August 2025: This Month In Huntington’s Disease Research

This month’s Huntington’s disease (HD) research roundup spans work from the dinner table to DNA repair. Scientists explored whether eating on a schedule could help clear toxic proteins, uncovered early signs of muscle loss in HD, and examined how childhood experiences shape adult mental health. Other teams investigated the gut–brain connection, identified new protein biomarkers, mapped toxic huntingtin clumps, and revealed how tiny changes in DNA repair genes might speed up disease onset. Together, these discoveries highlight both the complexity of HD and the many creative ways researchers are working to tackle it.

Appetite for Answers: Does Eating on a Schedule Help with Huntington’s Disease?

This month we covered work from researchers who are eyeing whether when (rather than what) you eat could benefit people with HD. Known as time‑restricted eating (TRE), the idea is to limit meals to a daily window, like 12 p.m. to 8 p.m., and let the body fast the rest of the time. In animals that model HD, this eating pattern appears to kick-start a cleanup process inside cells (called autophagy) that may help clear out harmful huntingtin protein clumps from the brain.

But before giving your fridge a curfew, remember this: these promising results are from animal studies, not people. And many folks with HD already struggle with unintended weight loss, problems with choking, and muscle wasting, so fasting could unintentionally make symptoms of the disease worse. So even though more research is needed before TRE is prescribed for HD, we know that a healthy diet filled with nutritious food has clear health benefits for everyone.

Body in Decline: Muscle Loss as an Early Symptom of Huntington’s Disease

A new study shows that HD doesn’t just impact the brain, it quietly reshapes the body too. In the earliest stages, people with HD already appear to have signs of reduced muscle mass (60%) and weaker grip strength (45%), even when walking still felt normal. On top of that, over half (55%) seemed to be at risk for or already experiencing malnutrition, a worrying early red flag.

These early physical declines aren’t just numbers, they’re affecting daily life. Reduced strength and nutrition were linked to worse motor symptoms, increased dependence on others, and trouble planning or organizing tasks. The good news is that there’s hope with practical solutions that can be implemented today. Nutritional support, high-calorie or easy-to-eat meals, and staying active with exercises like walking or resistance training could help towards preserving muscle, brain health, and independence. Looking ahead, measuring changes in body composition may one day offer a simple, non-invasive way to monitor disease progression.

Carried from Childhood: Childhood Experiences and Adult Mental Health in Families with Huntington’s Disease

Some childhood memories stick with us in surprising ways, even long into adulthood. A study from Italy looked at adults who grew up with a parent affected by HD and discovered that it wasn’t major crises, but ongoing emotional turbulence, like constant criticism, unpredictable moods, or feeling unsafe speaking up, that had the strongest impact on adult mental health.

Those who grew up in HD families were more likely to struggle with low mood, anxiety, and feeling overwhelmed, even when major traumatic events hadn’t happened. The research helps name what many people have quietly carried for years and why emotional support matters just as much as practical help. Most importantly, it reminds us that healing is possible, and you don’t have to carry it alone. 

If you would like to learn more about support systems and resources available for young people impacted by HD, we encourage you to reach out to the Huntington’s Disease Youth Organization (HDYO) or the Huntington’s Disease Society of America (HDSA) National Youth Alliance (NYA). You are not alone, and support is available. 

The Gut–Brain Superhighway in Huntington’s Disease: Clues From the Microbes Inside Us

Our gut and brain are always chatting – think of it like a busy two-way highway where nerves, immune signals, and gut microbes all send messages back and forth. In HD, this roadway gets bumpy: gut and brain barriers become leaky, inflammation kicks in, and the usual balance of gut microbes gets thrown off, like traffic patterns suddenly going haywire.

Researchers are looking into how we might ease the congestion. Lifestyle factors like exercise or a stimulating environment have helped gut health in animal models, and certain antibiotics showed less inflammation and better nerve cell protection in lab studies. While broad spectrum antibiotics aren’t a realistic option for intervening with the HD microbiome long term, these studies help identify molecular players that could be targeted with new medicines down the road to improve gut and, potentially, brain health in HD. 

City Under the Microscope: How Two Proteins Could Help Track Huntington’s Disease

Scientists are on the hunt for better ways to measure HD progression, even before symptoms show. In recent work, two proteins, CAP1 and CAPZB, identified using a blood test, have become lead candidates . In a study from Cyprus, researchers scanned the entire blood protein landscape and discovered that CAP1 levels dip in people in the very earliest stage of HD, while CAPZB levels rise consistently throughout the disease.

This month’s Huntington’s disease (HD) research roundup spans work from the dinner table to DNA repair. Together, these discoveries highlight both the complexity of HD and the many creative ways researchers are working to tackle it.

This is important research because we need more biomarkers that track with HD progression. Right now, neurofilament light (NfL), the leading HD biomarker, only tells part of the story. But having others like CAP1 and CAPZB joining the team would give researchers more ways to track disease progress and test treatments earlier and more accurately. If future studies in larger, more diverse groups confirm these findings, one day a simple blood test could reveal whether a new treatment is slowing HD before noticeable symptoms take hold, an exciting possibility for an early intervention.

Cracking the Protein Puzzle in HD: New Blueprints Offer Hope for Stopping Damage Early

Researchers have advanced what we know by mapping the structure of the huntingtin protein fragments, piece by piece, using ultra-precise imaging. Sticky protein clumps, called exon 1 fibrils, are the misfolded proteins that accumulate in HD and participate in the havoc that is wreaked in brain cells. Scientists discovered that these toxic clumps have a tight, dense core wrapped in a loose, fuzzy coat. With this new work, we can see exactly how each part fits together.

In a clever follow-up, researchers added a tiny amount of curcumin, the active ingredient in turmeric, to the mix in lab dishes. This gentle tweak seemed to reshape the protein clumps into forms that were slower to assemble, less sticky, and less harmful to neurons. The studies offer a new kind of blueprint as a way not just to clean up damage after it happens, but potentially to build safer versions from the start. 

But don’t start downing massive amounts of curcumin or turmeric with the hopes of altering the expanded huntingtin structure. These findings are early-stage and in a lab setting only and more work is needed to better understand the effects in people. However, they give scientists an exciting map to start designing treatments that target the blueprint of the huntingtin protein.

When DNA Repair Goes Off-Script: How a Small Change in FAN1 Can Accelerate Huntington’s Disease

Deep inside our cells, proteins work like stagehands keeping DNA maintenance running smoothly. But researchers have spotlighted a tiny change, called the R507H mutation, in one of the DNA repair proteins, FAN1, that causes it to trip up its performance. This small slip weakens FAN1’s grip on PCNA, a partner protein that helps it stay on track during DNA repair, ultimately letting harmful DNA loops accumulate in the huntingtin gene, seemingly speeding up disease onset.

This work is important because it helps explain why two people with identical CAG repeat numbers within their huntingtin gene might start showing symptoms at very different times. Understanding the R507H change in FAN1 gives researchers a new target. If they can restore FAN1’s grip or stabilize its teamwork with PCNA, they may be able to slow the progression of HD. This opens up a fresh strategy in the hunt for therapies by targeting genes that modify the onset of HD.