#inflammation?🧠💊
LightNews LightNews
lifespannews.bsky.social
Scientists have found that a gene on the X chromosome, 🧬which escapes silencing, promotes inflammation 🔥 and neurodegeneration 🧠in a mouse model of multiple sclerosis, but the effects can be reversed with metformin. 💊

www.lifespan.io/news/female-...
By: @arkadimazin.bsky.social
Female-Specific Mechanism of Neurodegeneration Discovered
Scientists have found that a gene on the X chromosome, which escapes silencing, promotes inflammation and neurodegeneration in a mouse […]
www.lifespan.io
October 17, 2025 at 4:26 PM
amjeditor.bsky.social
🧠💊 Omega-3 supplements reduced key markers of inflammation and oxidative stress in moderate-to-severe head injuries, but no improvement was seen in long-term recovery outcomes, researchers report.

www.emjreviews.com/en-us/amj/ne...

#AMJNeurology #BrainInjury #Neuroinflammation
Omega-3s Reduce Inflammation but Not Outcomes in Head Injuries
Omega-3 supplementation lowered inflammatory and oxidative stress markers in moderate-to-severe head injury patients but did not improve long-term clinical outcomes, trial results show.
www.emjreviews.com
October 2, 2025 at 1:33 PM
biologicalpsych.bsky.social
How does socioeconomic status 💰 impact reward processing 🧠, inflammation 🔥, and antidepressant efficacy 💊 in depression 😔?

Find out more 👇
Socioeconomic status is associated with reward processing, interleukin 1β, striatal connectivity and antidepressant outcomes in individuals with major depressive disorder: A CAN-BIND-1 report.
Major depressive disorder (MDD) is a common condition with heterogeneous risk factors. Socioeconomic status (SES) is one such risk factor, which is negatively linked to MDD treatment outcomes and symp...
www.bpsgos.org
November 3, 2025 at 1:38 PM
newsmedical.bsky.social
Long-term NSAID use may lower dementia risk 🧠💊📉 www.news-medical.net/news/2025030... #Dementia #NSAIDs #Brain #Health #Inflammation #Alzheimers #HealthyAging #MedicalNews #Neurology @agsjournal.bsky.social
Long-term NSAID use may lower dementia risk
Long-term NSAID use reduces dementia risk, particularly in those without the APOE-ε4 gene, highlighting the importance of sustained anti-inflammatory treatment over dosage levels.
www.news-medical.net
March 9, 2025 at 11:25 PM
tonnomartinez.bsky.social
Do you want to work as a #postdoc in our group in a Hospital Research Institute in Madrid?🏥🔬

Interested in how #mitochondria and #redox signalling/stress can influence #stroke outcome and #inflammation?🧠💊

Apply up to 26 December at n9.cl/iunkw (ref 72/2024)
Full call n9.cl/gijjd

Please repost 😉
Postdoctoral position in the group of Dr. Antonio Martínez Ruiz in Madrid
December 16, 2024 at 10:23 AM
dlingenfelter.bsky.social
Persistent SARS-CoV-2 in the gut drives systemic inflammation and diverse Long COVID symptoms via barrier damage and microbiome disruption.

