at Abbott puts it, “We have blood tests used in the hospital to detect injury throughout the body. For example, your heart, kidney and liver. Yet, we don’t have a blood test to detect injury in the brain. This research shows that a blood test has the potential to help doctors evaluate and treat patients suspected of brain injury quickly and accurately to get them back to better health. Our blood test in development could be the first point-of-care blood test for assessing concussions.”

Dr. Manley adds, “This study demonstrates that these blood-based biomarkers are more sensitive at detecting brain injury than a CT scan. Even when we found that the CT scan was negative, the research found that these blood proteins levels were elevated above both the healthy and orthopedic controls.” As part of the study, the diagnosis of brain injury was by an MRI scan. Importantly, even when the MRI scan was negative, this protein was elevated more than it was in the controls – suggesting that similar to CT scans, it may be more sensitive than MRI imaging. “And this research suggests,” says Manley, “that proteins have the potential to improve our ability to triage patients with traumatic brain injury.”

While there are still many research milestones for TRACK-TBI, the detection of TBI and identification of patients who need brain injury treatment and care could be a significant game changer – principally for emergency situations. Using only a few drops of blood, assessment of the brain could literally, change lives in a matter of minutes.

https://www.forbes.com/sites/nicolefisher/2019/08/24/study-finds-new-blood-test-could-help-detect-brain-injury-in-minutes/#3ea8cc4e3ac8


Brain tissue from deceased patients with Alzheimer’s has more tau protein buildup (brown spots) and fewer neurons (red spots) as compared to healthy brain tissue.

By Yasemin Saplakoglu

Alzheimer’s disease might be attacking the brain cells responsible for keeping people awake, resulting in daytime napping, according to a new study.

Excessive daytime napping might thus be considered an early symptom of Alzheimer’s disease, according to a statement from the University of California, San Francisco (UCSF).

Some previous studies suggested that such sleepiness in patients with Alzheimer’s results directly from poor nighttime sleep due to the disease, while others have suggested that sleep problems might cause the disease to progress. The new study suggests a more direct biological pathway between Alzheimer’s disease and daytime sleepiness.

In the current study, researchers studied the brains of 13 people who’d had Alzheimer’s and died, as well as the brains from seven people who had not had the disease. The researchers specifically examined three parts of the brain that are involved in keeping us awake: the locus coeruleus, the lateral hypothalamic area and the tuberomammillary nucleus. These three parts of the brain work together in a network to keep us awake during the day.

The researchers compared the number of neurons, or brain cells, in these regions in the healthy and diseased brains. They also measured the level of a telltale sign of Alzheimer’s: tau proteins. These proteins build up in the brains of patients with Alzheimer’s and are thought to slowly destroy brain cells and the connections between them.

The brains from patients who had Alzheimer’s in this study had significant levels of tau tangles in these three brain regions, compared to the brains from people without the disease. What’s more, in these three brain regions, people with Alzheimer’s had lost up to 75% of their neurons.

“It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network,” lead author Jun Oh, a research associate at UCSF, said in the statement. “This means that the brain has no way to compensate, because all of these functionally related cell types are being destroyed at the same time.”

The researchers also compared the brains from people with Alzheimer’s with tissue samples from seven people who had two other forms of dementia caused by the accumulation of tau: progressive supranuclear palsy and corticobasal disease. Results showed that despite the buildup of tau, these brains did not show damage to the neurons that promote wakefulness.

“It seems that the wakefulness-promoting network is particularly vulnerable in Alzheimer’s disease,” Oh said in the statement. “Understanding why this is the case is something we need to follow up in future research.”

Though amyloid proteins, and the plaques that they form, have been the major target in several clinical trials of potential Alzheimer’s treatments, increasing evidence suggests that tau proteins play a more direct role in promoting symptoms of the disease, according to the statement.

The new findings suggest that “we need to be much more focused on understanding the early stages of tau accumulation in these brain areas in our ongoing search for Alzheimer’s treatments,” senior author Dr. Lea Grinberg, an associate professor of neurology and pathology at the UCSF Memory and Aging Center, said in the statement.

The findings were published Monday (Aug. 12) in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

https://www.livescience.com/alzheimers-attacks-wakefulness-neurons.html?utm_source=notification