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Ancestor membership does not transfer phenotype values between groups.","importantHtml":""},"sections":[{"bodyHtml":"

Genetic changes that cause a disease are called pathogenic variants. Pathogenic variants in the OAT gene can cause gyrate atrophy. The OAT gene provides instructions for making an enzyme called ornithine aminotransferase (OAT). This enzyme helps break down a molecule called ornithine. Ornithine is involved in the urea cycle, which gets rid of the excess nitrogen (in the form of ammonia) that is made when proteins are broken down to provide energy.

In addition to its role in the urea cycle, ornithine helps ensure the proper balance of protein building blocks (amino acids) in the body. This balance is important because a specific sequence of amino acids is required to build each of the many different proteins needed for the body's functions. OAT allows ornithine to be converted into another molecule called pyrroline-5-carboxylate (P5C). P5C can be converted into two amino acids: proline and glutamate. Glutamate serves as an important chemical messenger (neurotransmitter).

The pathogenic variants that are associated with gyrate atrophy reduce the amount of functional OAT protein, which impairs the conversion of ornithine into P5C. As a result, excess ornithine can build up in the blood, in the fluid that surrounds the brain and spinal cord (cerebrospinal fluid), and in the clear fluid in the front of the eye (aqueous humor).

Although it is not clear exactly how these changes result in the specific signs and symptoms of gyrate atrophy, researchers have suggested that a buildup of ornithine may be toxic for cells in the retina. It has also been proposed that excess ornithine may reduce the production of a molecule called creatine. Creatine is needed for many tissues in the body to properly store and use energy. It helps provide energy for muscle contraction and is also important for nervous system functioning, a feature that may explain the peripheral neuropathy and muscle weakness seen in some people with gyrate atrophy.

MedlinePlus Genetics: Causes

","key":"forms","title":"What causes Gyrate atrophy of the choroid and retina?"},{"bodyHtml":"

Most people with gyrate atrophy have no symptoms other than vision loss, but some have additional features of the disorder. Occasionally, newborns with gyrate atrophy develop excess ammonia in the blood (hyperammonemia), which may lead to poor feeding, vomiting, seizures, or coma. Neonatal hyperammonemia associated with gyrate atrophy generally responds quickly to treatment and does not recur after the newborn period.

Gyrate atrophy usually does not affect intelligence; however, abnormalities may be observed in brain imaging or other neurological testing. In some cases, mild to moderate intellectual disability is associated with gyrate atrophy.

Gyrate atrophy may also cause disturbances in the nerves connecting the brain and spinal cord to muscles and sensory cells (peripheral nervous system). In some people with the disorder these abnormalities lead to numbness, tingling, or pain in the hands or feet, while in others they are detectable only by electrical testing of the nerve impulses.

In some people with gyrate atrophy, a particular type of muscle fibers (type II fibers) break down over time. While this muscle abnormality usually causes no symptoms, it may result in mild weakness.

Source: MedlinePlus Genetics

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