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The etiology of HD is primarily attributed to the huntingtin protein (HTT) gene contains an abnormal number of CAG repeats, leading to the amplification of trinucleotide repeat sequences (TNR), specifically the CAG codon, resulting in the synthesis of an abnormal protein with an expanded polyglutamine (polyQ) tract (210, 211)

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Thus, HSPA12B appears to act through both eNOS activation and TLR4 modulation, likely contributing to the mitigation of tissue damage