The study published in Cell demonstrates that DNA-repair proteins could serve as promising targets for therapeutics against Huntington's disease, potentially delaying onset or progression.
Researchers discovered that the neurons targeted by Huntington's disease accumulate a significant number of CAG repeats over time, especially the striatal projection neurons.
Understanding why Huntington's symptoms appear late in life has revealed that a faulty DNA-repair mechanism in neurons delays critical cellular damage until adulthood.
Frontline neuroscience efforts show that an inherited mutation must cross a threshold of neuronal damage before symptoms manifest, highlighting the disease's complex biological timeline.
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