Huntington's disease (HD) is a rare neurodegenerative disease characterized by motor, cognitive, and psychiatric symptoms. The earliest known description of the disease was in 1841 by American physician Charles Oscar Waters. The condition was described in further detail in 1872 by American physician George Huntington. In 1993, the Huntington's gene (Huntingtin, HTT), on chromosome 4p was identified. This disease is caused by an expanded CAG repeat in the HTT gene that encodes an expanded polyglutamine (polyQ) repeat in exon-1 of the human mutant huntingtin (mHTT) protein. The presence of this polyQ repeat results in neuronal degeneration, for which there is no cure or treatment that modifies disease progression. HD is dominantly inherited with a completely penetrant neurological condition. The frequency is 10-100 times higher in the population descended from Europe than in East Asia. Through various processes, including impairment of proteostasis, transcription, and cell function, as well as direct toxicity of the mutant protein, mutated huntingtin triggers neuronal malfunction and loss at the cellular level.
　　The characteristic pathologic change in HD is diffuse, marked atrophy of the neostriatum that may be worse in the caudate than in the putamen.
　　Since there are presently few medications that can change the course of the disease, palliative therapy, and symptom control are the cornerstone of treatment. Studying the cellular pathology and gross structural changes to the brain which occur as the illness advances have made enormous progress in recent years. There's been a substantial increase in medical studies and possible treatment options over the past ten years. The new treatments that aim to reduce amounts of mutant huntingtin are the most optimistic. However, one strategy is antisense oligonucleotide treatment, for which clinical trials are currently being conducted. These control trials might help us get another inch ahead of managing and perhaps even eliminating this disastrous disease.