Targeting the gut reservoir may unlock effective treatments.
davidlingenfelter.substack.com/p/sars-cov-2...
🧬 Scientific Announcement: A Paradigm Shift in Long COVID Pathophysiology We are pleased to share a groundbreaking synthesis of emerging evidence that redefines our understanding of Long COVID. Dr. David Lingenfelter's latest report presents a unifying pathophysiological model positioning the gastrointestinal tract as a persistent viral reservoir for SARS-CoV-2—an upstream driver of systemic inflammation and multisystemic symptoms. Key findings include: Persistent Viral Reservoir: The intestinal epithelium, rich in ACE2 and TMPRSS2, supports prolonged SARS-CoV-2 replication, with viral RNA and proteins detectable up to 676 days post-infection. Barrier Dysfunction & Dysbiosis: Chronic inflammation and microbiome disruption compromise gut integrity, facilitating translocation of viral antigens and microbial products into systemic circulation. Systemic Inflammatory Cascade: This “two-hit” model—viral and microbial—triggers sustained low-grade inflammation, contributing to hallmark symptoms such as cognitive dysfunction, fatigue, and dysautonomia. Gut-Brain Axis Implications: Aberrant vagus nerve signaling, serotonin depletion, and neuroinflammation link gut pathology to neurological and psychiatric manifestations of Long COVID. This integrative framework not only reconciles disparate clinical observations but also highlights novel therapeutic targets, including antiviral strategies, microbiome modulation, and barrier-repair interventions. We invite researchers, clinicians, and policy stakeholders to explore the full report and consider its implications for diagnostics, treatment stratification, and future clinical trials. 🔗 Read the full analysis on David Lingenfelter’s Substack Here's a concise summary of the main points from the article “SARS-CoV-2 Persistence in the Gastrointestinal Tract: A Unifying Pathophysiological Model for Systemic Long COVID” by David Lingenfelter, PhD: 🧠 Central Thesis Persistent SARS-CoV-2 in the gut may be a key driver of Long COVID. The gastrointestinal tract acts as a viral reservoir, triggering systemic inflammation and diverse symptoms. 🔬 Biological Mechanism The gut has high ACE2 receptor expression, making it highly susceptible to infection. SARS-CoV-2 disrupts local renin-angiotensin system (RAS), creating a pro-inflammatory environment. Viral persistence leads to chronic antigen shedding, immune activation, and gut barrier dysfunction. 🦠 Evidence of Viral Persistence SARS-CoV-2 RNA and proteins have been found in gut tissue months to years post-infection. Viral antigens (e.g., spike protein) detected in blood of Long COVID patients suggest ongoing shedding. The gut’s immune-tolerant environment may allow viral evasion and persistence. 🔁 Pathophysiological Cascade Local inflammation → gut dysbiosis → leaky gut → systemic inflammation. Translocation of viral and microbial products (e.g., LPS, β-glucan) into bloodstream fuels chronic inflammation. 🧠 Gut-Brain Axis & Neurological Symptoms Inflammation affects the vagus nerve, contributing to autonomic dysfunction (e.g., POTS). Neuroinflammation and serotonin depletion linked to cognitive symptoms like “brain fog” and anxiety. 🔄 Integration with Other Hypotheses Gut reservoir may drive or exacerbate: Immune dysregulation Endothelial dysfunction & microclots Latent virus reactivation Mitochondrial dysfunction 💊 Therapeutic Implications Targeting the gut may offer treatment paths: Antivirals to clear the reservoir Zonulin antagonists to restore barrier integrity Probiotics/synbiotics/FMT to correct dysbiosis Anti-inflammatory agents to manage systemic effects 🔍 Future Research Priorities Develop biomarkers for viral persistence Create animal models replicating gut pathology Understand host predisposition factors Design stratified clinical trials based on pathology This model reframes Long COVID as a gut-originating, systemic disease—suggesting that healing the gut could be key to resolving its wide-ranging symptoms.
September 9, 2025 at 7:06 PM
drruth.bsky.social
🩺Senolytic therapy alleviates human brain aging and COVID-19 neuropathology buff.ly/3MGvd9O

🧠SARS-CoV-2 causes the brain to age prematurely by increasing brain inflammation.

💊Senolytic drugs reduce this in brain organoids and may provide treatment for COVID neuroinflammation.

#neuroskyence 🧪
Brain organoids are treated with different senolytic drugs (navitoclax, abt-737, and D+Q).
November 16, 2023 at 8:23 PM
dlingenfelter.bsky.social
The gastrointestinal tract is a central driver of Long COVID pathogenesis, w/ SARS-CoV-2 infecting intestinal cells & causing inflammation, microbiome dysbiosis, & more.

