ME/CFS Evidence Browser — Classified Studies on Myalgic Encephalomyelitis

101–120 of 184 studies

E3 PreliminaryCohortPEM not requiredCase-Control

Stellate ganglion block reduces symptoms of Long COVID: A case series.

Liu, Luke D, Duricka, Deborah L·Journal of neuroimmunology·2022

This small study looked at a procedure called a stellate ganglion block, which uses local anesthetic to temporarily quiet the nerve signals in the neck that control your 'fight or flight' response. Two Long COVID patients received this procedure, and their symptoms—including fatigue, brain fog, and dizziness upon standing—improved. The authors suggest that an imbalance in the autonomic nervous system (the system that controls automatic body functions) may be contributing to Long COVID symptoms.

Neuroinflammation

E3 PreliminaryReviewPEM unclearReview-Narrative

Molecular Mechanisms of Neuroinflammation in ME/CFS and Long COVID to Sustain Disease and Promote Relapses.

Tate, Warren, Walker, Max, Sweetman, Eiren et al.·Frontiers in neurology·2022

This study explores why ME/CFS and Long COVID symptoms persist and come and go in cycles. The researchers propose that after an initial trigger—like a viral infection, chemical exposure, or major stress—inflammation spreads to the brain through damaged blood vessels, causing ongoing brain inflammation that keeps the illness cycling. They suggest that similar mechanisms may explain why both ME/CFS (from various causes) and Long COVID (from COVID-19) produce remarkably similar symptoms despite different starting triggers.

NeuroinflammationImmune SystemPost-Exertional Malaise

E3 PreliminaryReviewPEM unclearReview-Narrative

Mucosal Immunity and the Gut-Microbiota-Brain-Axis in Neuroimmune Disease.

Sterling, Kathryn G, Dodd, Griffin Kutler, Alhamdi, Shatha et al.·International journal of molecular sciences·2022

This review article examines the connection between gut bacteria, immunity, and the brain in diseases like ME/CFS. The authors explain that the bacteria in our gut can communicate with our brain through chemical signals and nerves, but this communication can be disrupted in certain illnesses. They focus on how the immune system in the gut lining controls which bacteria thrive there, and how changes in these bacterial communities might contribute to neuroimmune diseases.

NeuroinflammationGut MicrobiomeImmune System

E3 PreliminaryReviewPEM unclearReview-Narrative

At the Root of 3 "Long" Diseases: Persistent Antigens Inflicting Chronic Damage on the Brain and Other Organs in Gulf War Illness, Long-COVID-19, and Chronic Fatigue Syndrome.

James, Lisa M, Georgopoulos, Apostolos P·Neuroscience insights·2022

This review explores why some people develop long-lasting illnesses after exposure to viruses or bacteria, while others recover normally. The researchers propose that certain infections may persist in the body longer in people with specific immune system markers (HLA types), potentially causing ongoing damage to the brain and other organs. They suggest this mechanism might explain symptoms seen in ME/CFS, long-COVID, and Gulf War Illness.

NeuroinflammationImmune System

E3 PreliminaryMechanismPEM unclearMechanistic

Aberrations in the Cross-Talks Among Redox, Nuclear Factor-κB, and Wnt/β-Catenin Pathway Signaling Underpin Myalgic Encephalomyelitis and Chronic Fatigue Syndrome.

Maes, Michael, Kubera, Marta, Kotańska, Magdalena·Frontiers in psychiatry·2022

This study examined proteins and metabolites in ME/CFS patients to understand how the disease works at a molecular level. Researchers found that ME/CFS involves problems with three interconnected cellular systems: how cells handle harmful oxidative stress, how the immune system responds through inflammation, and how cells communicate through a pathway called Wnt/β-catenin. The study suggests ME/CFS may be triggered by various causes—like infections or toxic exposures—but they all damage these same three systems.

NeuroinflammationImmune System

E3 PreliminaryReviewPEM unclearReview-Narrative

Dissecting the Molecular Mechanisms Surrounding Post-COVID-19 Syndrome and Neurological Features.

