Posts tagged neuroscience
Articles and news from the latest research reports.
Novel compound halts cocaine addiction and relapse behaviors
A novel compound that targets an important brain receptor has a dramatic effect against a host of cocaine addiction behaviors, including relapse behavior, a University at Buffalo animal study has found.
The research provides strong evidence that this may be a novel lead compound for treating cocaine addiction, for which no effective medications exist.
The UB research was published as an online preview article in Neuropsychopharmacology last week.
In the study, the compound, RO5263397, severely blunted a broad range of cocaine addiction behaviors.
“This is the first systematic study to convincingly show that RO5263397 has the potential to treat cocaine addiction,” said Jun-Xu Li, MD, PhD, senior author and assistant professor of pharmacology and toxicology in the UB School of Medicine and Biomedical Sciences.
“Our research shows that trace amine associated receptor 1 – TAAR 1—holds great promise as a novel drug target for the development of novel medications for cocaine addiction,” he said.
TAAR 1 is a novel receptor in the brain that is activated by minute amounts of brain chemicals called trace amines.
The findings are especially important, Li added, since despite many years of research, there are no effective medications for treating cocaine addiction.
The compound targets TAAR 1, which is expressed in key drug reward and addiction regions of the brain.
“Because TAAR 1 anatomically and neurochemically is closely related to dopamine – one of the key molecules in the brain that contributes to cocaine addiction – and is thought to be a ‘brake’ on dopamine activity, drugs that stimulate TAAR 1 may be able to counteract cocaine addiction,” Li explained.
The UB research tested this hypothesis by using a newly developed TAAR 1 agonist RO5263397, a drug that stimulates TAAR 1 receptors, in animal models of human cocaine abuse.
One of the ways that researchers test the rewarding effects of cocaine in animals is called conditioned place preference. In this type of test, the animal’s persistence in returning to, or staying at, a physical location where the drug was given, is interpreted as indicating that the drug has rewarding effects.
In the UB study, RO5263397 dramatically blocked cocaine’s rewarding effects.
“When we give the rats RO5263397, they no longer perceive cocaine rewarding, suggesting that the primary effect that drives cocaine addiction in humans has been blunted,” said Li.
The compound also markedly blunted cocaine relapse in the animals.
“Cocaine users often stay clean for some time, but may relapse when they re-experience cocaine or hang out in the old cocaine use environments,” said Li. “We found that RO5263397 markedly blocked the effect of cocaine or cocaine-related cues for priming relapse behavior.
“Also, when we measured how hard the animals are willing to work to get an injection of cocaine, RO5263397 reduced the animals’ motivation to get cocaine,” said Li. “This compound makes rats less willing to work for cocaine, which led to decreased cocaine use.”
The UB researchers plan to continue studying RO5263397, especially its effectiveness and mechanisms in curbing relapse to cocaine addiction.
(Image: Shutterstock)
Neuroscientists discover brain circuits involved in emotion
Neuroscientists have discovered a brain pathway that underlies the emotional behaviours critical for survival.
New research by the University of Bristol, published in the Journal of Physiology, has identified a chain of neural connections which links central survival circuits to the spinal cord, causing the body to freeze when experiencing fear.
Understanding how these central neural pathways work is a fundamental step towards developing effective treatments for emotional disorders such as anxiety, panic attacks and phobias.
An important brain region responsible for how humans and animals respond to danger is known as the PAG (periaqueductal grey), and it can trigger responses such as freezing, a high heart rate, increase in blood pressure and the desire for flight or fight.
This latest research has discovered a brain pathway leading from the PAG to a highly localised part of the cerebellum, called the pyramis. The research went on to show that the pyramis is involved in generating freezing behaviour when central survival networks are activated during innate and learnt threatening situations.
The pyramis may therefore serve as an important point of convergence for different survival networks in order to react to an emotionally challenging situation.
Dr Stella Koutsikou, first author of the study and Research Associate in the School of Physiology and Pharmacology at the University of Bristol, said: “There is a growing consensus that understanding the neural circuits underlying fear behaviour is a fundamental step towards developing effective treatments for behavioural changes associated with emotional disorders.”
Professor Bridget Lumb, Professor of Systems Neuroscience, added: “Our work introduces the novel concept that the cerebellum is a promising target for therapeutic strategies to manage dysregulation of emotional states such as panic disorders and phobias.”