Persistent viral reservoirs in the gut lead to systemic and metabolic disruption.
davidlingenfelter.substack.com/p/the-gut-ce...
Here’s a structured summary of the main points from the Substack article titled “The Gut-Centric Pathogenesis of Long COVID” by David Lingenfelter, PhD: ________________________________________ 🧠 Executive Summary • Long COVID (PASC) is a chronic, multisystemic condition affecting millions post–SARS-CoV-2 infection. • The gastrointestinal (GI) tract is proposed as a central driver of Long COVID pathogenesis. • SARS-CoV-2 infects intestinal cells, triggering inflammation, microbiome dysbiosis, and barrier dysfunction. • Persistent viral reservoirs in the gut lead to systemic inflammation and metabolic disruption. • Gut-targeted diagnostics and therapies (e.g., synbiotics, zonulin antagonists) show promise. ________________________________________ 🧬 Mechanistic Evidence (Part I) 1.1 Viral Tropism • SARS-CoV-2 infects intestinal enterocytes via ACE2 and TMPRSS2. • Human intestinal organoids confirm productive viral replication. • Individuals with higher ACE2 expression may be more susceptible to gut infection and Long COVID. 1.2 Animal Models • Mouse, hamster, and primate models show gut involvement post-respiratory infection. • Viral replication and microbiome disruption observed in GI tissues. 1.3 Gut Barrier & Immune Impact • Infection induces local inflammation and damages Paneth/goblet cells. • Leads to compromised gut barrier (“leaky gut”) and dysbiosis. ________________________________________ 🧍‍♂️ Observational Human Evidence (Part II) 2.1 Acute COVID-19 Microbiome • Decreased microbial diversity and loss of butyrate-producing bacteria. • Enrichment of opportunistic pathogens correlates with disease severity. 2.2 Persistent Viral Reservoir • Viral RNA and antigens found in stool and gut tissue months to years post-infection. • Active replication in gut even after respiratory clearance. 2.3 Long COVID Microbiome • Chronic dysbiosis persists in Long COVID patients. • Microbiome composition during acute phase predicts Long COVID risk. • Specific microbial patte… ________________________________________ 🔄 Unified Pathophysiological Model (Part III) 3.1 Leaky Gut & Inflammation • Overexpression of zonulin disrupts tight junctions. • Viral antigens and microbial products (e.g., LPS) leak into bloodstream. • Drives chronic systemic inflammation. 3.2 Metabolic Disruption • Butyrate deficiency impairs immune regulation and energy metabolism. • Tryptophan metabolism disrupted → serotonin depletion → vagus nerve dysfunction. • Leads to fatigue, mood disorders, and cognitive symptoms. 3.3 Gut-Brain Axis • Neuroinflammation via cytokine leakage and vagus nerve impairment. • Altered microbial metabolites affect neurogenesis and myelination. • Parallels with ME/CFS suggest shared mechanisms. ________________________________________ 💊 Clinical & Therapeutic Implications (Part IV) 4.1 Diagnostics • Microbiome profiles can predict Long COVID risk and aid diagnosis. • Multi-omics platforms (e.g., BioMapAI) offer ~90% accuracy in related conditions. 4.2 Therapies • Synbiotics (e.g., SIM01) improve symptoms and restore microbial balance. • Fecal Microbiota Transplantation (FMT) under investigation. • Zonulin antagonists (e.g., larazotide) may restore barrier integrity and reduce inflammation. ________________________________________ 🔭 Conclusion: Toward Precision Medicine • Gut-centric model offers a coherent framework for understanding Long COVID. • Future research should focus on: o Longitudinal multi-omics studies o Stratified clinical trials o Personalized interventions based on microbial and metabolic profiles Source: https://davidlingenfelter.substack.com/p/the-gut-centric-pathogenesis-of-long
July 31, 2025 at 8:01 PM
drtanakabluesky.bsky.social
📚Have you read it?🧠✨🔬
Could #AdipoRon be the next breakthrough in #Alzheimer’s treatment?🏥💊New #Research reveals its #Neuroprotective effects—reducing #Inflammation, improving #Cognition & more! 🚀 MDPI Biomedicines #Neuroscience #BrainHealth
Curious? www.mdpi.com/1422-0067/26...
AdipoRon’s Impact on Alzheimer’s Disease—A Systematic Review and Meta-Analysis
Alzheimer’s disease (AD) remains a leading cause of cognitive decline and mortality worldwide, characterized by neurodegeneration, synaptic deficiencies, and neuroinflammation. Despite advancements in...
www.mdpi.com
February 2, 2025 at 8:13 AM
sigma1europe.bsky.social
🧠 Prof. Michael Decker (Univ. of Würzburg) spoke at LIOS on hybrid molecules & photopharmacology.

