NeuroVoices: Brian Callaghan, MD, on Recapping the 2026 Peripheral Nerve Society Annual Meeting

The 2026 Peripheral Nerve Society (PNS) Annual Meeting, held June 13 to 16 in Maastricht, Netherlands, brought together leading voices in peripheral nerve disease to discuss the latest research, debate unresolved questions, and preview what is coming next across conditions ranging from CIDP and GBS to hereditary neuropathies and TTR amyloidosis. From real-world treatment data to the early stages of CRISPR-based therapies, the meeting reflected a field in the middle of meaningful transformation.

For this week's NeuroVoices, NeurologyLive^® sat down with Brian Callaghan, MD MS, associate professor at the University of Michigan, for a post-conference recap of the themes, studies, and conversations clinicians may have missed. Callaghan has been deeply involved in peripheral nerve disease research across several of the conditions discussed at PNS 2026 and brought his perspective on both what stood out and what remains unresolved.

In this Q&A, Callaghan discusses emerging methodology in GBS research, the continued momentum in SMA and TTR neuropathy, why RFC1 is now commanding more attention than ever, the evolving conversation around IVIG discontinuation in CIDP, and where he is looking as PNS 2027 comes into view.

NeurologyLive: From a clinical perspective, what were some of the biggest themes or emerging concepts that came out of this year's meeting?

Brian Callaghan, MD: One of the interesting ideas that came out involved the IGOS, the International GBS Observational Study, which has been ongoing for a number of years. Researchers used that infrastructure as a way to create control groups for comparing new therapies, using a statistical technique called matching adjusted indirect comparison. They were able to study a new medicine, imlifidase, combined with IVIG, and compare it to patients who received IVIG alone.

That is conceptually exciting because it allows us to start generating data on a medication before committing to a large, randomized trial, which is expensive and difficult to execute. The idea that we can use this long-standing infrastructure and apply it to potentially new therapies is really quite clever.

What sorts of studies or clinical trials stood out from a therapeutic perspective, and which have the greatest potential to influence practice in the near future?

I would point to two areas. One is SMA, and the other is TTR amyloidosis, or hereditary TTR neuropathy. One of our main talks covered the full arc of SMA treatment data over the years, and what was fascinating is that we now have three medicines that can treat children with SMA and improve their motor function, survival, and quality of life.

But we keep pushing further. At this meeting we were talking about not just treating symptomatic patients, but also treating children identified through newborn screening in countries around the world, and even prenatal treatment. It is remarkable to see how far we have come, and how many more questions we are now in a position to answer.

Similarly, with TTR amyloid neuropathy, we were discussing real-world usage of therapies that knock down TTR, and it is exciting to see that these medicines not only work in trial settings, but continue to work outside of them and over prolonged periods of time.

What are some emerging concepts that are starting to come into their own, things that may have been lightly discussed a few years ago but are now moving closer to the forefront?

One I would highlight is RFC1. RFC1 is a cause of CANVAS, a condition that affects the nerves, the cerebellum, and the vestibular system. What has evolved into a growing consensus is that RFC1 is also quite a common cause of isolated sensory neuropathy. It is a repeat expansion disorder, which made the gene very difficult to discover, but once we identified it, we realized it is far more common than previously thought. It can present as cerebellar disease alone, neuropathy alone, or the full combination.

A lot of this progress is coming through long-read sequencing, a newer genetic testing technique that allows us to identify these repeat expansions and revolutionize our ability to diagnose certain inherited neuropathies. The other thing I would highlight is the evolving consensus around IVIG discontinuation in CIDP. A study presented at this meeting, drawing on data across multiple trials, showed that when patients are taken off IVIG, even those physicians believe still need it, roughly half do fine without it. That is an important finding, because if IVIG is not helping a patient, it can cause harm through side effects, cost, and inconvenience.

Where do you feel the field still has significant unanswered questions, or what came out of the meeting that still stumps us?

PNS had a lot of debates this year, which I thought was great, because it highlighted where real uncertainty exists. I was involved in one where Bruce Perkins and I debated whether diabetic peripheral neuropathy is reversible. He took the no side and I took the yes side. In the end, the honest answer is we do not know.

We do not have good enough treatments for diabetic peripheral neuropathy right now. There are encouraging signals from TTR neuropathy, which gives us hope, but the core question we were debating is whether reversal is even biologically possible. I was on the optimistic side, but it is a legitimate and unresolved question for the community.

Looking ahead to PNS 2027, what areas of investigation are you most looking forward to, and what does the future of the meeting look like from your perspective?

I think the future is bright. Two areas I would highlight. First, CRISPR technology. At this meeting, early-phase studies were presented on using CRISPR to knock down TTR with a single infusion, and the results were quite promising. Now I want to see how it plays out in patients with TTR neuropathy, how it compares to our current therapies, and whether it is complementary or a potential replacement.

Second, in the CMT space, we are starting to see gene silencing therapies coming for CMT1A and gene replacement therapies for CMT2s, and hopefully more beyond that. The big question I am watching is whether we can take the gains we have made in SMA and TTR and start expanding them to some of the other conditions the PNS community has been studying for many years.

Transcript edited for clarity. Click here for more PNS 2026 coverage.