Hutchinson-Gilford Progeria Treatment Market Revenue Growth Predicted by 2026

Hutchinson-Gilford Progeria Treatment Market
Expansion to be Persistent During 2018 – 2026
Hutchinson-Gilford Progeria Treatment Market - Global Industry Insights,
Trends, Outlook, and Opportunity Analysis, 2018-2026
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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Hutchinson-Gilford progeria is a rare condition that affects about one in four million newborns
worldwide according to the National Institutes of Health (NIH). Until now more than 130 cases have
been reported as per the NIH statistics. The affected patients live up to 30 years maximum, with an
average life span of 13 years. Nearly 90% of the patients die from complications related to
atherosclerosis. Till 2012 there wasn’t any effective treatment therapy discovered for HutchinsonGilford progeria syndrome. The treatments available focused mostly on reducing cardiovascular
symptoms and growth abnormalities.
Farnesyltransferase Inhibitor (FTI)
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 child’s 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.
Researchers are working to determine how genetic changes further leading to the characteristic features
of Hutchinson-Gilford progeria syndrome. Continuous advancement in research with increased
understanding of the human aging will provide valuable insights and aid in the treatment of this
disease. Click To Read More On Hutchinson-Gilford Progeria Treatment Market.
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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.