Tag: press release

Experts Gather in Montreal to Develop International Research Agenda on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

MONTREAL, April 25, 2018 /PRNewswire/ – International experts will participate in the first-ever Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Canadian Collaborative Team Conference on May 3–5, 2018 at CHU Sainte-Justine.  The conference will bring together 250 researchers and healthcare professionals from various disciplines to develop an international research agenda for this debilitating disease, for which there is no known cause or effective treatment.

“I am extremely encouraged by the interest shown by leading researchers and clinicians, who recognize the importance of establishing research priorities that will advance our understanding of ME/CFS and identify new strategies for treating patients,” says Dr. Alain Moreau, Head, Viscogliosi Laboratory in Molecular Genetics of Musculoskeletal Diseases, CHU Sainte-Justine Research Center and Scientific Chair of the Conference.

The conference will focus on:

  • Methods to properly diagnose patients with ME/CFS;
  • The role of biomarkers in diagnosing ME/CFS;
  • Benefits of establishing a biobank to advance research;
  • Ways to improve clinical care for ME/CFS patients; and
  • How to initiate, support, sustain and advance research on ME/CFS.

“There is an urgent need to get to the bottom of this devastating disease. To do this, we need many people looking at it from different perspectives and sharing as many ideas as possible so that we are better able to understand ME/CFS at the molecular level,” explains Dr. Ronald Davis, Professor, Biochemistry and Genetics and Director, Stanford Genome Technology Center.

Speakers include Dr. Jonas Bergquist, Professor, Uppsala University; Dr. Alison C. Bested, Clinical Director, Institute for Neuro-Immune Medicine at Nova Southeastern University; Dr. Peter Rowe, Director, Children’s Center Chronic Fatigue Clinic, Johns Hopkins University; Dr. Eleonor Stein, Clinical Assistant Professor, Department of Psychiatry, University of Calgary; and Dr. Derya Unutmaz, Professor, The Jackson Laboratory.

The conference is made possible through the support of the Canadian Institutes of Health Research and other partners.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
While severe chronic fatigue is one well-known symptom, ME/CFS affects a person’s cognitive and physical abilities and primarily strikes the neurological, endocrine and immune systems. A 2015 Statistics Canada unpublished Canadian Community Health Survey (CCHS) reports that just over 560,000 patients were diagnosed with ME/CFS, an increase of 37.6% from 2014.  In Quebec, tens of thousands of individuals are affected. ME/CFS is recognized by the World Health Organization.

To view the program, click here.

NIH announces centers for myalgic encephalomyelitis/chronic fatigue syndrome research

Press Release: NIH, September 27, 2017. The National Institutes of Health (NIH) will award four grants to establish a coordinated scientific research effort on myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). The total cost of the projects for fiscal year 2017 will be over $7 million, with support from multiple NIH Institutes and Centers that are part of the Trans-NIH ME/CFS Working Group.

The grants will support the creation of a consortium made up of three Collaborative Research Centers (CRC) and a Data Management Coordinating Center (DMCC). The CRCs will each conduct independent research but will also collaborate on several projects, forming a network to help advance knowledge on ME/CFS. The data will be managed by the DMCC and will be shared among researchers within the CRCs and more broadly with the research community.

“These important grants will provide a strong foundation for expanding research in ME/CFS, and lead to knowledge about the causes and ways to treat people affected by this mysterious, heartbreaking, and debilitating disease,” said NIH Director Francis S. Collins, M.D., Ph.D.

ME/CFS, which affects more than 1 million Americans, is characterized by profound fatigue that does not improve with rest, and may include problems with thinking and memory, pain and a range of other symptoms that negatively impact everyday life. A key feature of the disease is post-exertional malaise, which is a worsening of symptoms following mental or physical activity. The disease can last for years or decades, with those most severely impacted ending up house- or bed-bound. It is unknown what causes the disease and there are no proven treatments.

“These grants will use innovative technologies and research methods to unravel this devastating disease, which we know so little about,” said Walter Koroshetz, M.D., director of NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and chair of the Trans-NIH ME/CFS Working Group.