The researchers involved in this work are all members of Bristol Neuroscience which fosters interactions across one of the largest communities of neuroscientists in the UK.
Professor Richard Apps said: “This is a great example of how Bristol Neuroscience brings together expertise in different fields of neuroscience leading to exciting new insights into brain function.”
Exercise Keeps Hippocampus Healthy in People at Risk for Alzheimer’s
A study of older adults at increased risk for Alzheimer’s disease shows that moderate physical activity may protect brain health and stave off shrinkage of the hippocampus – the brain region responsible for memory and spatial orientation that is attacked first in Alzheimer’s disease. Dr. J. Carson Smith, a kinesiology researcher in the University of Maryland School of Public Health who conducted the study, says that while all of us will lose some brain volume as we age, those with an increased genetic risk for Alzheimer’s disease typically show greater hippocampal atrophy over time. The findings are published in the open-access journal Frontiers in Aging Neuroscience.
"The good news is that being physically active may offer protection from the neurodegeneration associated with genetic risk for Alzheimer’s disease," Dr. Smith suggests. "We found that physical activity has the potential to preserve the volume of the hippocampus in those with increased risk for Alzheimer’s disease, which means we can possibly delay cognitive decline and the onset of dementia symptoms in these individuals. Physical activity interventions may be especially potent and important for this group."
Dr. Smith and colleagues, including Dr. Stephen Rao from the Cleveland Clinic, tracked four groups of healthy older adults ages 65-89, who had normal cognitive abilities, over an 18-month period and measured the volume of their hippocampus (using structural magnetic resonance imaging, or MRI) at the beginning and end of that time period. The groups were classified both for low or high Alzheimer’s risk (based on the absence or presence of the apolipoprotein E epsilon 4 allele) and for low or high physical activity levels.
Of all four groups studied, only those at high genetic risk for Alzheimer’s who did not exercise experienced a decrease in hippocampal volume (3 percent) over the 18-month period. All other groups, including those at high risk for Alzheimer’s but who were physically active, maintained the volume of their hippocampus.
"This is the first study to look at how physical activity may impact the loss of hippocampal volume in people at genetic risk for Alzheimer’s disease," says Dr. Kirk Erickson, an associate professor of psychology at the University of Pittsburgh. "There are no other treatments shown to preserve hippocampal volume in those that may develop Alzheimer’s disease. This study has tremendous implications for how we may intervene, prior to the development of any dementia symptoms, in older adults who are at increased genetic risk for Alzheimer’s disease."
Individuals were classified as high risk for Alzheimer’s if a DNA test identified the presence of a genetic marker – having one or both of the apolipoprotein E-epsilon 4 allele (APOE-e4 allele) on chromosome 19 – which increases the risk of developing the disease. Physical activity levels were measured using a standardized survey, with low activity being two or fewer days/week of low intensity activity, and high activity being three or more days/week of moderate to vigorous activity.
"We know that the majority of people who carry the E4 allele will show substantial cognitive decline with age and may develop Alzheimer’s disease, but many will not. So, there is reason to believe that there are other genetic and lifestyle factors at work," Dr. Smith says. "Our study provides additional evidence that exercise plays a protective role against cognitive decline and suggests the need for future research to investigate how physical activity may interact with genetics and decrease Alzheimer’s risk."
Dr. Smith has previously shown that a walking exercise intervention for patients with mild cognitive decline improved cognitive function by improving the efficiency of brain activity associated with memory. He is planning to conduct a prescribed exercise intervention in a population of healthy older adults with genetic and other risk factors for Alzheimer’s disease and to measure the impact on hippocampal volume and brain function.
(Source: umdrightnow.umd.edu)
Loss of Memory in Alzheimer’s Mice Models Reversed through Gene Therapy
Alzheimer’s disease is the first cause of dementia and affects some 400,000 people in Spain alone. However, no effective cure has yet been found. One of the reasons for this is the lack of knowledge on the cellular mechanisms which cause alterations in nerve transmissions and the loss of memory in the initial stages of the disease.
Researchers from the Institute of Neuroscience at the Universitat Autònoma de Barcelona have discovered the cellular mechanism involved in memory consolidation and were able to develop a gene therapy which reverses the loss of memory in mice models with initial stages of Alzheimer’s disease. The therapy consists in injecting into the hippocampus - a region of the brain essential to memory processing - a gene which causes the production of a protein blocked in patients with Alzheimer’s, the “Crtc1” (CREB regulated transcription coactivator-1). The protein restored through gene therapy gives way to the signals needed to activate the genes involved in long-term memory consolidation.
