#braininflammation — Public Fediverse posts
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DATE: July 30, 2026 at 11:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Researchers find evidence connecting a specific blood protein to brain tissue loss
Higher levels of a blood protein called growth differentiation factor 15 during midlife were associated with approximately twice the rate of dementia over the following twenty years. This protein is released by cells during aging, inflammation, and other forms of biological stress. The research, published in Science Advances, provides evidence linking this protein to future cognitive decline.
Previous research identified the protein as a possible early warning sign for dementia. However, scientists were uncertain whether it merely reflected poor health or actually contributed to damaging brain processes. To find out, researchers investigated whether blood levels of this protein predicted different forms of dementia. They also examined whether it was connected to brain changes, inherited risk, and immune activity.
Led by Cassandra O. Blew at the US National Institutes of Health, the team combined evidence from six large studies that tracked participants over time. The principal midlife analysis included 11,595 American adults with an average age of fifty-seven. These participants were followed for about twenty years. The scientists also analyzed data from older American adults, British participants, and Icelandic adults, with average ages ranging from sixty to seventy-six.
The researchers measured the protein in blood samples and examined subsequent diagnoses of all forms of dementia, including Alzheimer’s disease and vascular dementia. The statistical models accounted for factors like age, sex, kidney function, smoking, obesity, diabetes, and genetic susceptibility. Results revealed that in the midlife American sample, each doubling of the protein’s levels was associated with a 55 percent greater risk of developing dementia.
Among participants with protein levels in the top half of the group, 7.5 percent developed dementia over twenty years, compared with 3.9 percent of those in the bottom half. A similar pattern emerged in the older American group over a seven-year period. In that older group, 18.7 percent of individuals with high levels developed dementia, compared to 9.5 percent of those with lower levels.
The relationship was stronger for vascular dementia than for Alzheimer’s disease. Vascular dementia develops through reduced blood flow and damage to the brain’s blood vessels, while Alzheimer’s is associated with abnormal protein buildups. In the British sample, each doubling of the protein was associated with a 101 percent higher vascular dementia risk but only a 20 percent higher Alzheimer’s risk. The Icelandic group produced similar estimates, showing a 106 percent higher risk for vascular dementia compared with a 24 percent increase for Alzheimer’s.
Brain scans provided matching evidence. Higher levels of the protein were associated with smaller brain volumes, thinner brain tissue, and greater damage to white matter, which is the network of nerve fibers connecting different brain regions. The elevated protein also predicted increased odds of small strokes and microscopic brain bleeds. The findings suggest the protein relates more strongly to blood vessel damage, general brain tissue loss, and inflammation rather than the specific protein pathways of Alzheimer’s disease.
Genetic analyses provided evidence suggesting the protein might play a direct role in causing brain changes. To explore this, the team conducted an experiment using macrophages, which are immune cells that engulf and destroy cellular debris. The scientists exposed macrophages from six adults to the growth differentiation factor 15 protein. This exposure altered immune and energy-related pathways in the cells, such as reducing antiviral signaling and disrupting the removal of free heme, an iron-rich molecule that can be toxic when released from red blood cells.
The authors concluded that their findings support the role of this circulating protein as an early warning sign, particularly for vascular dementia and brain inflammation. They noted that the results also help identify the biological mechanisms by which the protein might drive dementia risk.
A few limitations restrict the study’s conclusions. The blood protein added only modest predictive information for dementia risk beyond a person’s age. The research design also cannot conclusively establish that the protein causes the disease. Finally, the association between the protein and dementia was not statistically significant in a smaller Japanese group of 340 people, suggesting further research is needed across different populations.
