By Linda Thomas
I was scrolling through a myositis newsletter the other night, the kind of scrolling I do when I can’t sleep because my legs won’t settle down, and I thought, when did I become a person who reads medical journal abstracts for fun? I used to read novels at midnight. Now I read about T cells. I guess inclusion body myositis changes what counts as entertainment.
But here is the thing I want to tell you, the thing that actually kept me reading past the first paragraph: there is more happening in IBM research right now than there has been in years. Not a cure. I want to be honest with you, because platitudes don’t serve us any better in research news than they do at the grocery store. But real movement. The kind where scientists who have been arguing with each other for a decade are finally starting to agree on something.
The degeneration people and the inflammation people finally shook hands
For years there have been basically two camps studying IBM. One camp said the muscle is just wearing out on its own, dying from the inside, and the immune system shows up afterward like bystanders at an accident. The other camp said no, the T cells are the ones doing the damage, they’re the arsonists, not the firefighters. If you’ve ever sat in a specialist’s office and heard two different explanations of your own disease, you know how unsatisfying that split has been.
This year, researchers found something that ties both stories together, and I think it’s the most important thing that’s happened in IBM science in a long time. It turns out a protein called TDP- 43, which normally sits inside the nucleus of our muscle cells doing housekeeping, starts leaking out of the nucleus in IBM. When it leaves, it stops suppressing certain bits of genetic code that are usually kept switched off. Those bits get switched on, get turned into odd little proteins the body has never seen before, and the immune system reacts to them like they’re foreign invaders. So the degeneration causes the inflammation. It’s not either/or. It’s one long chain reaction, and now there’s a name for the link in the middle. I read that and thought about how many times I’ve explained IBM to someone as “part autoimmune, part just degenerative, nobody really knows,” and shrugged. Now I have a slightly better shrug.
The big drug trial that didn’t work, except where it did…kind of
You’ve probably heard of ulviprubart, also called ABC008, the antibody designed to knock out the specific T cells (the KLRG1 positive ones) that are thought to be attacking our muscle. The big Phase 2/3 trial results came out this spring, and the honest headline is: it missed its main goal. Across the whole group of patients, it didn’t slow disease progression by a statistically meaningful amount.
Here’s the part that doesn’t usually make the headline, though. When researchers looked specifically at people who started the trial with less severe disease, both drug doses showed the decline slowing by about half compared to placebo. Half. That’s not nothing, even if it wasn’t the pre-planned way to prove a drug works. The company is now raising money for a new trial aimed specifically at that group, people with less severe disease. I have complicated feelings about this. Part of me wants to shout “sooner, please, we needed this yesterday.” Part of me recognizes that a drug working better in earlier-stage disease is exactly why people keep telling us diagnosis speed matters so much. If you know someone newly diagnosed, this is your nudge to get them into a specialist and a registry now, not in two years.
The metabolism angle, and why exercise keeps showing up in every conversation
There was also a small study on pioglitazone, an old diabetes drug, looking at whether it could nudge the broken energy metabolism inside IBM muscle back toward normal. It’s the same pathway that gets activated when we do endurance exercise, which is probably why every myositis specialist eventually tells us to keep moving even when moving is the last thing we want to do. The study was small and didn’t prove pioglitazone changes outcomes, but it reinforced something I already believed out of stubbornness: our muscles aren’t just wasting away for no reason, there’s a fixable-sounding metabolic story underneath some of it, and that gives researchers another door to try.
Speaking of exercise, I laughed out loud at one study this year. A group of physical therapists sat down and quizzed ChatGPT on exercise advice for IBM, then graded its answers. Mostly safe, mostly accurate, a little vague when the questions got complicated. So apparently even the robots are being tested on their bedside manner now. I don’t know whether to feel reassured or replaced.
Quiet progress on swallowing
Dysphagia doesn’t get the flashy headlines that new drugs do, but it’s the complication that scares me more than the cane or the walker ever did. There’s been steady work this year on recognizing IBM earlier in people whose only symptom, at first, is trouble swallowing, and on better ways to see exactly what’s happening in the throat when we swallow, using more precise imaging than before. None of it is a fix. But better recognition means fewer people spending years being told it’s just reflux or just aging, and more people getting into a myositis clinic before the disease has had a decade’s head start.
Where that leaves us
None of this is a cure landing in my mailbox tomorrow. I know that. But I’ve been doing this long enough to remember when there was almost nothing to read at midnight except the same three old papers. Now there’s a mechanism that finally makes sense of why my body is doing what it’s doing, a drug trial that failed in a way that still taught us something useful, a gene therapy in early safety testing, and researchers paying real attention to swallowing instead of treating it as an afterthought.
I have IBM. It does not have me. And apparently, neither does the news cycle, because I read all of this and went back to sleep just fine.
Linda Thomas was diagnosed with IBM in 2023. Her disease has progressed slowly so far. She journals about her journey in a blog at ibmwarrior.com and has written three books on self-improvement, including The Life That’s Still Mine: Learning to Adapt and Find Meaning When Your Body Changes in Unexpected Ways. After several jobs in leadership positions, she failed retirement three times but is now getting the hang of it.
In case you’d like to go down the rabbit hole with Linda, here’s her list of sources:
TDP-43 / cryptic exon mechanism (the “unifying” discovery)
- Suzuki N, Izumi R, Ikeda K, et al. “Paradigm shift in the pathomechanisms and treatment of inclusion body myositisv” — Current Opinion in Neurology, Oct 2026 (PubMed)
- “TDP-43 pathology induces CD8+ T cell activation through cryptic epitope recognition” — bioRxiv preprint / PMC, 2026 (the HDGFL2/IgLON5 neoantigen work)
Ulviprubart (ABC008) trial
- Abcuro press releases: topline results (Feb 24, 2026) and detailed GCOM 2026 presentation (Mar 26, 2026)
- Cure IBM blog coverage of the same trial, including the subgroup analysis and the $66M raise for a follow-on Phase 3
- ClinicalTrials.gov listing NCT05721573
Pioglitazone study
- “Modifying muscle metabolic dysregulation in inclusion body myositis with pioglitazone: a single-arm trial” — Nature Communications, March 2026
- Cure IBM’s plain-language write-up of the same study
Gene therapy (AVGN7.2) — mentioned only lightly in the post, but I researched it
- Herring & Rodgers, “Murine toxicology assessment of avgn7.2…” — Gene Therapy, 2026 (Nature)
ChatGPT exercise-advice study
- Schütze, Bagg, Cooper, et al., “Evaluating ChatGPT’s advice and recommendations regarding exercise for people with inclusion body myositis” — Neuromuscular Disorders, May 2026 (ScienceDirect)
Dysphagia / earlier recognition
- Yale IBM Disease Registry publications page — several 2025–2026 papers on isolated-dysphagia presentations and swallowing kinematics (e.g., Kaneko et al., cricopharyngeal myotomy case; Ambrocio et al. on swallowing kinematics)