Mohamed, Mohamed S, Johansson, Anton, Jonsson, Jörgen et al.·International journal of molecular sciences·2022

This study reviews how the virus that causes COVID-19 may damage the nervous system and brain, leading to long-term symptoms similar to those seen in other coronavirus outbreaks. The authors identify specific brain mechanisms—involving inflammation, nerve cell communication problems, and hormone regulation—that could explain why some people develop persistent neurological symptoms after COVID-19. These findings suggest potential targets for future treatments.

Neuroinflammation

E3 PreliminaryReviewPEM requiredReview-Narrative

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure.

Renz-Polster, Herbert, Tremblay, Marie-Eve, Bienzle, Dorothee et al.·Frontiers in cellular neuroscience·2022

This study suggests that ME/CFS might be caused by problems with certain support cells in the brain called glia, which help protect and maintain nerve cells. The researchers reviewed existing research on two key ME/CFS symptoms—feeling worse after activity and reduced blood flow to the brain—and found evidence that brain cell dysfunction could explain many of the different problems seen in ME/CFS.

NeuroinflammationPost-Exertional Malaise

E3 PreliminaryMechanismPEM unclearMechanistic

Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE).

Gottschalk, Gunnar, Peterson, Daniel, Knox, Konstance et al.·Molecular and cellular neurosciences·2022

Researchers found that people with ME/CFS have higher levels of a protein called ATG13 in their blood compared to healthy people. When they tested this protein on brain immune cells in the lab, it triggered the production of harmful molecules called free radicals (oxidative stress). This suggests that a breakdown in the body's cellular recycling system (autophagy) might contribute to the inflammation and stress response seen in ME/CFS.

NeuroinflammationImmune System

E3 PreliminaryReviewPEM unclearReview-Narrative

Inflammation From Peripheral Organs to the Brain: How Does Systemic Inflammation Cause Neuroinflammation?

Sun, Yuanjie, Koyama, Yoshihisa, Shimada, Shoichi·Frontiers in aging neuroscience·2022

This review explores how inflammation in the body's organs—like the gut, lungs, or joints—can trigger inflammation in the brain. The authors describe several pathways by which this happens, including damage to the protective barrier around the brain, activation of immune cells in the brain, and communication through nerves connecting organs to the brain. ME/CFS is highlighted as one disease where this peripheral-to-brain inflammation mechanism may be important.

NeuroinflammationImmune System

E3 PreliminaryMechanismPEM not requiredMechanistic

Differential Impacts of HHV-6A versus HHV-6B Infection in Differentiated Human Neural Stem Cells.

Bahramian, Elham, Furr, Mercede, Wu, Jerry T et al.·Frontiers in immunology·2022

This study examined how two closely related viruses called HHV-6A and HHV-6B infect different types of nerve cells in the brain. Researchers found that both viruses can infect certain brain cells that use glutamate and dopamine (chemical messengers), but neither virus infected a third type of brain cell that uses GABA. Importantly, HHV-6A appeared to cause more damage to infected cells than HHV-6B, suggesting it may be more harmful to nerve tissue.

Neuroinflammation

E3 PreliminaryMechanismPEM not requiredMechanistic

[Electroacupuncture improves cognitive function by inhibiting NF-κB activity in rats with chronic fatigue syndrome].

Feng, Chu-Wen, Qu, Yuan-Yuan, Sun, Zhong-Ren et al.·Zhen ci yan jiu = Acupuncture research·2021

This study tested whether electroacupuncture (a form of acupuncture with electrical stimulation) could help rats with chronic fatigue syndrome recover cognitive abilities like memory and learning. The researchers found that electroacupuncture reduced inflammation in the brain's memory center (hippocampus) and improved the rats' ability to learn and remember, likely by blocking a inflammatory protein called NF-κB.

Neuroinflammation

E3 PreliminaryReviewPEM unclearReview-Narrative

Persistent Brainstem Dysfunction in Long-COVID: A Hypothesis.