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Chronic fatigue syndrome linked to imbalanced microbiome

Press Release: Columbia University's Mailman School of Public Health, April 26. 2017. Scientists at the Center for Infection and Immunity (CII) at Columbia University's Mailman School of Public Health have discovered abnormal levels of specific gut bacteria related to chronic fatigue syndrome/myalgic encephalomyelitis, or ME/CFS, in patients with and without concurrent irritable bowel syndrome, or IBS. Findings are published in the journal Microbiome.

The study is among the first to disentangle imbalances in the gut bacteria in individuals with ME/CFS and IBS. ME/CFS is a complex, debilitating disorder characterized by extreme fatigue after exertion and other symptoms including muscle and joint pain, cognitive dysfunction, sleep disturbance, and orthostatic intolerance. Up to 90 percent of ME/CFS patients also have IBS.

The researchers followed 50 patients and 50 matched healthy controls recruited at four ME/CFS clinical sites. They tested for bacterial species in fecal samples, and for immune molecules in blood samples.

They report:

  • Levels of distinct intestinal bacterial species — Faecalibacterium, Roseburia, Dorea, Coprococcus, Clostridium, Ruminococcus, Coprobacillus — were strongly associated with ME/CFS; their combined relative abundance appeared to be predictive of diagnosis

  • Increased abundance of unclassified Alistipes and decreased Faecalibacterium were the top biomarkers of ME/CFS with IBS; while increased unclassified Bacteroides abundance and decreased Bacteroides vulgatus were the top biomarkers of ME/CFS without IBS

  • An analysis of bacterial metabolic pathways associated with disturbances in gut bacteria revealed distinct differences between ME/CFS and ME/CFS subgroups relative to healthy controls

  • In ME/CFS subgroups, symptom severity measures, including pain and fatigue, correlated with the abundance of distinct bacterial types and metabolic pathways

  • No changes were observed in immune markers — a finding that may reflect the dearth of participants who had been ill for a short time; earlier research suggests immune changes may only be evident when comparing short and long duration cases

"Individuals with ME/CFS have a distinct mix of gut bacteria and related metabolic disturbances that may influence the severity of their disease," says co-lead investigator Dorottya Nagy-Szakal, postdoctoral research scientist at CII.

"Our analysis suggests that we may be able to subtype patients with ME/CFS by analyzing their fecal microbiome," says co-lead investigator Brent L. Williams, assistant professor of Pathology and Cell Biology at CII. "Subtyping may provide clues to understanding differences in manifestations of disease."

"Much like IBS, ME/CFS may involve a breakdown in the bidirectional communication between the brain and the gut mediated by bacteria, their metabolites, and the molecules they influence," says senior author W. Ian Lipkin, director of CII and John Snow Professor of Epidemiology at Columbia's Mailman School. "By identifying the specific bacteria involved, we are one step closer to more accurate diagnosis and targeted therapies."

Journal Reference: Dorottya Nagy-Szakal, Brent L. Williams, Nischay Mishra, Xiaoyu Che, Bohyun Lee, Lucinda Bateman, Nancy G. Klimas, Anthony L. Komaroff, Susan Levine, Jose G. Montoya, Daniel L. Peterson, Devi Ramanan, Komal Jain, Meredith L. Eddy, Mady Hornig, W. Ian Lipkin. Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome, 2017; 5 (1) DOI: 10.1186/s40168-017-0261-y https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-017-0261-y

 

Characteristic chemical signature for chronic fatigue syndrome identified

Chronic fatigue syndrome (CFS) is a mysterious and maddening condition, with no cure or known cause. But researchers at the University of California San Diego School of Medicine, using a variety of techniques to identify and assess targeted metabolites in blood plasma, have identified a characteristic chemical signature for the debilitating ailment and an unexpected underlying biology: It is similar to the state of dauer, and other hypometabolic syndromes like caloric restriction, diapause and hibernation.

Dauer is the German word for persistence or long-lived. It is a type of stasis in the development in some invertebrates that is prompted by harsh environmental conditions. The findings are published online in the August 29 issue of PNAS.

“CFS is a very challenging disease,” said first author Robert K. Naviaux, MD, PhD, professor of medicine, pediatrics and pathology and director of the Mitochondrial and Metabolic Disease Center at UC San Diego School of Medicine. “It affects multiple systems of the body. Symptoms vary and are common to many other diseases. There is no diagnostic laboratory test. Patients may spend tens of thousands of dollars and years trying to get a correct diagnosis.”

