Adrenoleukodystrophy Market Set to Surge Significantly by 2025

Adrenoleukodystrophy Market to Witness an Outstanding Growth by 2025
Adrenoleukodystrophy is also known as Adrenomyeloneuropathy or Schilder-Addison Complex, it
is a hereditary condition that damages the myelin sheath (membrane surrounding nerve cells in your
brain) and disrupts the breakdown process of long-chain fatty acids (VLCFA).
Adrenoleukodystrophy is passed down from parents to their children in a form of X-linked genetic
trait. The genetic trait causes deposition of very-long chain fatty acids in the body tissues due to
impaired beta oxidation. Myelin sheath in central nervous system, the adrenal cortex and Ledydig
cells in the testes are the most severely affected tissues. Adrenoleukodystrophy give rise to three
major disease categories such as childhood cerebral form (observed between 4 to 8 years of age),
adrenomyelopathy and impaired adrenal gland function (also known as Addison disease).
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The major symptoms observed in a childhood cerebral form adrenoleukodystrophy patient are
muscle spasms, crossed eyes (strabismus), hearing loss, seizures and other disorders related with the
nervous system. In adrenomyelopathy the patients are observed with difficulty in controlling
urination, muscle weakness or leg stiffness, difficulties in thinking speed and lack of visual
memory. In Addison disease or adrenal gland failure the major symptoms observed are coma,
decreased apetite, skin pigmentation, loss of weight, muscle weakness and vomiting. According to
Centers for Disease Control and Prevention (CDC), approximately 1 in 20,000 people suffer from
X-linked adrenoleukodystrophy. The Office of Rare Diseases (ORD) of the National Institutes of
Health (NIH) has listed Adrenoleukodystrophy as a "rare disease". In addition to this, CDC also
reported that adrenoleukodystrophy, is a subtype of adrenoleukodystrophy, affects less than 200,000
people in the U.S. population annually.
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The adrenoleukodystrophy is diagnosed primarily with plasma very long chain fatty acid (VLCFA)
examination by application of gas chromatography and/or mass spectrometery. The other
diagnostics methods include chromosome studies that are carried out to understand the mutation in
ABCD 1 gene and magnetic resonance imaging (MRI) scan of head. Adrenoleukodystrophy is
treated with dietary therapy, transplant, adrenal insufficiency and gene therapy. The dietary therapy
consists of prohibiting the patient for the intake of very-long chain fatty acids (VLCFA) and this is a
supportive therapy to normalize the disease conditions of the patient.
The transplants are performed with allogeneic hematopoietic stem cells that assist in the
demyelination process where myelin sheath is restored and its deterioration is inhibited. In gene
therapy appropriate vectors are selected and modified according to the normal ABCD 1 and later
these are transplanted into patient’s bone marrow or stem cell transplant. Adrenal insufficiency is
the treatment still under research and trials as this process is ineffective and needs assistance form
hormonal replacement therapy. In some cases genetic counseling is recommended for prospective
parents with a family history of X-linked adrenoleukodystrophy.

Adrenoleukodystrophy Market Set to Surge Significantly by 2025