Yong, Shin Jie·ACS chemical neuroscience·2021

This paper suggests that long-COVID symptoms may be caused by damage to the brainstem, a part of the brain that controls basic functions like breathing, heart rate, and digestion. The authors propose that the coronavirus may directly infect the brainstem or cause inflammation there, and because brain cells heal slowly, this damage could persist long after the initial infection. This theory could help explain why long-COVID patients experience lasting fatigue, breathing problems, and other widespread symptoms.

Neuroinflammation

E3 PreliminaryCommentaryPEM requiredEditorial

A Paradigm for Post-Covid-19 Fatigue Syndrome Analogous to ME/CFS.

Mackay, Angus·Frontiers in neurology·2021

This study proposes that long-term fatigue following COVID-19 works similarly to ME/CFS—both may result from severe infection triggering dysfunction in a brain region called the hypothalamic paraventricular nucleus (PVN). In people genetically susceptible to this condition, the stress from COVID-19 infection could overwhelm this brain center, making it oversensitive to everyday stressors and causing the fatigue, post-exertional malaise, and other symptoms characteristic of ME/CFS.

NeuroinflammationPost-Exertional Malaise

E3 PreliminaryCommentaryPEM unclearEditorial

COVID-19 and chronic fatigue syndrome: Is the worst yet to come?

Wostyn, Peter·Medical hypotheses·2021

This paper proposes a theory about why some people develop prolonged fatigue after COVID-19 that resembles ME/CFS. The author suggests that COVID-19 may damage nerve cells in the nose, which could reduce the brain's ability to clear out waste products, leading to toxic buildup and fatigue. The paper calls for research to test whether treatments that help drain fluid from around the brain might help patients with post-COVID fatigue.

Neuroinflammation

E3 PreliminaryMechanismPEM requiredMechanistic

Moderate, intermittent voluntary exercise in a model of Gulf War Illness improves cognitive and mood function with alleviation of activated microglia and astrocytes, and enhanced neurogenesis in the hippocampus.

Kodali, Maheedhar, Mishra, Vikas, Hattiangady, Bharathi et al.·Brain, behavior, and immunity·2021

Researchers tested whether moderate exercise three times a week could help rats with a Gulf War Illness-like condition improve their memory, mood, and thinking skills. After 13 weeks, the exercising rats showed better memory and less anxiety, and their brains showed less inflammation and more growth of new brain cells. This suggests that gentle, part-time exercise might help people with similar conditions improve brain function.

NeuroinflammationPost-Exertional Malaise

E3 PreliminaryMechanismPEM not requiredMechanistic

Improvement Effects of Myelophil on Symptoms of Chronic Fatigue Syndrome in a Reserpine-Induced Mouse Model.

Song, Ji-Hye, Won, Seul-Ki, Eom, Geun-Hyang et al.·International journal of molecular sciences·2021

Researchers tested a herbal mixture called myelophil (made from two traditional medicinal plants) in mice engineered to show ME/CFS-like symptoms including fatigue, pain, and depression. The treatment improved all three symptoms and appeared to work by increasing important brain chemicals like dopamine and serotonin, reducing inflammation, and protecting against cell damage. While these results are encouraging, this study was only in mice, so it's too early to know if the same benefits would occur in people with ME/CFS.

Neuroinflammation

E3 PreliminaryCommentaryPEM unclearEditorial

Dorsal root ganglia: fibromyalgia pain factory?

Martínez-Lavín, Manuel·Clinical rheumatology·2021

This article explores whether structures called dorsal root ganglia (DRG)—small nerve clusters along the spine—might be the main source of pain in fibromyalgia. These ganglia contain pain-sensing nerve cells and immune molecules that can become overactive. Recent evidence suggests that in some fibromyalgia patients, these nerve clusters show signs of damage and increased pain signaling.

Neuroinflammation

E3 PreliminaryReviewPEM unclearReview-Narrative

Historical Insight into Infections and Disorders Associated with Neurological and Psychiatric Sequelae Similar to Long COVID.

