The study by Handsaker et al. (2025) provides new insights into how Huntington's disease progresses at the cellular level. The researchers focused on the CAG repeat—a specific sequence of DNA building blocks—that, when abnormally repeated many times, causes the disease. They discovered that the expansion of this repeat within individual cells is a driving force behind the neurodegeneration seen in Huntington's disease. This finding was made possible by measuring the length of the CAG repeat in single cells, which revealed that the extent of expansion is linked to the severity of the disease's effects on neurons.
The implications of this research are significant for developing treatments. By understanding that the somatic expansion of the CAG repeat is a key factor in disease progression, therapies can be tailored to target this process. This approach could potentially be applied not only to Huntington's disease but also to other disorders caused by similar DNA-repeat expansions. Handsaker et al.'s work thus opens new avenues for therapeutic strategies that could slow or halt the progression of these debilitating diseases.
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