As we age, our blood quietly shifts toward making more inflammation-prone immune cells and fewer of the ones that fight infections and cancer well — real bad news in old age. This paper found one specific immune cell is secretly driving that shift, and blocking a single signal from it reversed the effect in old mice, restoring muscle strength too. nature.com/articles/s43587-0…

Sanofi is taking us straight to the future with this monster in development for osteoarthritis It's a trispecific nanobody that anchors to cartilage (via CAP) and inhibits two cartilage-degrading enzymes, MMP13 and ADAMTS5

Thank you @Surgeon_General for acknowledging Lyme Infection Associated Chronic Illness (Lyme IACI). I’ve lived with it for 11+ years now, & it dominates all aspects of my life. We need better education, prevention, diagnostics, treatments, and INSURANCE PROTECTION. 💚

Could a cough syrup slow Parkinson’s disease? Ambroxol clinical trials move forward. Ambroxol is an expectorant cough medication that also acts as a chaperone, meaning it helps stabilize and improve the function of an important brain enzyme linked to Parkinson’s biology. Toffoli and colleagues describe in a new Viewpoint paper in Movement Disorders how Ambroxol, a frequently used cough medicine in many countries, is being studied as a potential disease modifying therapy for Parkinson’s disease. Key points: – Ambroxol increases glucocerebrosidase activity and may help clear alpha synuclein, a key protein linked to Parkinson’s pathology. – Early phase studies showed ambroxol reached the brain and was safe and well tolerated even at much higher doses than used for cough treatment. – A large phase III clinical trial called ASProPD began recruitment in 2025 and aims to enroll about 330 participants to test whether Ambroxol can slow disease progression, w/ results expected in 2029. My take: This is one of the most exciting drug repurposing efforts in Parkinson’s disease. Ambroxol targets a core biological pathway tied to lysosomes and alpha synuclein. The field is now moving from small safety and proof of mechanism studies into large definitive trials designed to answer whether this therapy can truly slow progression. Here are 5 points that resonated w/ me: 1- Ambroxol is appealing because it is already widely used and has a strong safety track record. 2- The drug crosses into the brain, which is essential if we want to influence Parkinson’s biology. 3- Early studies showed the drug engaged its intended target, which is a critical milestone in therapy development. 4- The ongoing phase III trial looks to be appropriately sized and designed to answer whether Ambroxol meaningfully slows symptoms. 5- Even if Ambroxol is not the final answer, could it open the door to targeting lysosomal pathways as a strategy for future Parkinson’s treatments? movementdisorders.onlinelibr… #parkinson

Sometimes scientific consensus is manufactured via a combination of deplatforming, publication cartels, and framing dissidents as crackpots or bigots. The more you believe it necessary to protect a consensus by authoritarian tactics, the less credible the consensus becomes.

Most patients, regardless of diagnosis, cannot get endothelial or anti-thrombotic drugs without getting referred to cardiology and hematology first. Many networks are trying to deny referrals to rheumatology at present for LC, ME/CFS, and FMS. They are the ones that run the full antinuclear anti-body panels. In this case the main one for endothelial and anti-thrombotic that should be ordered is a Anti-Cardiolipin Antibody IgM for clotting. You have to have 2 positive test results 7-8 weeks apart, then you can get your hematology referral “supposedly” to get started. I have my second retest in a a few weeks. We shall see how it goes. 😪 What you can try to do is get your doctor to order those anti-nuclear anti-body panels to override.

Hi all - I have a patient in France who I manage remotely who I recommended sulodexide as an alternative to my preferred drug, pentoxifyline, which apparently is not available there. It works as an anti-thrombotic, anti-inflammatory, endothelial protective agent.

We identify FKBP5 as a key regulator of myeloid-driven neuroinflammation in #MS 🔬 Elevated in CSF monocytes & microglia from MS 🧬 Inhibition boosts myelin clearance & reduces IFNγ signaling 🐭 SAFit2 improves EAE outcomes #JournalofNeuroinflammation rdcu.be/e3zGN

#WeekendRead! #ImmunometabolismPower! #InflammasomePower! Liu, Yin &co show @CellChemBiol that lactate driven by aerobic glycolysis is used to directly lactylates NLRP3 increasing ASC recruitment & inflammasome activation, exacerbating lethality in sepsis! sciencedirect.com/science/ar…

Important and personal op-ed by ⁦@ScottGottliebMD⁩ on the toll of a virus infection that is not adequately acknowledged. Gift link washingtonpost.com/opinions/…

Our body (cells) have fuel preference, e.g., burning fat vs. carbohydrates, which depends on the environment and nutritional states. How do cells decide which fuels to use?  Our new study found that carnitine biosynthesis is crucial for fuel switching science.org/doi/10.1126/scie…

With @jaiswal_ok, we built a single-cell + spatial atlas of ~4M cells in human IBD. IAFs reside in fibrotic niches, co-localize with inflammatory macrophages, and express ECM + cytokines, incl. IAF-specific IL-11.

📰New feature alert: “Functional Neurological Disorder, Reframed.” A compelling look at the science reshaping how we understand FND—an often overlooked but highly impactful condition. Essential reading for clinicians, researchers, and advocates magazine.hms.harvard.edu/art…)

Vagus nerve wins, big for autoimmune tx bro

12/ Mechanistically, GSTA4 detoxifies 4-HNE, a lipid peroxidation byproduct that progressively accumulates in aging RPE. Unlike generic antioxidants that just mop up ROS, GSTA4 repairs the damage.