Euroscreen Receives Exclusive GPCR License From Virginia

Euroscreen Receives Exclusive GPCR License From Virginia

(PRWEB) December 20, 2001

BRUSSELS, Belgium.—December 20, 2001--Euroscreen s.a. these days announced an exclusive license agreement with The University of Virginia Patent

Foundation (UVAPF) for psychosine (TDAG8) receptor technologies that was developed at the University of Virginia.

Several lysophospholipids are thought to act as additional-cellular mediators in cell signaling by way of G protein coupled receptors (GPCRs). Earlier this year, researchers at the University of Virginia deorphanized a new G protein-coupled receptor, named TDAG8 (T cell Death Associated Gene protein# 8 GPR 65), which is a receptor for the glycosphingolipid, psychosine. In the lipid storage disorder known as Krabbe's illness psychosine accumulates to inordinately high levels. KrabbeÂ’s illness is a genetic disorder characterized by multinuclear, globoid cells in the white matter of the brain and global de-myelination of central and peripheral neurons. It is plausible for that reason that psychosine activation of TDAG8 in brain microglia might be the molecular basis underlying the patho-physiology of Krabbe's disease, a illness in which there is a lack of the production of galactosylceramidase, the enzyme which catalyzes the cleavage of psychosine to galactose and sphingosine. This invention need to significantly facilitate the discovery and characterization of psychosine receptor agonists and antagonists, which might be of therapeutic value in a variety of diseases which involve this receptor and its natural ligand. Euroscreen has a study team seeking to identify such drug candidates, but is also willing to sublicense to significant investigation partners to assist in this effort.

Euroscreen integrates its world class G protein-coupled receptor (GPCR)

study capabilities with its patented AequoScreen cellular assay

technology to provide new, innovative solutions to GPCR drug discovery. With its corporate partners as well as by means of its own internal development efforts Euroscreen continues to uncover crucial new drug leads and to boost its patent portfolio with the pivotal patent applications for the utility of CCR5 for HIV being an outstanding example. The Organization has corporate partnerships with Solvay, Merck & Co., Syngenta, Galapagos, Sosei and Nanosyn as well as licensing agreements with the Brussels University, the University of Virginia Patent Foundation and the University of Georgia Investigation Foundation. The Business applies its GPCR and ligand technology approaches to deorphanize certain targets and believes that its unique technique increases the chances of successfully creating commercial goods. Far more data about Euroscreen's goods and services can be discovered at http://www.euroscreen.be.

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What is Krabbe Disease?

Write-up by Peter Hutch

Krabbé disease is a rare, inherited degenerative disorder of the central and peripheral nervous systems. It is characterized by the presence of globoid cells (cells that have a lot more than one nucleus), the breakdown of the nerve’s protective myelin coating, and destruction of brain cells. Krabbé disease is 1 of a group of genetic disorders referred to as the leukodystrophies. These disorders impair the growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fibers, and cause severe degeneration of mental and motor abilities.

Krabbe disease is component of a group of disorders recognized as leukodystrophies, which result from the loss of myelin (demyelination). This disorder is also characterized by the abnormal presence of globoid cells, which are globe-shaped cells that usually have a lot more than 1 nucleus.

Krabbe Disease patients show symptoms within the 1st year of life, there have been instances diagnosed at all ages, via late adulthood. In general, the earlier the diagnosis, the more rapid the progression of the illness. Those who initial show symptoms at ages 2-14 will regress and become severely incapacitated, and generally die 2-7 years following diagnosis. Some patients who have been diagnosed in the adolescent and adult years have symptoms that remain confined to weakness without any intellectual deterioration, whilst other people may possibly become bedridden and deteriorate both mentally and physically.

In all individuals with Krabbe disease, galactocerebrosidase (GALC) enzyme activity is deficient in leukocytes isolated from whole heparinized blood or in cultured skin fibroblasts. Carrier testing by measurement of GALC enzyme activity in leukocytes or in cultured skin fibroblasts is unreliable simply because of the wide range of enzymatic activities observed in carriers and non-carriers. Molecular genetic testing of GALC, the only gene known to be associated with Krabbe disease, may be used for carrier detection in at-risk relatives if the illness-causing alleles have been identified in an affected family members member.

In most instances, Krabbe illness develops in babies prior to six months of age, even though it can occur in older children and in adults. Krabbe disease might be very best known in the United States for the media attention it received when former professional football quarterback Jim Kelly raised awareness and research funds for the disorder, which had been diagnosed in his son, Hunter.

Krabbe illness is 1 of a group of genetic conditions called leukodystrophies. Doctors often refer to Krabbe disease as globoid cell leukodystrophy â€" the globoid cells are storage cells that play a role in the disorder. The illness is named right after the Danish neurologist who first reported infants with the condition in 1916.

If the symptoms suggest Krabbe disease, a blood test can be carried out to see if the child or adult has GALC deficiency, which would confirm the diagnosis. A lumbar puncture can be done to sample the cerebrospinal fluid, which in Krabbe disease has abnormally high levels of protein. The test for GALC deficiency can also be done on an unborn child if the parents carry the defective gene (on chromosome 14).

Infants with Krabbe illness are regular at birth. Symptoms begin between the ages of 3 and 6 months with irritability, fevers, limb stiffness, and seizures, feeding difficulties, vomiting, and slowing of mental and motor development. In the first stages of the illness, doctors typically mistake the symptoms for those of cerebral palsy. Other symptoms incorporate muscle weakness, spasticity, deafness, optic atrophy and blindness, paralysis, and difficulty when swallowing. Prolonged weight loss may also occur. There are also juvenile- and adult-onset instances of Krabbe illness, which have similar symptoms but slower progression.