The paper, “Plasma GDF15 affects long-term dementia risk and alters neuroimmune signaling,” was authored by Cassandra O. Blew, Michael R. Duggan, Dimitrios Tsitsipatis, Gabriela T. Gomez, Zulema Rodriguez-Hernandez, Luke C. Pilling, Jingsha Chen, Eva Jacobsen, Heather E. Dark, Yifei Lu, Shannon M. Drouin, Cassandra M. Joynes, Minhao Yao, Murat Bilgel, Abhay Moghekar, Qu Tian, Julián Candia, Mary Kaileh, Aditi Gupta, Krystyna Mazan-Mamczarz, Myriam Gorospe, Alexey Lyashkov, Yevgeniya Lukyanenko, Mika Kivimaki, Philipp Frank, Lori L. Jennings, Valborg Gudmundsdottir, Vilmundur Gudnason, Lenore J. Launer, Naoto Kaneko, Shintaro Kato, Makio Furuichi, Masaki Shibayama, Masahisa Katsuno, Keita Hiraga, Yukiko Nishita, Rei Otsuka, James R. Pike, Mary R. Rooney, Pascal Schlosser, Yuhan Cui, Guray Erus, Christos Davatzikos, Rebecca F. Gottesman, Iwao Waga, Priya Palta, Christie Ballantyne, Michael Griswold, Zhonghua Liu, Luigi Ferrucci, Allison B. Herman, and Keenan A. Walker.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #GDF15 #dementiarisk #vasculardementia #braininflammation #neuroimmunology #bloodprotein #midlifestudies #brainscanmarkers #agingbiology #SciAdvResearch
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DATE: July 30, 2026 at 08:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Long COVID symptoms linked to measurable damage in the brain’s dopamine system
A recent study published in eBioMedicine provides evidence that individuals suffering from long COVID show a measurable reduction in the brain’s dopamine-releasing neurons. These physical brain changes tend to be associated with common persistent symptoms such as apathy, memory problems, and a slowing of physical movements. The findings suggest that treatments aimed at boosting dopamine function could offer a new therapeutic direction for people experiencing the neuropsychiatric effects of long COVID.
Long COVID is a condition where individuals experience ongoing physical and mental symptoms long after their initial infection with the COVID-19 virus has resolved. Many people report persistent brain-related symptoms, including a profound lack of motivation, difficulty experiencing pleasure, memory lapses, and general cognitive sluggishness. The biological mechanisms responsible for these lingering issues remain poorly understood by the medical community.
Past medical research primarily focused on how immune system overreactions and persistent brain inflammation might drive these symptoms. Jeffrey Meyer, a Canada Research Chair, senior research scientist, and professor in the department of psychiatry at the University of Toronto, authored the new study. His prior work focused extensively on similar inflammatory processes.
“We had top international level expertise in measuring brain inflammation in psychiatric illnesses,” Meyer said. “When COVID came, I decided to use the same imaging tools to study long COVID.”
During that earlier research, Meyer found a distinct pattern linking inflammation and specific brain networks. He noted that the most intense areas of inflammation overlapped with the brain’s dopamine pathways.
“When I discovered evidence for brain inflammation in long COVID, I noticed that the greatest elevations in the inflammation marker were in regions where there are nerve terminals that release dopamine,” Meyer said.
These brain regions also control basic physical movements. Dopamine is a chemical messenger in the brain that regulates motivation, learning, and physical movement, and its neurons are highly concentrated in a deep brain structure called the striatum.
“Also, the inflammation marker correlated with a measure of movement speed that can be affected by injury to dopamine releasing nerves so I speculated that injury to dopamine releasing nerves could account for the symptom of slowed movement speed, and be related to inflammation in the same region,” Meyer said. “Sometimes inflammation can damage dopamine releasing nerves.”
Scientists had additional reasons to look at the dopamine system in relation to COVID-19. The specific cells that produce dopamine contain high levels of the receptor proteins that the COVID-19 virus uses to enter and infect human cells.
“Also, the key binding site for the virus to enter cells is higher density on nerves that release dopamine which is another reason to see if their terminals are lost,” Meyer added.
To measure the health of dopamine neurons, the researchers looked at a protein called vesicular monoamine transporter 2. This protein acts like a microscopic pump, packaging dopamine into tiny cellular sacs so that it can be released to communicate with neighboring cells. Because this protein is almost exclusively found within dopamine-releasing neurons in the striatum, measuring its presence provides a highly accurate estimate of how many intact dopamine nerve terminals exist.
The researchers conducted a case-control study involving 24 adults diagnosed with long COVID and 24 healthy adults matched closely for age. The healthy control group was later expanded to 43 participants for additional exploratory comparisons. Participants in the long COVID group had experienced only mild to moderate illness during their initial infection. However, they all developed significant neuropsychiatric symptoms within three months of their acute illness, and these symptoms had persisted for at least three months.
The scientists established strict exclusion criteria for all participants to ensure the accuracy of their measurements. Anyone with a history of neurological illness prior to their COVID-19 infection was excluded from the study. The team also excluded individuals with a history of moderate or severe substance abuse, as well as anyone who had smoked cigarettes or used recreational drugs within the past two months.