As many as 2.5 million Americans are believed to have CFS. It most often afflicts women in their 30s to 50s, though both genders and all ages can be affected. The primary symptom is severe fatigue lasting at least six months, with corollary symptoms ranging from muscle pain and headaches to sleep and memory problems.

Naviaux and colleagues studied 84 subjects: 45 men and women who met the diagnostic criteria for CFS and 39 matched controls. The researchers targeted 612 metabolites (substances produced by the processes of metabolism) from 63 biochemical pathways in blood plasma. They found that individuals with CFS showed abnormalities in 20 metabolic pathways. Eighty percent of the diagnostic metabolites measured were decreased, consistent with hypometabolic syndrome or reduced metabolism. The diagnostic accuracy rate exceeded 90 percent.

“Despite the heterogeneity of CFS, the diversity of factors that lead to this condition, our findings show that the cellular metabolic response is the same in patients,” said Naviaux. “And interestingly, it’s chemically similar to the dauer state you see in some organisms, which kicks in when environmental stresses trigger a slow-down in metabolism to permit survival under conditions that might otherwise cause cell death. In CFS, this slow-down comes at the cost of long-term pain and disability.”

Naviaux said the findings show that CFS possesses an objectively identifiable chemical signature in both men and women and that targeted metabolomics, which provide direct small molecule information, can provide actionable treatment information. Only 25 percent of the metabolite disturbances found in each person were needed for the diagnosis of CFS. Roughly 75 percent of abnormalities were unique to each individual, which Naviaux said is useful in guiding personalized treatment.

“This work opens a fresh path to both understanding the biology of CFS and, more importantly to patients, a robust, rational way to develop new therapeutics for a disease sorely in need of them.”

The study authors noted additional research using larger groups of participants from diverse geographical areas is needed to validate both the universality and specificity of the findings.

 

Journal Reference: Robert K. Naviaux, Jane C. Naviaux, Kefeng Li, A. Taylor Bright, William A. Alaynick, Lin Wang, Asha Baxter, Neil Nathan, Wayne Anderson, Eric Gordon. Metabolic features of chronic fatigue syndrome. Proceedings of the National Academy of Sciences, 2016; 201607571 DOI: 10.1073/pnas.1607571113

 

Source: University of California – San Diego. “Characteristic chemical signature for chronic fatigue syndrome identified: Discovery, along with revealed underlying biology, could lead to faster, more accurate diagnoses and more effective, personalized therapies.” ScienceDaily. ScienceDaily, 29 August 2016. https://www.sciencedaily.com/releases/2016/08/160829163253.htm

 

Chronic fatigue syndrome is in your gut, not your head

Physicians have been mystified by chronic fatigue syndrome, a condition where normal exertion leads to debilitating fatigue that isn’t alleviated by rest. There are no known triggers, and diagnosis requires lengthy tests administered by an expert.

Now, for the first time, Cornell University researchers report they have identified biological markers of the disease in gut bacteria and inflammatory microbial agents in the blood.

In a study published June 23 in the journal Microbiome, the team describes how they correctly diagnosed myalgic encephalomyeletis/chronic fatigue syndrome (ME/CFS) in 83 percent of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.

“Our work demonstrates that the gut bacterial microbiome in chronic fatigue syndrome patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” said Maureen Hanson, the Liberty Hyde Bailey Professor in the Department of Molecular Biology and Genetics at Cornell and the paper’s senior author. “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”

“In the future, we could see this technique as a complement to other noninvasive diagnoses, but if we have a better idea of what is going on with these gut microbes and patients, maybe clinicians could consider changing diets, using prebiotics such as dietary fibers or probiotics to help treat the disease,” said Ludovic Giloteaux, a postdoctoral researcher and first author of the study.

In the study, Ithaca campus researchers collaborated with Dr. Susan Levine, an ME/CFS specialist in New York City, who recruited 48 people diagnosed with ME/CFS and 39 healthy controls to provide stool and blood samples.

