Authors : Mohammad Shaheen; Tejomurtula Hari Chandana; Guddanti Hema; Gayathri Paturi

Volume/Issue : Volume 9 - 2024, Issue 5 - May

Google Scholar : https://tinyurl.com/32h3k2p5

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DOI : https://doi.org/10.38124/ijisrt/IJISRT24MAY1659

Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.

Abstract : Huntington's disease (HD) is a severe genetic illness caused by a CAG expansion on chromosome 4 in the huntingtin gene. This results in an excessively long polyglutamine tract, which has negative consequences. The normal huntingtin protein serves important tasks, however the mutant version causes a variety of detrimental effects. Disruptions in cellular processes such as autophagy, decreased mitochondrial activity, lysosomal dysfunction, and others are involved in the etiology of HD. Inflammation, oxidative stress, and transcriptional alterations all contribute to neurodegeneration. Despite great progress in understanding the genetic basis of HD, there is currently no cure. The current approach to management focuses on symptomatic control, but as our understanding of genetics advances, targeted medicines might become available. Although HD is still a difficult condition to treat, there is optimism for future advancements in research. Clinical techniques mostly focus on symptom management, with genetic testing assisting in diagnosis. Promising research looks on potential disease-modifying therapies, such as ways to reduce mutant huntingtin levels and improve clearance. Ongoing clinical research provide promise for future treatments, bringing hope to HD patients and their families.

Keywords : Huntington’s Illness, Diagnosis, Treatment, Inflammation.

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