[PDF] Hutchinson-Gilford Progeria Treatment Market to Witness Robust Expansion Throughout by 2027 UNLV The Rebel Yell – UNLV The Rebel Yell

Hutchinson-Gilford progeria syndrome is a genetic condition characterized by the dramatic, rapid, appearance of aging from the childhood. Hutchinson-Gilford progeria syndrome is caused by a mutation in the lamin A (LMNA) gene. The affected children develop a characteristic facial experience including prominent eyes, small chin, protruding ears, thin lips and a thin nose with a beaked tip. This syndrome also causes hair loss (alopecia), joint abnormalities, aged-looking skin, and a loss of fat under the skin (subcutaneous fat). Moreover, patients of Hutchinson-Gilford progeria syndrome experiences severe hardening of the arteries (arteriosclerosis) from the childhood. The condition worsens with age and increases the risk of heart attack or stroke even at a young age.

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The prominent players in the Hutchinson-Gilford Progeria Treatment Market are Technology & Research (A*STAR)

In 2012, findings of the first clinical trial of the drug Lonafarnib, a farnesyltransferase inhibitor (FTI), gave a new hope for the treatment of children with Hutchinson-Gilford progeria syndrome. Clinical trial results demonstrated improvement in weight gain, increase in bone mineral density, reduced vascular stiffness, and improved sensorineural hearing in patients with progeria. Previous treatments with growth hormone, and Sulforaphane helped in reducing the symptoms, and prolong a childs life. However, it is essential that the patient regularly visits the cardiologist. Rapamycin is one other drug used before, that demonstrated to reverse nuclear blebbing, retard cellular senescence, and facilitate degradation of progerin.

Recently in 2015, the scientists at the Agency for Science, Technology & Research (A*STAR) successfully established a model of Hutchinson-Gilford progeria syndrome. The study conducted by this organization proposed a model which implies that progerin is linked to telomeres. Progerin induces a reduction in heterochromatin, a tightly packed form of DNA, making telomeres in the cell more fragile and susceptible to damage. The damaged telomeres in turn trigger premature cellular aging. This model is radically different from the one believed earlier the gene progerin caused the nucleus to be deformed, thereby weakening the ability of cells to divide and proliferate. The altered progerin protein makes the nuclear envelope unstable and progressively damages the nucleus, making cells more likely to die prematurely.

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Important Features that are under Offering and Key Highlights of Hutchinson-Gilford Progeria Treatment Market Report:

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[PDF] Hutchinson-Gilford Progeria Treatment Market to Witness Robust Expansion Throughout by 2027 UNLV The Rebel Yell - UNLV The Rebel Yell