The researchers sequenced regions of microbial DNA from the stool samples to identify different types of bacteria. Overall, the diversity of types of bacteria was greatly reduced and there were fewer bacterial species known to be anti-inflammatory in ME/CFS patients compared with healthy people, an observation also seen in people with Crohn’s disease and ulcerative colitis.

At the same time, the researchers discovered specific markers of inflammation in the blood, likely due to a leaky gut from intestinal problems that allow bacteria to enter the blood, Giloteaux said.

Bacteria in the blood will trigger an immune response, which could worsen symptoms.

The researchers have no evidence to distinguish whether the altered gut microbiome is a cause or a whether it is a consequence of disease, Giloteaux added.

In the future, the research team will look for evidence of viruses and fungi in the gut, to see whether one of these or an association of these along with bacteria may be causing or contributing to the illness.

 

Journal Reference: Ludovic Giloteaux, Julia K. Goodrich, William A. Walters, Susan M. Levine, Ruth E. Ley, Maureen R. Hanson. Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome, 2016; 4 (1) DOI: 10.1186/s40168-016-0171-4

 

Source: Cornell University. “Chronic fatigue syndrome is in your gut, not your head.” ScienceDaily. ScienceDaily, 27 June 2016. https://www.sciencedaily.com/releases/2016/06/160627160939.htm

 

Chronic fatigue syndrome flare-ups caused by straining muscles and nerves

A recent study conducted by researchers at the University of Alabama at Birmingham and Johns Hopkins University School of Medicine published in PLOS ONE shows that symptoms of chronic fatigue syndrome, a complex and disabling multisystem disorder, can be provoked by imposing a mild to moderate strain to the muscles and nerves.

Eighty individuals, 60 with CFS and 20 without CFS, reported their levels of fatigue, body pain, lightheadedness, concentration difficulties and headache every five minutes while undergoing 15 minutes of either a passive supine straight leg raise — the raising and holding up of one of an individual’s legs while they lie on their back on an exam table — or a sham leg raise that did not cause strain.

Participants were contacted 24 hours later and again reported their symptoms. Compared to those with CFS who underwent the sham leg raise, individuals with CFS who underwent the passive leg raise that actually strained their muscles and nerves reported significantly increased body pain and concentration difficulties during the procedure. After 24 hours, these same individuals who underwent the true strain also reported greater symptom intensity for lightheadedness and the overall combined score for symptoms. The individuals with CFS who underwent the true strain also reported more symptoms during, and 24 hours after, the true strain compared to individuals without CFS.

“These findings have practical implications for understanding why exercise and the activities of daily living might be capable of provoking CFS symptoms,” said Kevin Fontaine, Ph.D., professor and chair of the UAB School of Public Health Department of Health Behavior and a co-author of the paper. “If simply holding up the leg of someone with CFS to a degree that produces a mild to moderate strain is capable of provoking their symptoms, prolonged or excessive muscle strain beyond the usual range of motion that occurs during daily activities might also produce symptom flares.”

As Peter Rowe, M.D., lead author and director of Johns Hopkins Children’s Center Chronic Fatigue Clinic, noted in the article, “The lengthwise strain applied to the nerves and muscles of the lower limb is capable of increasing symptom intensity in individuals with CFS for up to 24 hours, indicating that increased mechanical sensitivity may be a contributor to the provocation of symptoms in this disorder.”

Rowe and Fontaine, and their physical therapist collaborator Rick Violand, intend to extend this work to further understand the effects that strains to the muscles and nerves have on CFS, as well as whether specific physical therapy methods could be used to improve neuromuscular function to reduce symptoms.

Journal Reference: Peter C. Rowe, Kevin R. Fontaine, Megan Lauver, Samantha E. Jasion, Colleen L. Marden, Malini Moni, Carol B. Thompson, Richard L. Violand. Neuromuscular Strain Increases Symptom Intensity in Chronic Fatigue Syndrome. PLOS ONE, 2016; 11 (7): e0159386 DOI: 10.1371/journal.pone.0159386

 

Source: University of Alabama at Birmingham. “Chronic fatigue syndrome flare-ups caused by straining muscles and nerves.” ScienceDaily. ScienceDaily, 18 July 2016. https://www.sciencedaily.com/releases/2016/07/160718194125.htm

 

Further clues in the fight against chronic fatigue syndrome

New findings regarding the pathology of Chronic Fatigue Syndrome (CFS) are bringing Griffith University researchers closer to identifying the cause of this disabling illness.

