Abstract
Huntington’s disease (HD) is an irreversible neurodegenerative disorder that is inherited in an autosomal dominant manner. In HD, many regions of the human brain are affected, including the striatum, thalamus, and cortex. The mechanism is by the expansion of CAG repeats, which encode glutamine (Q) in the Huntingtin gene on chromosome 4p16.3. Patients with more CAG repeats tend to have a younger age of onset and a higher risk. Mutant HTT protein, translated from mtHtt, would congregate or interact with other proteins, causing damage to the human body. Patients with HD show symptoms like chorea, which is an involuntary motor disability, cognitive deterioration, and psychiatric disturbances. Except for the genetic pathology of HD, the epigenetic mechanism of this disease has made a lot of progress in recent years. This paper primarily focuses on the alternation of deoxyribonucleic acid (DNA) methylation, histone modification, and non-coding ribonucleic acids (ncRNAs) in HD as well as the advancements of epigenetic therapy and healthcare in HD.
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