Twenty-eight people with relapsing-remitting multiple sclerosis added a weekly diabetes shot to their usual treatment for a year. The two things the trial was built to measure, a blood protein that climbs when nerve fibers are dying and the slow shrinkage of the brain on MRI, did not change.
That null is the honest center of a small randomized study published online June 20 in Neurology and Therapy ↗. The drug was dulaglutide ↗, the GLP-1 receptor agonist sold as Trulicity for type 2 diabetes and a cousin of Ozempic and Wegovy. GLP-1 drugs have been floated for years as possible nerve protectors, on the idea that the GLP-1 receptor sitting on brain cells does something useful when you switch it on. This is one of the first randomized tests of that idea in MS, and it put the hard markers first.
What the trial did
The setup was deliberately clean for a first look. All 28 patients were already on natalizumab, a strong antibody therapy that suppresses MS relapses, and their disease was stable. The team, led by Pavel Šiarnik, randomized 15 of them to add dulaglutide at 0.75 mg under the skin once a week for 12 months and left 13 on natalizumab alone. Everyone was measured at the start and again a year later.
The primary readouts were neurofilament light chain, or NfL, a protein that leaks into the blood when nerve axons break down, and MRI volumetry, which tracks how much brain tissue is left. Both are standard proxies for whether the disease is still quietly eating away at the nervous system. If dulaglutide were protecting neurons, these are the numbers that should have bent.
They did not. Over the year, dulaglutide did not modify plasma NfL or the MRI volume measures.
What did move
What the drug did do is exactly what GLP-1 drugs always do. Patients lost weight, body-mass index, body fat, and visceral fat, the deep abdominal fat tied to metabolic disease, and their glucose tolerance improved, measured as a smaller blood-sugar spike after a sugar drink. None of that is surprising, and none of it is the question the trial asked.
Two functional tests did wobble in the drug's favor. Walking speed on a timed 25-foot walk trended better in the treated group (p = 0.005), and dexterity in the non-dominant hand improved on a standard nine-hole peg test (p = 0.039). A test of cognitive processing speed showed no difference between groups. The authors label these findings exploratory, and they are right to. The trial was open-label, meaning patients and assessors knew who was getting the drug, and effort-dependent functional tests are exactly the kind that drift when people know they are being treated. With 28 patients split two ways, one unusually fast or slow walker moves the average.
Why the null is the story
NfL is a hard biological signal, not a performance you can talk yourself into, and it stayed flat. The cleanest reading is that a year of a low-dose GLP-1 drug, layered on top of an already effective MS therapy that may already be holding NfL down, added no measurable neuroprotection. That is worth knowing, because the neuroprotection pitch for GLP-1 in neurological disease keeps getting made on the strength of animal data and soft endpoints. A small trial that measured the hard markers and reported them plainly is more useful than a larger one built to chase a walking-speed headline.
It also fits a pattern this section keeps hitting. A GLP-1 drug infused during open-heart surgery did not protect the lungs ↗ in a controlled substudy reported this week either. The metabolic effects of these drugs are real and reproducible. The organ-protection halo around them keeps shrinking every time someone measures it cleanly.
One thing the trial does confirm is safety: no adverse events and no dropouts in either arm over 12 months. For someone with MS who also has diabetes or obesity, that is a fair reason to use dulaglutide. Slowing the MS itself is not, at least not on this evidence.