To identify this protein, researchers compared gene expression in the hippocampus of healthy control mice with that of transgenic mice which had developed the disease. Through DNA microchips, they identified the genes (“transcriptome”) and the proteins (“proteome”) which expressed themselves in each of the mice in different phases of the disease. Researchers observed that the set of genes involved in memory consolidation coincided with the genes regulating Crtc1, a protein which also controls genes related to the metabolism of glucose and to cancer. The alteration of this group of genes could cause memory loss in the initial stages of Alzheimer’s disease.
In persons with the disease, the formation of amyloid plaque aggregates, a process known to cause the onset of Alzheimer’s disease, prevents the Crtc1 protein from functioning correctly. “When the Crtc1 protein is altered, the genes responsible for the synapsis or connections between neurons in the hippocampus cannot be activated and the individual cannot perform memory tasks correctly”, explains Carlos Saura, researcher of the UAB Institute of Neuroscience and head of the research. According to Saura, “this study opens up new perspectives on therapeutic prevention and treatment of Alzheimer’s disease, given that we have demonstrated that a gene therapy which activates the Crtc1 protein is effective in preventing the loss of memory in lab mice”.
The research, published today as a featured article in The Journal of Neuroscience, the official journal of the US Society of Neuroscience, paves the way for a new therapeutic approach to the disease. One of the main challenges in finding a treatment for the disease in the future is the research and development of pharmacological therapies capable of activating the Crtc1 protein, with the aim of preventing, slowing down or reverting cognitive alterations in patients.
Toward unraveling the Alzheimer’s mystery
Getting to the bottom of Alzheimer’s disease has been a rapidly evolving pursuit with many twists, turns and controversies. In the latest crook in the research road, scientists have found a new insight into the interaction between proteins associated with the disease. The report, which appears in the journal ACS Chemical Neuroscience, could have important implications for developing novel treatments.
Witold K. Surewicz, Krzysztof Nieznanski and colleagues explain that for years, research has suggested a link between protein clumps, known as amyloid-beta plaques, in the brain and the development of Alzheimer’s, a devastating condition expected to affect more than 10 million Americans by 2050. But how they inflict their characteristic damage to nerve cells and memory is not fully understood. Recent studies have found that a so-called prion protein binds strongly to small aggregates of amyloid-beta peptides. But the details of how this attachment might contribute to disease — and approaches to treat it — are still up for debate. To resolve at least part of this controversy, Surewicz’s team decided to take a closer look.
Contrary to previous studies, they found that the prion protein also attaches to large fibrillar clumps of amyloid-beta and do not break them down into smaller, more harmful pieces, as once thought. This finding bodes well for researchers investigating a novel approach to treating Alzheimer’s — using prion-protein-based compounds to stop these smaller, toxic amyloid-beta pieces from forming, the authors conclude.
On the Defensive
TAU discovers that protein clusters implicated in neurodegenerative diseases actually serve to protect brain cells
People diagnosed with Huntington’s disease, most in their mid-thirties and forties, face a devastating prognosis: complete mental, physical, and behavioral decline within two decades. “Mutant” protein clusters, long blamed for the progression of the genetic disease, have been the primary focus of therapies in development by pharmaceutical companies. But according to new research from Prof. Gerardo Lederkremer and Dr. Julia Leitman of Tel Aviv University’s Department of Cell Research and Immunology, in collaboration with Prof. Ulrich Hartl of the Max Planck Institute for Biochemistry, these drugs may not only be ineffective — they may pose a serious threat to patients.
In two ground-breaking studies, published in the journals PLOS ONE and Nature Communications, Prof. Lederkremer and his team demonstrated that protein clusters are not the cause of toxicity in Huntington’s disease. On the contrary, these aggregates actually serve as a defense mechanism for “stressed” brain cells. Conducted on tissue cultures using cutting-edge microscopic technology, their studies identified a different causative agent — the “stress response” of affected brain cells.
"The upsetting implication for therapy of this disease is that drugs being developed to interfere with the formation of protein aggregates may in fact be detrimental," said Prof. Lederkremer. "The identification of the new cause will hopefully lead to the development of new therapeutic approaches. This may hold true for other neurodegenerative diseases as well."