Participants underwent brain imaging using positron emission tomography. This is a medical imaging technique that uses a safe, mildly radioactive tracer to visualize and measure specific cellular processes in the body. For this study, the scientists used a specific tracer designed to bind directly to the vesicular monoamine transporter 2 protein.
In addition to brain scans, participants completed a battery of psychological and physical assessments. Motivation levels were measured using the Marin Apathy Evaluation Scale. Fine motor speed was gauged using the Finger Tapping Test, which requires participants to tap a mechanical counter as quickly as possible. Memory retention and cognitive function were assessed using the Hopkins Verbal Learning Test-Revised and the Cognitive Failures Questionnaire.
The brain imaging revealed that the 24 individuals with long COVID had significantly lower levels of the dopamine transporter protein compared to the healthy controls. Specifically, the long COVID group showed an overall reduction in protein binding across three key regions of the striatum.
“The magnitude of loss is about 18% of the dopamine nerve terminals on average,” Meyer told PsyPost. “In other illnesses this magnitude of loss is associated with symptoms i.e. loss in one region is associated with trouble with motivational energy problems, loss in another region is associated with some slowness of movement and loss in a third region is associated with memory trouble.”
Lower protein levels in specific brain regions correlated directly with the severity of the participants’ symptoms. In the ventral striatum, which helps process motivation, reduced dopamine cell density was associated with higher apathy scores and increased reports of daily cognitive failures. In the dorsal putamen, a region heavily involved in movement, lower cell density correlated with slower performances on the physical finger-tapping test. In the dorsal caudate, which supports learning, reduced cell density was linked to poorer scores on the delayed memory recall test.
“The correlations in loss of the marker of dopamine nerves with symptoms were stronger than expected and correlated with a wider range of symptoms than expected,” Meyer said.
The scientists also tested blood samples from the participants to see if peripheral biomarkers of dopamine metabolism or general nerve damage matched the brain scan results. They found no significant correlations between the blood markers and the imaging data in the long COVID group. This indicates that simple blood tests may not accurately reflect the specific dopamine cell damage occurring deep within the central nervous system.
Observational studies of this nature cannot definitively prove causality. The data shows an association between lower dopamine cell density and long COVID symptoms, but it does not confirm that the virus directly killed the cells. Other biological responses triggered by the virus could potentially contribute to both the brain changes and the neuropsychiatric symptoms.
Another limitation relates to what the positron emission tomography scans physically measure. The imaging tracks the density of the transporter proteins rather than the physical brain cells themselves. It is theoretically possible that the neurons remain structurally intact but have simply stopped producing normal levels of the transporter protein.
The study utilized a relatively small sample size of 24 long COVID patients, and all these individuals suffered from a specific set of severe psychological and cognitive symptoms. As a result, these findings might not apply to people whose long COVID primarily involves respiratory or cardiovascular issues. Future research will need to replicate these brain scans in much larger and more diverse groups of patients to confirm the generalizability of the findings.
A key consideration is that these findings represent a specific point in time, and the long-term trajectory for patients remains unknown. The nervous system has a capacity to heal, and symptom persistence varies from person to person.
“It doesn’t mean people can’t regrow the nerve terminals without treatment or that it is permanent for everyone,” Meyer said. “But it may be that some people will need additional treatment to help.”
The authors suggest that these findings point toward new potential treatments for long COVID. Because the data suggests a localized loss of dopamine function, clinical trials could explore whether existing dopamine-enhancing medications might alleviate symptoms.
“People with long COVID with symptoms of low motivational energy, slowed speed taking longer to complete activities and problems with remembering words probably have lost nerves that release a chemical called dopamine,” Meyer said. “Some people may grow new nerve terminals and recover but for those who do not, there is an opportunity to make treatments to help nerves either release more dopamine or regrow nerve terminals.”
Medications that inhibit dopamine breakdown or provide precursors to dopamine might help restore motivation and cognitive speed in affected patients. The research team is currently working to test this hypothesis in a clinical setting.
“I am close to receiving approval for a clinical study to repurpose a medication for long COVID,” Meyer said. “The medication would help nerves release more dopamine and lower some types of brain inflammation. We hope it will help with memory problems and difficulty with motivational energy.”
