Abstract
Cellular mechanisms associated with neurodegenerative diseases, such as oxidative stress, mitochondrial impairment, protein aggregation, and inflammation, have all been implicated in Huntington's disease.1,2 However, in contrast to many other neurodegenerative diseases, the underlying cause of Huntington's disease—a mutation of the HTT gene—is known. This knowledge enables the investigation of mutation-induced changes over decades, even before the symptomatic manifestation of the disease. Thus, biomarkers and potential treatments can be evaluated in the premanifest stage of the disease, which offers a potentially large advantage for the development of new therapies and biomarkers for Huntington's disease compared with neurodegenerative diseases that are not inherited, such as most cases of Alzheimer's disease or Parkinson's disease.
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