Starting from genetic scratch
Prof. Lederkremer and his team chose to examine the effect of protein aggregates in the pathology of Huntington’s disease because its genetic cause is well-known, unlike those of other neurodegenerative diseases, such as Parkinson’s, whose origins remain less clear.
"What we found in this study — a surprise, although we suspected it — was that damage to the cells, the cell ‘stress’ that leads to death of cells, appeared well before the protein aggregates did," said Prof. Lederkremer. "And even more surprising, when the aggregates finally appeared, the stress was reduced, in some cases even stopping. The actual process of forming an aggregate was protective, isolating and segregating the problematic proteins. This explains why in autopsies of people who died of Huntington’s and other diseases like Alzheimer’s or old age, the protein aggregates in the brains were all quite similar, reflecting no specific disease link."
By interfering with the stress response of brain cells, rather than the formation of protein clusters, scientists may be able to slow, or even halt, the progression of neurodegenerative diseases. According to Prof. Lederkremer, this research paves the way for a revolutionary new direction for pharmaceutical research to treat Huntington’s, Alzheimer’s, Parkinson’s, and other neurodegenerative diseases.
Response to stress
"The practical consequences are that several companies are already in advanced stages of development of drugs inhibiting this form of protein aggregate, interfering with the body’s natural process to protect the brain," said Prof. Lederkremer. "But the drugs should be focused on another area altogether, and the protein aggregates, a protective resource for the brain, should be left intact."
Samples of brain cells from mouse models afflicted with Huntington’s disease were examined using “live cell imaging,” the study of live cells through time-lapse microscopy. Prof. Lederkremer and his team were thus able to identify a compound that modified brain cells’ response to stress, promoting their survival.
"Our approach was to interfere with the stress response instead of the formation of the protein aggregates, and the lab succeeded in identifying a compound that altered the response, rescuing affected cells from death," said Prof. Lederkremer. "Our findings are most encouraging for the development of a therapy for this devastating disease, which is presently incurable."
(Source: aftau.org)
Brain size matters when it comes to animal self-control
Chimpanzees may throw tantrums like toddlers, but their total brain size suggests they have more self-control than, say, a gerbil or fox squirrel, according to a new study of 36 species of mammals and birds ranging from orangutans to zebra finches.
Scientists at Duke University, UC Berkeley, Stanford, Yale and more than two-dozen other research institutions collaborated on this first large-scale investigation into the evolution of self-control, defined in the study as the ability to inhibit powerful but ultimately counter-productive behavior. They found that the species with the largest brain volume – not volume relative to body size – showed superior cognitive powers in a series of food-foraging experiments.
Moreover, animals with the most varied diets showed the most self-restraint, according to the study published in the journal of the Proceedings of the National Academy of Sciences.
“The study levels the playing field on the question of animal intelligence,” said UC Berkeley psychologist Lucia Jacobs, a co-author of this study and of its precursor, a 2012 paper in the journal, Animal Cognition.
This latest study was led by evolutionary anthropologists Evan MacLean, Brian Hare and Charles Nunn of Duke University. The findings challenge prevailing assumptions that “relative” brain size is a more accurate predictor of intelligence than “absolute” brain size. One possibility, they posited, is that “as brains get larger, the total number of neurons increases and brains tend to become more modularized, perhaps facilitating the evolution of new cognitive networks.”
While participating researchers all performed the same series of experiments, they did so on their own turf and on their own animal subjects. Data was provided on bonobos, chimpanzees, gorillas, olive baboons, stump-tailed macaques, golden snub-nosed monkeys, brown, red-bellied and aye-aye lemurs, coyotes, dogs, gray wolves, Asian elephants, domestic pigeons, orange-winged amazons, Eurasian jays, western scrub jay, zebra finches and swamp sparrows.
Food inside a tube used as bait
In one experiment, creatures large and small were tested to see if they would advance toward a clear cylinder visibly containing food – showing a lack of self-restraint – after they had been trained to access the food through a side opening in an opaque cylinder. Large-brained primates such as gorillas quickly navigated their way to the treat or “bait.” Smaller-brained animals did so with mixed results.
Jacobs and UC Berkeley doctoral student Mikel Delgado contributed the only rodent data in the study, putting some of the campus’s fox squirrels and some Mongolian gerbils in their lab through food-foraging tasks.
