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Disease List:

3 6 A B C D E F G H I J K L M N O P R S T U V W Z

Pituitary Hormone Deficiency, Combined 3

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What is Pituitary Hormone Deficiency, Combined 3?

Pituitary Hormone Deficiency, Combined 3 (CPHD3) is an autosomal recessive disorder that causes growth problems, short stature, spine and neck stiffness, sensorineural hearing loss, and other health problems due to lack of pituitary hormones in the body.  Pituitary hormones are made in the brain by the pituitary gland.  Affected infants have low blood sugar (hypoglycemia), seizures, underactive thyroid, and growth delays.  If the condition is not treated, it causes short stature and may cause delayed or absent puberty and infertility (inability to have biological children), and intellectual disability.  Treatment includes lifelong pituitary hormone replacement therapy.

What causes Pituitary Hormone Deficiency Combined-3?

Pituitary Hormone Deficiency Combined-3 (CPHD3) is caused by a change, or mutation, in both copies of the LHX3 gene pair.  These mutations cause the genes to not work properly or not work at all. When both copies of this gene do not work correctly, the body cannot make the needed pituitary hormones, leading to the symptoms described above.

Polycystic Kidney Disease, Autosomal Recessive

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What is Polycystic Kidney Disease, Autosomal Recessive?

Polycystic Kidney Disease, Autosomal Recessive (ARPKD) is an autosomal recessive disorder that affects the kidneys and other organs, including the liver.  Affected children are typically born with enlarged kidneys with multiple fluid-filled sacs called cysts.  The kidneys do not work properly causing serious health problems.  The fetal kidney problems begin in pregnancy and often affect fetal lung development.  Lung development is affected by low fluid levels in the pregnancy (oligohydramnios) resulting from the kidney disease. Children born with Polycystic Kidney Disease, Autosomal Recessive often have very serious lung disease that may lead to death.  Liver disease (congenital hepatic fibrosis) happens in about 45% of infants and children with Polycystic Kidney Disease, Autosomal Recessive.  The disorder often leads to death in early infancy; however, some children have less severe symptoms and can survive with medical treatments.  In very rare cases, symptoms do not start until adolescence or early adulthood.

What causes Polycystic Kidney Disease, Autosomal Recessive?

Polycystic Kidney Disease, Autosomal Recessive is caused by a gene change, or mutation, in both copies of the PKHD1 gene pair.  These mutations cause the genes to not work properly or not work at all.  When both copies of this gene do not work correctly, the kidneys do not develop properly and liver disease may also occur, leading to the symptoms described above.

Pontocerebellar Hypoplasia, RARS2-Related

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What is Pontocerebellar Hypoplasia, RARS2-Related?

Pontocerebellar Hypoplasia, RARS2-Related is an autosomal recessive disorder that causes abnormal brain development. The two parts of the brain that are underdeveloped in children with this condition are called the pons and the cerebellum. These parts of the brain help send signals through the brain and also coordinate movement of the body.  The underdeveloped pons and cerebellum cause a child to have a smaller head size (microcephaly), intellectual disability, decreased muscle tone, and vision loss.  This condition usually results in death in infancy or early childhood.  However there have been a few people with Pontocerebellar Hypoplasia, RARS2-Related who have lived into adulthood.

What causes Pontocerebellar Hypoplasia, RARS2-Related?

Pontocerebellar Hypoplasia, RARS2-Related is caused by a gene change, or mutation, in both copies of the RARS2 gene pair. These mutations cause the genes to not work properly or not work at all. Normal function of the RARS2 genes is important for development of the brain. When both copies of the RARS2 gene do not work correctly, it leads to the symptoms described above. 

Pontocerebellar Hypoplasia, Type 1A

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What is Pontocerebellar Hypoplasia, Type 1A?

Pontocerebellar Hypoplasia, Type 1A is an autosomal recessive disorder that causes abnormalities in the parts of the brain called the pons and cerebellum, leading to problems with muscle movement.  Signs and symptoms are usually present at birth and include a small head size, severe muscle weakness (hypotonia), feeding and breathing problems, joint problems called contractures, intellectual disability, and vision problems.  Lifespan is shortened and death often occurs in infancy or early childhood. There is no cure or specific treatment for this disorder.

Very rarely, specific mutations in the same genes cause a related condition called Hereditary Motor and Sensory Neuropathy, VRK1-Related.  Hereditary Motor and Sensory Neuropathy, VRK1-Related affects the peripheral and sensory nerves leading to weak muscle tone and reduced sense of touch, pain, and temperature.  Children with Hereditary Motor and Sensory Neuropathy, VRK1-Related also have delayed development and a small head size.  Intelligence is normal. 