The study, “Loss of vesicular monoamine transporter 2 in striatum of long COVID and relationship to neuropsychiatric symptoms,” was authored by Yuhan Karida Liu, Devina Persaud, Erica L. Vieira, Joeffre Braga, Pablo Rusjan, Laura Miler, Jennifer S. Rabin, Tina McCluskey, Isabelle Boileau, Thomas Chao, Michael Bagby, Lucas Narciso, Lauren Rose Gray, Neil Vasdev, Kimberly Desmond, Stefan Kloiber, Jerry Warsh, Muhammad Ishrat Husain, Kelly Smart, Wei Wang, and Jeffrey H. Meyer.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #LongCOVID #DopamineBrain #NeuropsychiatricSymptoms #BrainInflammation #DopaminePathways #VesicularMonoamineTransporter2 #Striatum #MotivationMemoryMovement #NeurodegenerativeResearch #ClinicalTrials
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Chemical in #Roundup that causes brain damage found in common #cereals, new study finds
December 5, 2024 | Vivek Saxena
"Brief exposure to a weed killer found in breakfast cereals, oats, and orange juice has been shown to cause damage to the human body and brain.
"The weed killer, glyphosate (also known as Roundup), 'is the most widely used herbicide in the US,' according to the Center for Environmental Health.
" 'It is the most commonly used pesticide [#herbicide] in parks and is even found in foods that adults and kids love,' the center notes.
"Yet a new study conducted by Arizona State University researcher Ramon Velazquez and his team has found that active exposure to glyphosate 'can result in significant #BrainInflammation, and increase the risk of #neurodegenerative disease and #Alzheimer’s-like effects,' as reported by Arizona State University (#ASU).
" 'Our work contributes to the growing literature highlighting the brain’s vulnerability to glyphosate,' Velazquez said in a statement. 'Given the increasing incidence of #CognitiveDecline in the aging population, particularly in rural communities where exposure to glyphosate is more common due to large-scale #farming, there is an urgent need for more basic research on the effects of this herbicide.'
" 'My hope is that our work drives further investigation into the effects of glyphosate exposure, which may lead to a reexamination of its long-term safety and perhaps spark discussion about other prevalent toxins in our environment that may affect the brain,' additional study author Samantha Bartholomew added.
"The study involved testing both a high dose and low dose of glyphosate exposure on mice, with the lower dose being around the level that’s found in common foods like cereal and orange juice. While the high dosage dose caused issues, so did the lower dose.
" '[The] lower dose still led to harmful effects in the brains of mice, even after exposure ceased for months,' according to ASU. 'While reports show that most Americans are exposed to glyphosate daily, these results show that even a short period could potentially cause neurological damage.'
"A previous study commissioned by #MomsAcrossAmerica in 2017 found that one of the most popular #OrangeJuices in America, #Tropicana, also contains glyphosate.
" 'The discovery of glyphosate residue in orange juice is unacceptable, especially since a branch of the World Health Organization designated glyphosate a probable #carcinogen two years ago, back in the spring of 2015,' Moms Across America founder Zen Honeycutt said in a statement at the time.
" 'The EPA has had ample time to revoke the license of this chemical and restrict its use in our food and beverage crops. As confirmed by the American Academy of Pediatrics, our children (who frequently drink orange juice for breakfast) are especially vulnerable to pesticides and measures should be taken immediately to protect them,' she added.
"What remains to be seen is how the upcoming Trump Environmental Protection Agency will deal with this." [We know how that went!!! More #EPAFails!]
#EPAFail #Bayer #ToxicPesticides
#Monocrops #Monocrap #BigAg
#BigChem #Corruption #Poison #Crapitalism #CapitalismKills #RoundUpKills #USPol #WorldPol #Roundup #Glyphosate #BreakfastCereals #OrangeJuice -
#PhotoBioModulation #RedLightTherapy #NearInfrared #inflammation #me #cfs #logcovid #MECFS #BrainInflammation #microglia
dr. Jarred Younger on studies with near infrared light to reduce brain inflammation
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#ME/CFS #CFS #LongCovid #fatiguesyndrome #ClinicalResearch #BrainInflammation #JarredYounger
Developing treatment for brain inflammation at University of Alabama at Birmingham
https://www.youtube.com/watch?v=KpsK6RmqLNI
Lab donation page:
https://go.uab.edu/youngerLarge Donations and Questions:
Julia Ann Starke (Senior Director of Development at UAB)
Email: [email protected]