Mixed results on campus squirrels’ self-restraint
In the case of the fox squirrels, the red-hued, bushy-tailed critters watched as the food was placed in a side opening of an opaque cylinder. Once they demonstrated a familiarity with the location of the opening, the food was moved to a transparent cylinder and the real test began. If the squirrels lunged directly at the food inside the bottle, they had failed to inhibit their response. But if they used the side entrance, the move was deemed a success.
“About half of the squirrels and gerbils did well and inhibited the direct approach in more than seven out of 10 trials,” Delgado said. “The rest didn’t do so well.”
In a second test, three cups (A, B and C) were placed in a row on their sides so the animals could see which one contained food. It was usually cup A. The cups were then turned upside down so the “baited” cup could no longer be seen. If the squirrels touched the cup with the food three times in a row, they graduated to the next round. This time, the food was moved from cup A to cup C at the other end of the row.
“The question was, would they approach cup A, where they had originally learned the food was placed, or could they update this learned response to get the food from a new location?” Delgado said. “The squirrels and gerbils tended to go to the original place they had been trained to get food, showing a failure to inhibit what they originally learned.” Click here for video showing other animals doing the cup test.
“It might be that a squirrel’s success in life is affected the same way as in people,” Jacobs said. “By its ability to slow down and think a bit before it snatches at a reward.”
(Source: newscenter.berkeley.edu)
Newly-Approved Brain Stimulator Offers Hope for Individuals With Uncontrolled Epilepsy
A recently FDA-approved device has been shown to reduce seizures in patients with medication-resistant epilepsy by as much as 50 percent. When coupled with an innovative electrode placement planning system developed by physicians at Rush, the device facilitated the complete elimination of seizures in nearly half of the implanted Rush patients enrolled in the decade-long clinical trials.
That’s good news for a large portion of the nearly 400,000 people in the U.S. living with epilepsy whose seizures can’t be controlled with medications and who are not candidates for brain surgery.
Epilepsy is a chronic neurological condition characterized by recurrent seizures that disrupt the senses, or can involve short periods of unconsciousness or convulsions. “Many people with epilepsy have scores of unpredictable seizures every day that make it impossible for them to drive, work or even get a good night’s sleep,” said Dr. Marvin Rossi, co-principal investigator of the NeuroPace Pivotal Clinical Trial and assistant professor of neurology at the Rush Epilepsy Center.
The NeuroPace RNS System uses responsive, or ‘on-demand’ direct stimulation to detect abnormal electrical activity in the brain and deliver small amounts of electrical stimulation to suppress seizures before they begin.
The device is surgically placed underneath the scalp within the skull and connected to electrodes that are strategically placed within the brain where the seizures originate (called the seizure focus). A programmed computer chip in the skull communicates with the system to record data and to help regulate responsive stimulation.
The unique electrode placement planning modeling system developed at Rush uses a computer-intensive mapping system that facilitates surgical placement of electrodes at the precise location in the brain’s temporal lobe circuitry. When stimulated, these extensive epileptic circuits are calmed. The modeling system predicts where in the brain the activity begins and spreads, so that the device can better influence the maximal extent of the epileptic pathway.
The device also acts as an implanted EEG for recording brain activity. This function was first shown at Rush to help determine whether the patient will further benefit from a surgical resection, in which surgeons remove a portion of the temporal lobe network. Dr. Richard Byrne, chairman of Neurosurgery at Rush, implants the electrodes in the temporal lobes.
As a result, physicians at Rush can offer patients the new implantable neurostimulator device, a surgical resection or both with the possibility of completely eliminating seizures. “This device is also being used at Rush as a foundation and inspiration for building cutting-edge hybrid stimulation therapy-drug molecule delivery systems,” said Rossi.
“Devices that treat epilepsy may offer new hope to patients when medication is ineffective and resection is not an option,” said Rossi. “Not long ago, it was highly unlikely that these patients would ever be free of their seizures. Now, several of our Rush patients with this device are actually able to drive, lower or even eliminate their medications and aren’t as limited as they once were. There is no doubt that quality of life of the majority of our implanted patients is significantly improved.”
According to the Centers for Disease Control and Prevention, in 2010, epilepsy affected approximately 2.3 million adults in the U.S. and 467,711 children under the age of 17.
(Source: rush.edu)
Depressed? Researchers identify new anti-depressant mechanisms, therapeutic approaches
Researchers at UT Southwestern Medical Center are making breakthroughs that could benefit people suffering from depression.