This is the news from a team at the National Centre for Neuroimmunology and Emerging Diseases at the Menzies Health Institute Queensland.

Professors Marshall-Gradisnik and Don Staines and their research team have identified significant impairments in cellular function of people with CFS.

CFS — sometimes known as ME (myalgic encephalomyelitis) — is a complex illness characterized by impaired memory and concentration, metabolic, cardiac, gut and immune dysfunction and debilitating muscle pain and fatigue on exertion (also known as neuroimmune exhaustion).

It is estimated that the prevalence rate of CFS/ME worldwide is between 1 and 2 per cent.

“While the patho-mechanism of CFS/ME is unknown, these recent findings by NCNED researchers provide further evidence for the pathology of this illness,” says Professor Sonya Marshall-Gradisnik, who speaks as we approach International CFS Awareness Day on Thursday May 12.

Published in the Journal of Translational Medicine, the results report significant differences in intracellular signalling of cells with CFS patients.

“In this group, we see that dysfunctional signalling may contribute to impaired cell activity. These findings are consistent with our previous findings and align with the presentation of symptoms in patients,” says Professor Staines.

The current research findings build upon recent discoveries including novel identification of key genetic changes in cells of the immune system.

The NCNED — internationally recognised for research into CFS/ME — will present a seminar on current research findings on this disease on International CFS/ME Awareness Day, Thursday May 12 at Griffith University, Gold Coast Campus, commencing 1pm, location G17, Lecture theatre 3.

Griffith University will also be illuminating the Griffith Health Centre in blue to further help raise awareness for CFS/ME.

Journal Reference: Teilah Kathryn Huth, Donald Staines, Sonya Marshall-Gradisnik. ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in CD56dimCD16 and CD56brightCD16dim/− natural killer cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients. Journal of Translational Medicine, 2016; 14 (1) DOI: 10.1186/s12967-016-0859-z

 

Source: Griffith University. “Further clues in the fight against chronic fatigue syndrome.” ScienceDaily. ScienceDaily, 10 May 2016. https://www.sciencedaily.com/releases/2016/05/160510093906.htm

 

Chronic fatigue syndrome: Inherited virus can cause cognitive dysfunction and fatigue

Many experts believe that chronic fatigue syndrome (CFS) has several root causes including some viruses. Now, lead scientists Shara Pantry, Maria Medveczky and Peter Medveczky of the University of South Florida’s Morsani College of Medicine, along with the help of several collaborating scientists and clinicians, have published an article in the Journal of Medical Virology suggesting that a common virus, Human Herpesvirus 6 (HHV-6), is the possible cause of some CFS cases.

Over 95 percent of the population is infected with HHV-6 by age 3, but in those with normal immune systems the virus remains inactive. HHV-6 causes fever and rash (or roseola) in infants during early childhood, and is spread by saliva. In immunocompromised patients, it can reactivate to cause neurological dysfunction, encephalitis, pneumonia and organ failure.

“The good news reported in our study is that antiviral drugs improve the severe neurological symptoms, including chronic pain and long-term fatigue, suffered by a certain group of patients with CFS,” said Medveczky, who is a professor of molecular medicine at USF Health and the study’s principal investigator. “An estimated 15,000 to 20,000 patients with this CFS-like disease in the United States alone may ultimately benefit from the application of this research including antiviral drug therapy.”

The link between HHV-6 infection and CFS is quite complex. After the first encounter, or “primary infection,” all nine known human herpesviruses become silent, or “latent,” but may reactivate and cause diseases upon immunosuppression or during aging. A previous study from the Medveczky laboratory showed that HHV-6 is unique among human herpesviruses; during latency, its DNA integrates into the structures at the end of chromosomes known as telomeres.

Furthermore, this integrated HHV-6 genome can be inherited from parent to child, a condition commonly referred to as “chromosomally integrated HHV-6,” or CIHHV-6. By contrast, the “latent” genome of all other human herpesviruses converts to a circular form in the nucleus of the cell, not integrated into the chromosomes, and not inheritable by future generations.

