A new study uses ultra-sensitive research techniques to map DNA changes across the entire spectrum of CAG repeat lengths, revealing where intermediate repeats fit in the genetic landscape
A new study identifies small molecules that target a DNA repair machine, opening a potential path to delay Huntington’s disease onset.
A new study shows that lowering MSH3, a key DNA repair protein, with antisense oligonucleotide (ASO) therapy can stop CAG repeat expansions in HD patient-derived brain cells. This could be a promising way to slow symptom onset and progression.
In a surprising twist, oral HTT-lowering drugs also slow somatic expansion in the HTT gene. A new study that used cells in a dish for this fortuitous discovery identified the gene PMS1 as a key player in the slowing of CAG expansions.
Scientists have looked at CAG expansions in brains from people with HD to see which cells are affected
The gene MSH3 is getting a lot of attention in HD research lately. New findings suggest MSH3 lowering could halt CAG repeat expansions, offering a new therapeutic avenue.
CAG repeats expand in some parts of the body and brain as people with HD get older, a phenomenon known as somatic instability. Learn more about how researchers are exploring somatic instability and DNA repair to design therapies for HD.
HDBuzz has ramped up to match the accelerating pace of Huntington’s disease research. April 2025 brought us insight on somatic expansion, replacing lost brain cells, and clinical trial updates. Read on for the highlight reel from this month!
From stem-cell “tooth fairy therapy” to gene therapy roadblocks and new genetic insights, November was big for HD research. Catch all of these stories in our monthly summary!