A team of physician-scientists at UT Southwestern has identified a major mechanism by which ghrelin (a hormone with natural anti-depressant properties) works inside the brain. Simultaneously, the researchers identified a potentially powerful new treatment for depression in the form of a neuroprotective drug known as P7C3.
The study, published online in April’s issue of Molecular Psychiatry, is notable because although a number of anti-depressant drugs and other treatments are available, an estimated one in 10 adults in the U.S. still report depression, according to the Centers for Disease Control and Prevention.
"By investigating the way the so-called ‘hunger hormone’ ghrelin works to limit the extent of depression following long-term exposure to stress, we discovered what could become a brand new class of anti-depressant drugs," said Dr. Jeffrey Zigman, Associate Professor of Internal Medicine and Psychiatry at UT Southwestern, and co-senior author of the study.
Ghrelin, a hormone produced in the stomach and intestines, has several widely known functions, including the ability to stimulate appetite. The latest research builds on a 2008 study led by Dr. Zigman, in which the team discovered that ghrelin exhibited natural anti-depressant effects that manifest when its levels rise as a result of caloric restriction or prolonged psychological stress.
The current findings identify ghrelin’s ability to stimulate adult hippocampal neurogenesis, the formation of new neurons, in animal models. In addition, Dr. Zigman and his colleagues also found that the regenerative process inside the hippocampus – a region of the brain that regulates mood, memory, and complex eating behaviors – is crucial in limiting the severity of depression following prolonged exposure to stress.
"After identifying the mechanism of ghrelin’s anti-depressant actions, we investigated whether increasing this ghrelin effect by directly enhancing hippocampal neurogenesis with the recently reported P7C3 class of neuroprotective compounds would result in even greater anti-depressant behavioral effects," Dr. Zigman said.
The P7C3 compounds were discovered in 2010 by a team of UT Southwestern researchers led by Dr. Steven McKnight, Chair of Biochemistry, Dr. Joseph Ready, Professor of Biochemistry, and Dr. Andrew Pieper, a former UT Southwestern faculty member and co-senior author of the current study. Previous research demonstrated P7C3’s promising neuroprotective abilities in instances of Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and traumatic brain injury. Today, researchers hope that it can have a transformative impact on depression treatment too.
"We found that P7C3 exerted a potent anti-depressant effect via its neurogenesis-promoting properties," said Dr. Pieper, who is now Associate Professor of Neurology and Psychiatry at the University of Iowa Carver College of Medicine. "Also exciting, a highly active P7C3 analog was able to quickly enhance neurogenesis to a much greater level than a wide spectrum of currently marketed anti-depressant drugs."
Based on the study’s behavioral findings, researchers believe that individuals with depression associated with chronic stress or with altered ghrelin levels or ghrelin resistance, as has been described or theorized for conditions such as obesity and anorexia nervosa, might be particularly responsive to treatment with highly neuroprotective drugs, such as the P7C3 compounds.
Future studies will examine the ability to apply these findings to other forms of depression, including the possibility of developing clinical trials aimed at identifying whether or not P7C3 compounds have anti-depressant effects in people with major depression, as predicted. The three main types of depressive disorders include major depression, dysthymia, and bipolar disorder.
Sleep disorder linked to brain disease
Researchers at the University of Toronto say a sleep disorder that causes people to act out their dreams is the best current predictor of brain diseases like Parkinson’s and many other forms of dementia.
"Rapid-eye-movement sleep behaviour disorder (RBD) is not just a precursor but also a critical warning sign of neurodegeneration that can lead to brain disease," says associate professor and lead author Dr. John Peever. In fact, as many as 80 to 90 per cent of people with RBD will develop a brain disease."
As the name suggests, the disturbance occurs during the rapid-eye-movement (REM) stage of sleep and causes people to act out their dreams, often resulting in injury to themselves and/or bed partner. In healthy brains, muscles are temporarily paralyzed during sleep to prevent this from happening.
"It’s important for clinicians to recognize RBD as a potential indication of brain disease in order to diagnose patients at an earlier stage," says Peever. "This is important because drugs that reduce neurodegeneration could be used in RBD patients to prevent (or protect) them from developing more severe degenerative disorders."
His research examines the idea that neurodegeneration might first affect areas of the brain that control sleep before attacking brain areas that cause more common brain diseases like Alzheimer’s.
Peever says he hopes the results of his study lead to earlier and more effective treatment of neurodegenerative diseases.
(Source: eurekalert.org)