Detailed analysis of Hutchinson-Gilford Progeria Treatment market, growth factors, major key companies, trends, developments and forecast by 2027
Hutchinson-Gilford progeria syndrome is a genetic disorder characterized by the rapid and dramatic onset of aging in children. This condition is caused by a mutation in the lamin A gene (LMNA). Affected children develop a characteristic facial appearance, including prominent eyes, a small chin, protruding ears, thin lips, and a thin nose with a beak tip. In addition, this syndrome leads to hair loss (alopecia), joint abnormalities, aged-looking skin, and loss of subcutaneous fat (subcutaneous fat). People with Hutchinson-Gilford progeria syndrome are known to experience severe hardening of the arteries (arteriosclerosis) from early childhood. The disease worsens with age and thus increases the risk of heart attack or stroke at a young age.
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Hutchinson-Gilford progeria is a rare disease known to affect at least one in four million newborns worldwide, according to a National Institutes of Health (NIH) survey. So far, around 130 cases have been reported according to NIH statistics. Affected patients live up to a maximum of 30 years, with an average lifespan of 13 years. Almost 90% of patients die from complications related to atherosclerosis. Until 2012, no effective treatment option was discovered for this syndrome. However, the available treatment options focused primarily on reducing cardiovascular symptoms and growth abnormalities.
Farnesyltransferase inhibitor (FTI)
In 2012, the results of the first clinical trial of the drug Lonafarnib, a farnesyltransferase inhibitor (FTI), offered new hope for the treatment of children with Hutchinson-Gilford progeria syndrome. Results from clinical trials have demonstrated massive improvement in weight gain, increased bone mineral density, reduced vascular stiffness, and improved sensorineural hearing in patients with progeria. Previous treatments with growth hormone and sulforaphane have helped reduce symptoms and prolong a child’s life. However, it is essential that the patient see the cardiologist regularly. Rapamycin is another drug used in the past that has been shown to be effective in reversing nuclear bubble formation, delaying cell senescence, and facilitating the breakdown of progerin.
In 2015, a team of scientists from the Agency for Science, Technology and Research (A * STAR) successfully established a model of Hutchinson-Gilford syndrome progeria market. The study conducted by this organization proposed a model implying that progerin is bound to telomeres. Progerin induces a reduction in heterochromatin, a very compact form of DNA, making the cell’s telomeres more fragile and susceptible to damage. Damaged telomeres in turn trigger premature cellular aging. This model was radically different from the previous one. The progerin gene causes the nucleus to deform, weakening the ability of cells to divide and proliferate. The altered progerin protein makes the nuclear envelope unstable and gradually damages the nucleus, making cells more likely to die prematurely.
Researchers are currently working to determine how genetic changes further lead to important features of Hutchinson-Gilford progeria syndrome. Continued advances in research, as well as a better understanding of human aging, should provide valuable information about the disease and therefore greatly aid in its treatment.
The research and development activities carried out by the main institutes, in order to find new therapies for age-related conditions, are expected to offer lucrative opportunities to players in the global market. For example, in August 2019, researchers at the Houston Methodist Research Institute at Texas Medical Center focused on using RNA-based therapies – a treatment focused on ribonucleic acids, a substance found in all living cells – to slow down and eventually reverse Hutchinson-Gilford Progeria. Likewise, in July 2019, a group of researchers from the University of Oviedo, Spain, established that fecal microbiota transplants can help prematurely old mice live longer. Research may help design targeted probiotic treatments for age-related conditions, such as Hutchinson-Gilford Progeria in humans. Additionally, in March 2019, researchers from the Centro Nacional de Investigaciones Cardiovasculares (CNIC) and the Universidad de Oviedo identified a new molecular mechanism involved in the premature development of atherosclerosis in mice with Hutchinson-Gilford syndrome. progeria. The newly identified therapeutic target could be used to block early atherosclerosis in progeria.
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Global Hutchinson-Gilford Progeria Treatment Market Research Report
Section 1: Global Hutchinson-Gilford Progeria Treatment Industry Overview
Section 2: Global Economic Impact on the Hutchinson-Gilford Progeria Processing Industry
Section 3: Competition in the world market by industry producers
Section 4: World productions, income (value), by region
Article 5: Global supply (production), consumption, export, import, geographically
Article 6: World productions, income (value), price trend, product type
Article 7: Global market analysis, based on the application
Article 8: Hutchinson-Gilford Progeria Treatment Market Price Analysis
Article 9: Market chain, sourcing strategy and downstream buyers
Article 10: Key strategies and policies of distributors / suppliers / traders
Article 11: Analysis of the key marketing strategy, by market suppliers
Article 12: Analysis of market effect factors
Article 13: Global Hutchinson-Gilford Progeria Treatment Market Forecast
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