What causes Pontocerebellar Hypoplasia, Type 1A?

Pontocerebellar Hypoplasia, Type 1A is caused by a gene change, or mutation, in both copies of the VRK1 gene pair.  These mutations cause the genes to not work properly or not work at all. Normal function of the VRK1 genes is important for the development of the brain. When both copies of the VRK1 gene pair do not work correctly, it leads to the symptoms described above. It is sometimes, but not always, possible to determine whether a specific mutation in the VRK1 gene will cause Pontocerebellar Hypoplasia, Type 1A or Hereditary Motor and Sensory Neuropathy, VRK1-Related. 

Pontocerebellar Hypoplasia, Type 2D

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What is Pontocerebellar Hypoplasia, Type 2D?

Pontocerebellar Hypoplasia, Type 2D (also called Progressive Cerebellocerebral Atrophy) is an autosomal recessive disorder that affects brain development. The two parts of the brain that are underdeveloped in this condition are the pons and the cerebellum. These parts of the brain help send signals through the brain and also coordinate movement of the body. Signs and symptoms of this disorder begin in infancy and include small head size (microcephaly), severe intellectual disability, delayed develop, poor muscle tone with stiff muscles, seizures, vision impairment, and abnormal movement. Death may occur in childhood; however survival into adulthood is possible. Currently there is no cure or specific treatment for this disorder.

What causes Pontocerebellar Hypoplasia, Type 2D?

Pontocerebellar Hypoplasia, Type 2D is caused by a gene change, or mutation, in both copies of the SEPSECS gene pair. These mutations cause the genes to not work properly or not work at all. Normal function of the SEPSECS gene pair is important for the development of the brain. When both copies of the SEPSECS gene do not work correctly, it leads to the symptoms described above. 

Primary Ciliary Dyskinesia, DNAH5-Related

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What is Primary Ciliary Dyskinesia, DNAH5-Related?

Primary Ciliary Dyskinesia, DNAH5-Related is an autosomal recessive disorder that causes recurrent, chronic respiratory tract infections, abnormal placement of the organs, and infertility.  Some affected newborns require oxygen following delivery due to respiratory distress.  However, the progression and severity of lung disease throughout life varies.  Chronic or recurrent ear infections may occur in infancy or young childhood and can result in hearing loss.  People with this condition may have abnormal organ placement, called ‘situs inversus totalis’ (mirror-image reversal of the organs in the chest and abdomen; for example, the heart is on the right instead of the left).  Affected males have infertility. 

What causes Primary Ciliary Dyskinesia, DNAH5-Related?

Primary Ciliary Dyskinesia, DNAH5-Related is caused by a gene change, or mutation, in both copies of the DNAH5 gene pair. These mutations cause the genes to not work properly or not work at all. Normal function of the DNAH5 genes is important in helping to make cilia (the hair-like structures on cells). Coordinated movement of cilia is necessary for many parts of the body to develop and work properly. When both copies of the DNAH5 gene do not work correctly, it leads to the symptoms described above. 

Primary Ciliary Dyskinesia, DNAI1-Related

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What is Primary Ciliary Dyskinesia, DNAI1-Related?

Primary Ciliary Dyskinesia, DNAI1-Related is an autosomal recessive disorder that causes recurrent, chronic respiratory tract infections, abnormal placement of the organs, and infertility.  Some affected newborns may require oxygen following delivery due to respiratory distress. However, the progression and severity of lung disease throughout life varies.  Chronic or recurrent ear infections may occur in infancy or young childhood and can result in hearing loss.  People with this condition may have abnormal organ placement, called ‘situs inversus totalis’ (mirror-image reversal of the organs in the chest and abdomen; for example, the heart is on the right instead of the left).  Affected males have infertility. 

What causes Primary Ciliary Dyskinesia, DNAI1-Related?

Primary Ciliary Dyskinesia, DNAI1-Related is caused by a gene change, or mutation, in both copies of the DNAI1 gene pair. These mutations cause the genes to not work properly or not work at all. Normal function of the DNAI1 gene pair is important in helping to make cilia (the hair-like structures on cells). Coordinated movement of cilia is necessary for many parts of the body to develop and work properly. When both copies of the DNAI1 gene do not work correctly, it leads to the symptoms described above. 

