February 2026: This Month in Huntington’s Disease Research

February is the shortest month, but the HD research community packed a lot into it. From peer-reviewed trial data finally hitting the journals to fundamental discoveries about how brain cells are wired, and even some tiny worms doing heavy lifting in the lab, there was plenty to keep up with. This month’s articles also shine a light on the human side of HD, reminding us that behind every data point is a person navigating real uncertainty. Let’s dig in.

Themes That Unified the Month

The value of published data: One of the most important stories this month wasn’t about a success, it was about making sure a setback gets properly documented so we can learn from them moving forward. The publication of results from the VIBRANT-HD trial testing the HTT-lowering drug branaplam are a reminder that science advances through honest accounting of what worked, what didn’t, and what we learned from it.

Genetics are complicated: Two articles this month pushed back against the idea that a single number, your CAG repeat count, tells the whole story. Whether it’s the specific DNA sequence around those repeats or the exact way brain cells are wired, the details turn out to matter enormously.

HD affects the whole person: February brought a much-needed spotlight on psychological wellbeing for people living at risk of HD, and an eye-opening review of how even the retina and eye movements can reveal what’s happening in the brain. HD is not just a movement disorder — it touches every aspect of life.

HD is not just a movement disorder — it touches every aspect of life.

Clinical Trial Updates

Putting it in print: oral drug branaplam lowered huntingtin, but safety concerns halted development

The results of the VIBRANT-HD trial that tested the oral HTT-lowering drug branaplam have been formally published in Nature Medicine. A positive takeaway from the trial was that branaplam worked, reducing levels of expanded HTT  in the spinal fluid by ~25% compared to placebo. This provided the first clear proof that a pill can be used to lower HTT in people with HD.

The bad news was that about three-quarters of participants showed signs of nerve damage, causing the trial to be stopped early. The damage was largely reversible after stopping the drug, and the knowledge gained, including the validation of NfL as an early-warning safety biomarker, continues to inform the next generation of oral HTT-lowering drugs now in clinical trials.

Understanding HD Biology

Worms to the Rescue: Separating the Good, the Bad, and the Clumpy Huntingtin

Not all HTT protein clumps are created equal, and a clever new study figured out which ones might be more dangerous by separating and feeding them to microscopic worms. The verdict from this study was that small, flexible clumps were highly toxic, while the large rigid structures often assumed to be the main culprit caused no harm at all in this study.

When researchers chemically “stapled” the small clumps together to make them less flexible, the worms fared better, suggesting that a clump’s flexibility, not its size, may be the key to its toxicity. This is still early-stage worm science, but it opens an intriguing new angle: could locking down toxic protein clumps become a treatment strategy for HD?

A Fault in the Supercomputer

Researchers at UCLA took a three-dimensional look at the brain circuits most vulnerable in HD, medium spiny neurons in the striatum, and found that these cells look different depending on where they sit within the brain, with varying spine lengths, densities, and branching patterns. More importantly, in a mouse that models HD, these neurons were less complex and had fewer connections than in healthy mice.

This suggests the striatum in HD may be progressively losing its connections to the rest of the brain, like a central processing core being slowly unplugged. Understanding exactly how this happens could open new avenues for therapies aimed at repairing or protecting these vital circuits.

A Hitch in the Stitch: Why DNA Sequence Patterns Matter in Huntington’s Disease

Your CAG repeat count isn’t the whole story. The exact pattern of the DNA sequence around those repeats matters enormously. A new study from researchers in Vancouver and Paris examined 328 people with CAG repeats in the 36–42 range and found that people missing key interruptions in the repeat sequence, called “loss of interruption” patterns, developed symptoms nearly 13 years earlier than predicted by repeat count alone, and progressed roughly twice as fast.

Standard genetic tests count the number of CAG repeats, but often miss these sequence variations. This means some people in the HD grey zone may face a higher risk than their result suggests. The findings have big implications for genetic counselling, disease prediction, and clinical trial design, and the team even identified a brand new sequence variant never described before.

Biomarkers

A Window into the Eyes: Using Ocular Biomarkers to Track HD Progression

Could a simple eye exam help track HD? A review from the University of Cambridge examined the evidence for retinal scans and eye movement tracking as potential biomarkers. Retinal imaging showed inconsistent results across studies and isn’t ready for clinical use, but eye movement tracking told a more promising story: people with HD, including those not yet showing symptoms, have measurable and progressive differences in how their eyes move.

The catch is that the technology is expensive and not widely available, and studies need to become more standardized before eye tracking could be rolled out as a clinical tool. But the consistency of the findings makes it one of the more exciting non-invasive biomarker candidates in the HD field right now.

Living with HD

Split Between Two Worlds: The Psychological Challenges for People at Risk of HD

An interview-based study from Lancaster, UK listened carefully to 12 people living at risk of HD and found that maintaining psychological wellbeing is an active, daily effort, not a fixed state. Participants described navigating between two worlds: one defined by the reality of HD, and one where ordinary life could exist alongside it, a conscious and skilled balancing act rather than denial.

Many also described a constant sense of urgency to live fully while they still can, alongside the exhausting work of protecting their identity and managing stigma from others. The study makes a clear case for better training among healthcare providers and more accessible psychological support for people at risk, because the invisible mental load of living with uncertainty deserves the same attention as the physical symptoms.

The people living at risk, navigating uncertainty every single day, deserve to see their experiences reflected in the science, and supported by the care they receive.

Looking Ahead

February’s articles paint a rich picture of HD research in 2026: a field that is maturing, diversifying, and increasingly attuned to the full complexity of the disease. The published VIBRANT-HD data close one chapter while next-generation oral HTT-lowering drugs continue their way through trials. 

The emerging science of CAG sequence patterns and brain circuit connectivity promises to sharpen our ability to predict and treat HD. And a growing focus on biomarkers, from eye movements to protein clump structure, is expanding the toolkit available to researchers and clinicians.

Most importantly, this month reminded us that HD research isn’t only about molecules and mechanisms. The people living at risk, navigating uncertainty every single day, deserve to see their experiences reflected in the science, and supported by the care they receive.

Summary

• Results from the VIBRANT-HD trial testing branaplam have been published. This study showed us that oral HTT-lowering is possible, but nerve damage side effects halted development of this drug. These lessons continue to inform next-gen drugs.

• A study in laboratory worms suggests small, flexible HTT protein clumps are the most toxic form.
• 3D mapping of HD-vulnerable brain circuits shows fewer connections in HD mice
• DNA sequence patterns within the CAG repeat region can shift symptom onset up to 13 years earlier and double progression speed. 
• Eye movement tracking is a promising early HD biomarker.
• An interview-based study highlights the daily psychological work of living at risk of HD and the urgent need for better support from healthcare professionals.