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Krabbe Disease â€" Causes, Symptoms and Treatment

Post by peter hutch

Krabbe illness is inherited in an autosomal recessive manner. If both parents are carriers, each child has a 25% chance of becoming affected, a 50% chance of becoming an asymptomatic carrier, and a 25% chance of being unaffected and not a carrier. Each and every healthy sib of a proband has a 2/3 chance of becoming a carrier. For genetic counseling purposes, a carrier frequency of 1 in 150 might be employed for the general population. Prenatal diagnosis is probable either by measurement of GALC enzyme activity or by molecular genetic testing if both illness-causing alleles in an affected family members member are identified.

Causes

Krabbe disease is caused by mutations in the GALC gene, which causes a deficiency of an enzyme called galactosylceramidase. The buildup of unmetabolized lipids affects the growth of the nerve's protective myelin sheath (the covering that insulates many nerves) and causes severe degeneration of mental and motor skills. As component of a group of disorders recognized as leukodystrophies, Krabbe illness results from the imperfect growth and development of myelin.

Persons with this gene defect do not make enough of a substance called galactocerebroside beta-galactosidase (galactosylceramidase). The body requirements this substance to make myelin, the material that surrounds and protects nerve fibers. Without having it, myelin breaks down, brain cells die, and nerves in the brain and other body areas do not work appropriately.

The trigger of Krabbe disease is a deficiency in an enzyme referred to as galactocerebrosidase (GALC), which is crucial for the maintenance of myelin â€" a fatty substance that insulates your nerve fibers. A child requirements to inherit an abnormal gene from each parent to trigger the disorder. Passing on the genes occurs in an inheritance pattern called autosomal recessive.

A defect in the GALC gene causes Krabbe illness. Persons with this gene defect do not make enough of a substance known as galactocerebroside beta-galactosidase (galactosylceramidase). The body needs this substance to make myelin, the material that surrounds and protects nerve fibers. With out it, myelin breaks down, brain cells die, and nerves in the brain and other body areas do not work properly.

Symptoms

The symptoms of Krabbe illness typically begin just before the age of 1 year (the infantile form). Initial signs and symptoms typically contain irritability, muscle weakness, feeding difficulties, episodes of fever without having any sign of infection, stiff posture, and slowed mental and physical development. As the disease progresses, muscles continue to weaken, affecting the infant's capacity to move, chew, swallow, and breathe. Affected infants also expertise vision loss and seizures.

The cause of Krabbe illness is a deficiency in an enzyme known as galactocerebrosidase (GALC), which is essential for the maintenance of myelin â€" a fatty substance that insulates your nerve fibers.

A child wants to inherit an abnormal gene from each and every parent to trigger the disorder. Passing on the genes occurs in an inheritance pattern referred to as autosomal recessive. Specifically, Krabbe illness has been linked to a defect in chromosome 14.

Treatment

There is no cure for Krabbé illness. Outcomes of a really modest clinical trial of patients with infantile Krabbé illness found that young children who received umbilical cord blood stem cells from unrelated donors prior to symptom onset developed with small neurological impairment. Outcomes also showed that disease progression stabilized quicker in patients who obtain cord blood compared to those who receive adult bone marrow. Bone marrow transplantation has been shown to benefit mild circumstances early in the course of the illness. Usually, treatment for the disorder is symptomatic and supportive.

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Information on Krabbe Disease

Article by Alicia Stock

Krabbe Illness is also identified as Globoid Cell Leukodystrophy. Krabbe illness is 1 of a group of inherited disorders known as the leukodystrophies. Krabbe illness could be very best known in the United States for the media attention. Approximately 2 million people in the United States are carriers of the genetic deficiency that causes Krabbe Illness. It is likely that Krabbe illness affects 1 in 100,000 individuals worldwide, with greater incidences reported in some areas. Krabbe disease is an inherited disorder characterized by a deficiency of the enzyme galactocerebroside beta-galactosidase (galactosylceramidase).

The enzyme galactosylceramide beta-galactosidase (GALC) breaks down a number of important compounds in the body. In Krabbe disease, there isn't adequate GALC accessible, and substances which need to be broken down start to accrue. The build-up of these substances damages the nerve cells in the central nervous program, destroying several of them and preventing the repair of others. Krabbe disease can influence muscle tone and movement, and trigger vision and hearing loss, amongst other effects. In most instances, Krabbe disease develops in babies before six months of age, despite the fact that it can happen in older kids and in adults.

Krabbe disease is affects both sexes similarly. It is also affects people of all ethnic backgrounds. A greater incidence has been reported in a couple of remote communities in Israel. Most patients with Krabbe disease have the infantile form. Couples with an affected child with every pregnancy have a 25% chance of an affected child, a 50% chance of a healthy child who is a carrier, and a 25% chance of a healthy child who is not a carrier. Infants with Krabbe illness are typical at birth. Symptoms start between the ages of three and 6 months with irritability, fevers, limb stiffness, and seizures, feeding difficulties, vomiting, and slowing of mental and motor development.

Other symptoms embrace muscle weakness, spasticity, deafness, optic atrophy and blindness, paralysis, and difficulty when swallowing. Prolonged weight loss may also occur. There are also juvenile and adult-onset circumstances of Krabbe illness, which have like symptoms but slower progression. There is no definite treatment for Krabbe disease. Bone marrow transplantation has been shown to benefit mild circumstances early in the course of the disease. Patients may benefit from physical and occupational therapy. Genetic counseling is suggested for persons with a family members history of Krabbe illness who are contemplating having kids.

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Alicia Stock writes articles for skin care suggestions. She also writes articles for haircut styles and beauty suggestions.

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