Most studies suggest that around 0.8 percent of the U.S. and U.K. population is CIHHV6 positive, thus carrying a copy of HHV-6 in each cell. While most CIHHV-6 individuals appear healthy, they may be less able to defend themselves against other strains of HHV-6 that they might encounter. Medveczky reports that some of these individuals suffer from a CFS-like illness. In a cohort of CFS patients with serious neurological symptoms, the researchers found that the prevalence of CIHHV-6 was over 2 percent, or more than twice the level found in the general public. In light of this finding, the authors of the study suggest naming this sub-category of CFS “Inherited Human Herpesvirus 6 Syndrome,” or IHS.

Medveczky’s team discovered that untreated CIHHV-6 patients with CFS showed signs that the HHV-6 virus was actively replicating: determined by the presence of HHV-6 messenger RNA (mRNA), a substance produced only when the virus is active. The team followed these patients during treatment, and discovered that the HHV-6 mRNA disappeared by the sixth week of antiviral therapy with valganciclovir, a drug used to treat closely related cytomegalovirus (HHV-5). Of note, the group also found that short-term treatment regimens, even up to three weeks, had little or no impact on the HHV-6 mRNA level.

The investigators assumed that the integrated virus had become reactivated in these patients; however, to their surprise, they found that these IHS patients were infected by a second unrelated strain of HHV-6.

The USF-led study was supported by the HHV-6 Foundation and the National Institutes of Health.

Further studies are needed to confirm that immune dysregulation, along with subsequent chronic persistence of the HHV-6 virus, is the root cause of the IHS patients’ clinical symptoms, the researchers report.

Journal Reference: Shara N. Pantry, Maria M. Medveczky, Jesse H. Arbuckle, Janos Luka, Jose G. Montoya, Jianhong Hu, Rolf Renne, Daniel Peterson, Joshua C. Pritchett, Dharam V. Ablashi, Peter G. Medveczky. Persistent human herpesvirus-6 infection in patients with an inherited form of the virus. Journal of Medical Virology, 2013; DOI:10.1002/jmv.23685

 

Source: University of South Florida (USF Health). “Chronic fatigue syndrome: Inherited virus can cause cognitive dysfunction and fatigue.” ScienceDaily. ScienceDaily, 26 July 2013. https://www.sciencedaily.com/releases/2013/07/130726092427.htm

 

New light shed on cause of chronic fatigue syndrome

New research findings may shed new light on the potential cause of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).

Researchers from Griffith University’s National Centre for Neuroimmunology and Emerging Diseases (NCNED) — part of the new Menzies Health Institute Queensland — have uncovered significant factors contributing to the pathology of this illness.

The results reveal genetic changes in important receptors associated with immunological and cellular function and contribute to the development of this complex illness.

“These findings have been achieved through a team effort involving researchers, patients, funding bodies, clinicians and the support of Griffith University and the Queensland Government,” say chief investigators Professor Sonya Marshall-Gradisnik and Professor Donald Staines.

Co-researcher and consultant immunologist Professor Pete Smith said that important signalling mechanisms are disrupted as a result of these genetic changes involving the detection and response to threats.

“These are primitive genes that are involved in many cellular signals in the brain, gut, cardiovascular and immune systems, as well as in the mediation of pain.”

These research findings coincide with International Neuroimmune Awareness week commencing Monday 11 May.

The Griffith Health Centre on the university’s Gold Coast campus is being lit up each evening from 10 -12 May to raise awareness of neurological conditions such as CFS/ME as well as other conditions such as Fibromyalgia and Gulf War Syndrome.

“The lighting up of the Griffith Health Centre signifies Griffith’s commitment to the CFS patient community and our team approach to this research,” says Pro-Vice Chancellor (Health) Professor Allan Cripps.

CFS/ME is a highly debilitating disorder characterized by profound fatigue, muscle and joint pain, cerebral symptoms of impaired memory and concentration, impaired cardiovascular function, gut disorder and sensory dysfunction such as noise intolerance and balance disturbance. Many cases can continue for months or years. It is believed to affect around 250,000 Australians.

The research findings are to be presented at an international conference in London later this month.