Stefano, George B·Medical science monitor : international medical journal of experimental and clinical research·2021

This review examines how long COVID causes long-term symptoms similar to those seen after other viral infections throughout history, particularly focusing on 'brain fog' and difficulty thinking clearly. By looking at past pandemics like the 1918 flu and other viral illnesses, researchers found that many infections can cause similar cognitive problems and fatigue that persist long after the initial infection. The study suggests that viruses may damage the brain's energy-producing structures (mitochondria), leading to reduced oxygen in the brain and chronic symptoms like those seen in ME/CFS and long COVID.

Neuroinflammation

E3 PreliminaryReviewPEM not requiredReview-Narrative

[Imaging and Manipulation of Stem and Progenitor Cells for Revealing the Novel Mechanism of Local Tissue Maintenance in the Brain].

Kataoka, Yosky·Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan·2021

This study examined special cells in the brain called glial progenitor cells that help maintain healthy brain tissue and manage inflammation. Researchers used imaging technology to track these cells and discovered that when these cells are removed, the brain develops harmful inflammation and immune activation. The findings suggest these cells may play a protective role and could be targeted to treat conditions associated with brain inflammation, including chronic fatigue syndrome.

Neuroinflammation

E3 PreliminaryReviewPEM unclearReview-Narrative

[Intestinal flora and neurological disorders].

Tang, Qianqian, Cao, Lihua·Sheng wu gong cheng xue bao = Chinese journal of biotechnology·2021

Your gut bacteria (microbiome) communicate with your brain through multiple pathways, including immune signals and nerve connections. When this gut-brain communication goes wrong, it may contribute to various neurological conditions, including chronic fatigue syndrome. This review summarizes what scientists know about how imbalanced gut bacteria might affect the nervous system and cause disease.

Neuroinflammation

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Stellate ganglion block reduces symptoms of Long COVID: A case series.

Molecular Mechanisms of Neuroinflammation in ME/CFS and Long COVID to Sustain Disease and Promote Relapses.

Mucosal Immunity and the Gut-Microbiota-Brain-Axis in Neuroimmune Disease.

At the Root of 3 "Long" Diseases: Persistent Antigens Inflicting Chronic Damage on the Brain and Other Organs in Gulf War Illness, Long-COVID-19, and Chronic Fatigue Syndrome.

Aberrations in the Cross-Talks Among Redox, Nuclear Factor-κB, and Wnt/β-Catenin Pathway Signaling Underpin Myalgic Encephalomyelitis and Chronic Fatigue Syndrome.

Dissecting the Molecular Mechanisms Surrounding Post-COVID-19 Syndrome and Neurological Features.

The Pathobiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Case for Neuroglial Failure.

Elevated ATG13 in serum of patients with ME/CFS stimulates oxidative stress response in microglial cells via activation of receptor for advanced glycation end products (RAGE).

Inflammation From Peripheral Organs to the Brain: How Does Systemic Inflammation Cause Neuroinflammation?

Differential Impacts of HHV-6A versus HHV-6B Infection in Differentiated Human Neural Stem Cells.

[Electroacupuncture improves cognitive function by inhibiting NF-κB activity in rats with chronic fatigue syndrome].

Persistent Brainstem Dysfunction in Long-COVID: A Hypothesis.

A Paradigm for Post-Covid-19 Fatigue Syndrome Analogous to ME/CFS.

COVID-19 and chronic fatigue syndrome: Is the worst yet to come?

Moderate, intermittent voluntary exercise in a model of Gulf War Illness improves cognitive and mood function with alleviation of activated microglia and astrocytes, and enhanced neurogenesis in the hippocampus.

Improvement Effects of Myelophil on Symptoms of Chronic Fatigue Syndrome in a Reserpine-Induced Mouse Model.

Dorsal root ganglia: fibromyalgia pain factory?

Historical Insight into Infections and Disorders Associated with Neurological and Psychiatric Sequelae Similar to Long COVID.

[Imaging and Manipulation of Stem and Progenitor Cells for Revealing the Novel Mechanism of Local Tissue Maintenance in the Brain].

[Intestinal flora and neurological disorders].

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