Primary Ciliary Dyskinesia, DNAI2-Related

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What is Primary Ciliary Dyskinesia, DNAI2-Related?

Primary Ciliary Dyskinesia, DNAI2-Related is an autosomal recessive disorder that causes recurrent, chronic respiratory tract infections, abnormal placement of the organs, and infertility.  Some affected newborns require oxygen following delivery due to respiratory distress. However, the progression and severity of lung disease throughout life varies.  Recurrent ear infections may occur in infancy or young childhood and can result in hearing loss. People with this condition may have abnormal organ placement, called ‘situs inversus totalis’ (mirror-image reversal of the organs in the chest and abdomen; for example, the heart is on the right instead of the left).  Affected males have infertility. 

What causes Primary Ciliary Dyskinesia, DNAI2-Related?

Primary Ciliary Dyskinesia, DNAI2-Related is caused by a gene change, or mutation, in both copies of the DNAI2 gene pair. These mutations cause the genes to not work properly or not work at all. Normal function of the DNAI2 gene pair is important in helping to making cilia (the hair-like structures on cells). Coordinated movement of cilia is necessary for many parts of the body to develop and work properly. When both copies of the DNAI2 gene do not work correctly, it leads to the symptoms described above. 

Primary Hyperoxaluria, Type 1

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What is Primary Hyperoxaluria, Type 1?

Primary Hyperoxaluria, Type 1 is a rare autosomal recessive disorder that causes the buildup of a substance called calcium oxalate, the main substance found in kidney stones.  Too much calcium oxalate in the body can cause kidney stones and may also damage other organs.  Most people with Primary Hyperoxaluria, Type 1 develop recurrent kidney stones beginning in late childhood but some have a more severe form of this condition that starts by 6 months of age and some do not show symptoms until early adulthood. Kidney damage worsens over time and can lead to kidney failure.  By early adulthood, about half of people with Primary Hyperoxaluria, Type 1 have kidney failure, which is treated with dialysis and then kidney transplantation. Treatment to prevent or reduce the formation of kidney stones includes a special medical diet, supplements, and other oral medications.

What causes Primary Hyperoxaluria, Type 1?

Primary Hyperoxaluria, Type 1 is caused by a gene change, or mutation, in both copies of the AGXT gene pair. These mutations cause the genes to not work properly or not work at all. When both copies of this gene pair do not work correctly, it leads to the symptoms described above.

Primary Hyperoxaluria, Type 2

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What is Primary Hyperoxaluria, Type 2?

Primary Hyperoxaluria, Type 2 is an autosomal recessive disorder that causes the buildup of a substance called calcium oxalate, the main substance found in kidney stones.  Too much calcium oxalate in the body can cause kidney stones and may also damage other organs.  Most people with Primary Hyperoxaluria, Type 2 develop recurrent kidney stones beginning in childhood; however, the age of onset can vary. Kidney damage worsens over time and can lead to kidney failure, which is treated with dialysis and then kidney transplantation. Treatment to prevent or reduce the formation of kidney stones includes a special medical diet, supplements, and other oral medications.

What causes Primary Hyperoxaluria, Type 2?

Primary Hyperoxaluria, Type 2 is caused by a gene change, or mutation, in both copies of the GRHPR gene pair. These mutations cause the genes to not work properly or not work at all. When both copies of this gene do not work correctly, it leads to the symptoms described above.

Primary Hyperoxaluria, Type 3

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What is Primary Hyperoxaluria, Type 3?

Primary Hyperoxaluria, Type 3 is an autosomal recessive disorder that causes the buildup of a substance called calcium oxalate, the main substance found in kidney stones.  Too much calcium oxalate in the body can lead to kidney stones and sometimes damages other organs.  Some people with Primary Hyperoxaluria, Type 3 develop kidney stones beginning in childhood, some not until adulthood, and some people never show symptoms. Type 3 is less severe than other forms of Primary Hyperoxaluria (Types 1 and 2).  While Primary Hyperoxaluria, Type 3 has not been reported to cause kidney failure, it is a very rare condition and there is little information available about the health of affected adults. Treatment to prevent or reduce the formation of kidney stones includes a special medical diet, supplements, and other oral medications.

What causes Primary Hyperoxaluria, Type 3?

Primary Hyperoxaluria, Type 3 is caused by a gene change, or mutation, in both copies of the HOGA1 gene pair. These mutations cause the genes to not work properly or not work at all. When both copies of this gene do not work correctly, it leads to the symptoms described above.