Journal Reference: Sonya Marshall-Gradisnik, Donald Staines, Pete Smith, Bernd Nilius, Ekua Brenu, Sandra Ramos. Examination of Single Nucleotide Polymorphisms (SNPs) in Transient Receptor Potential (TRP) Ion Channels in Chronic Fatigue Syndrome Patients. Immunology and Immunogenetics Insights, 2015; 1 DOI: 10.4137/III.S25147

 

Source: Griffith University. “New light shed on cause of chronic fatigue syndrome.” ScienceDaily. ScienceDaily, 11 May 2015. https://www.sciencedaily.com/releases/2015/05/150511172755.htm 

 

Brain imaging reveals clues about chronic fatigue syndrome

A brain imaging study shows that patients with chronic fatigue syndrome may have reduced responses, compared with healthy controls, in a region of the brain connected with fatigue. The findings suggest that chronic fatigue syndrome is associated with changes in the brain involving brain circuits that regulate motor activity and motivation.

Compared with healthy controls, patients with chronic fatigue syndrome had less activation of the basal ganglia, as measured by fMRI (functional magnetic resonance imaging). This reduction of basal ganglia activity was also linked with the severity of fatigue symptoms.

According to the Centers for Disease Control and Prevention, chronic fatigue syndrome is a debilitating and complex disorder characterized by intense fatigue that is not improved by bed rest and that may be worsened by exercise or mental stress.

The results are scheduled for publication in the journal PLOS One.

“We chose the basal ganglia because they are primary targets of inflammation in the brain,” says lead author Andrew Miller, MD. “Results from a number of previous studies suggest that increased inflammation may be a contributing factor to fatigue in CFS patients, and may even be the cause in some patients.”

Miller is William P. Timmie professor of psychiatry and behavioral sciences at Emory University School of Medicine. The study was a collaboration among researchers at Emory University School of Medicine, the CDC’s Chronic Viral Diseases Branch, and the University of Modena and Reggio Emilia in Italy. The study was funded by the CDC.

The basal ganglia are structures deep within the brain, thought to be responsible for control of movements and responses to rewards as well as cognitive functions. Several neurological disorders involve dysfunction of the basal ganglia, including Parkinson’s disease and Huntington’s disease, for example.

In previous published studies by Emory researchers, people taking interferon alpha as a treatment for hepatitis C, which can induce severe fatigue, also show reduced activity in the basal ganglia. Interferon alpha is a protein naturally produced by the body, as part of the inflammatory response to viral infection. Inflammation has also been linked to fatigue in other groups such as breast cancer survivors.

“A number of previous studies have suggested that responses to viruses may underlie some cases of CFS,” Miller says. “Our data supports the idea that the body’s immune response to viruses could be associated with fatigue by affecting the brain through inflammation. We are continuing to study how inflammation affects the basal ganglia and what effects that has on other brain regions and brain function. These future studies could help inform new treatments.”

Treatment implications might include the potential utility of medications to alter the body’s immune response by blocking inflammation, or providing drugs that enhance basal ganglia function, he says.

The researchers compared 18 patients diagnosed with chronic fatigue syndrome with 41 healthy volunteers. The 18 patients were recruited [not referred] based on an initial telephone survey followed by extensive clinical evaluations. The clinical evaluations, which came in two phases, were completed by hundreds of Georgia residents. People with major depression or who were taking antidepressants were excluded from the imaging study, although those with anxiety disorders were not.

For the brain imaging portion of the study, participants were told they’d win a dollar if they correctly guessed whether a preselected card was red or black. After they made a guess, the color of the card was revealed, and at that point researchers measured blood flow to the basal ganglia.

The key measurement was: how big is the difference in activity between a win or a loss? Participants’ scores on a survey gauging their levels of fatigue were tied to the difference in basal ganglia activity between winning and losing. Those with the most fatigue had the smallest changes, especially in the right caudate and the right globus pallidus, both parts of the basal ganglia.

Ongoing studies at Emory are further investigating the impact of inflammation on the basal ganglia, including studies using anti-inflammatory treatments to reduce fatigue and loss of motivation in patients with depression and other disorders with inflammation including cancer.

 

Source: Emory Health Sciences. “Brain imaging reveals clues about chronic fatigue syndrome.” ScienceDaily. ScienceDaily, 23 May 2014. https://www.sciencedaily.com/releases/2014/05/140523192427.htm