His dual-action molecules ⚖️ slow brain cell loss & cut inflammation 💊, protecting against memory decline in Alzheimer’s models.

#BrainHealth #Neurodegeneration #COSTaction #SIGMA1EUROPE
September 9, 2025 at 9:58 AM
reumatologiaj.bsky.social
🦴MSK involvement in #SSc
Affects up to 90% patients: arthralgia, arthritis, tendinitis, contractures,calcinosis,myositis
🧠Early joint pain may precede SSc diagnosis
🔍US/MRI detect subclinical inflammation
💊Physio+MTX/MMF/HCQ/RTX/TCZ;avoid high-dose GCs
doi.org/10.5114/reum...
October 19, 2025 at 11:42 AM
newsmedical.bsky.social
Ketogenic diet a potential therapy for autism by reshaping gut bacteria and brain inflammation 🧠💊🦠 www.news-medical.net/news/2024050... #Ketogenic #Diet #Autism #GutMicrobiome #Neuroinflammation #miRNA #Dietary #BrainGutAxis #Metabolic
Ketogenic diet a potential therapy for autism by reshaping gut bacteria and brain inflammation
Modified ketogenic diet modulates gut microbiome, inflammatory markers, and brain-related miRNAs in autistic children, correlating with improved behavioral symptoms. The diet increases beneficial gut ...
www.news-medical.net
May 9, 2024 at 11:50 PM
drtanakabluesky.bsky.social
💥 #Fat #Hormones aren’t just about weight—they regulate the brain! In #RRMS, #Fingolimod & natalizumab modulate #Adipocytokines, reshaping #Inflammation & #Therapy response! 🧠💊🔥 @IJMS_MDPI @MDPIOpenAccess#MultipleSclerosis #BrainScience
www.mdpi.com/1422-0067/26...
www.mdpi.com
September 8, 2025 at 6:13 AM
drtanakabluesky.bsky.social
📚Have you read it?🧠✨🔬
Could #AdipoRon be the next breakthrough in #Alzheimer’s treatment?🏥💊New #Research reveals its #Neuroprotective effects—reducing #Inflammation, improving #Cognition & more! 🚀 MDPI Biomedicines #Neuroscience #BrainHealth
Curious? www.mdpi.com/1422-0067/26...
AdipoRon’s Impact on Alzheimer’s Disease—A Systematic Review and Meta-Analysis
Alzheimer’s disease (AD) remains a leading cause of cognitive decline and mortality worldwide, characterized by neurodegeneration, synaptic deficiencies, and neuroinflammation. Despite advancements in...
www.mdpi.com
January 29, 2025 at 7:47 AM
apresj20.bsky.social
🧠🔥💊Mécanismes possibles :
- Persistance virale dans les reins
- Inflammation chronique
- Médicaments COVID
- Conditions économiques et sociales liées à la pandémie (ex : accès aux soins)
April 20, 2025 at 12:43 PM
apresj20.bsky.social
🔑Vers des solutions:
Des essais cliniques en cours testent :
💊 Antiviraux, anti-inflammatoires, immunomodulateurs
🧠 Traitements ciblant la neuro-inflammation
February 24, 2025 at 11:35 AM
drtanakabluesky.bsky.social
💥 #Fat #Hormones aren’t just about weight—they regulate the brain! In #RRMS, #Fingolimod & natalizumab modulate #Adipocytokines, reshaping #Inflammation & #Therapy response! 🧠💊🔥 @mdpiopenaccess.bsky.social #MultipleSclerosis #BrainScience
www.mdpi.com/1422-0067/26...
www.mdpi.com
September 19, 2025 at 5:25 AM