Progressive Familial Intrahepatic Cholestasis, Type 2

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What is Progressive Familial Intrahepatic Cholestasis, Type 2?

Progressive Familial Intrahepatic Cholestasis, Type 2 is an autosomal recessive disorder that causes liver disease that worsens over time. Symptoms typically begin in infancy and include severe itching, yellowing of skin and whites of eyes (jaundice), failure to gain weight and grow at the normal rate, high blood pressure in the vein that supplies blood to the liver, and enlarged liver and spleen. Liver failure often occurs within the first years of life and is usually treated with liver transplantation. People with Progressive Familial Intrahepatic Cholestasis, Type 2 are also at increased risk for liver cancer.  Some people have a milder form of this condition which is sometimes called Benign Recurrent Intrahepatic Cholestasis, Type 2.  Benign Recurrent Intrahepatic Cholestasis, Type 2 causes episodes of severe itching and jaundice but liver failure is less common.  It is sometimes, but not always, possible to determine whether a specific gene change, or mutation, will cause Progressive Familial Intrahepatic Cholestasis, Type 2 or Benign Recurrent Intrahepatic Cholestasis, Type 2.

What causes Progressive Familial Intrahepatic Cholestasis, Type 2?

Progressive Familial Intrahepatic Cholestasis, Type 2 is caused by mutations in both copies of the ABCB11 gene pair.  These mutations cause the genes to not work properly or not work at all. When both copies of the ABCB11 gene do not work correctly, bile salts cannot be released by liver cells and they build up in the liver, leading to the symptoms described above.

Propionic Acidemia, PCCA-Related

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What is Propionic Acidemia, PCCA-Related?

Propionic Acidemia, PCCA-Related (also called Propionic Acidemia, alpha subunit or Propionic Acidemia, Type 1) is an autosomal recessive condition that is one of a group of inherited disorders known as Organic Acid Disorders (OAs). People with Propionic Acidemia cannot break down certain components of proteins (amino acids) and fats. This causes organic acids to build up to toxic levels in the blood and body tissues. Symptoms usually appear soon after birth with hypotonia, feeding difficulties, vomiting, and lethargy. If untreated, children with this condition may develop metabolic acidosis leading to seizures, coma, and sometimes death. Long-term effects of Propionic Acidemia, alpha subunit may include developmental delays, learning disabilities or intellectual disability, involuntary movements, rigid muscle tone (spasticity), and heart problems. In rare cases, the symptoms may start later in life and be less severe. The condition can be managed with a medical diet and supplemental therapies; however, even with careful treatment, some children still have episodes of illness and may have life-long intellectual disability and seizures.

What causes Propionic Acidemia, PCCA-Related?

Propionic Acidemia, PCCA-Related is caused by a gene change, or mutation, in both copies of the PCCA gene pair. These mutations cause the genes to not work properly or not work at all. When both copies of this gene do not work correctly, it leads to the symptoms described above. 

Propionic Acidemia, PCCB-Related

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What is Propionic Acidemia, PCCB-Related?

Propionic Acidemia, PCCB-Related (also called Propionic Acidemia, beta subunit or Propionic Acidemia, Type 2) is an autosomal recessive condition that is one of a group of inherited disorders known as Organic Acid Disorders (OAs). People with Propionic Acidemia cannot break down certain building blocks of protein (amino acids) and certain fats. When food with protein is eaten, harmful substances build up in the blood and cause damage to the brain along with other serious health problems. Symptoms usually start shortly after birth and may include low muscle tone (hypotonia), poor feeding, vomiting, low energy (lethargy), dehydration, poor growth, breathing problems, low blood sugar (hypoglycemia), and seizures. Without treatment, coma or death may occur. Episodes of the above symptoms are often triggered by eating large amounts of protein, during illness, or after going a long time without food (fasting).

Long-term effects of these episodes may include developmental delays, learning disabilities or intellectual disability, involuntary movements, rigid muscle tone (spasticity), and heart problems. In rare cases, the symptoms may start later in infancy and may be less severe. Treatment includes a medical low-protein diet and formula, specific supplements and medications, and avoidance of fasting. If this condition is treated before symptoms start, children with Propionic Acidemia, PCCB-Related may have normal growth and development. However, even with careful treatment, some children have life-long learning problems or intellectual disability, seizures, and involuntary movements.

What causes Propionic Acidemia, PCCB-Related?

Propionic Acidemia, PCCB-Related is caused by a gene change, or mutation, in both copies of the PCCB gene pair. These mutations cause the genes to not work properly or not work at all. When both copies of this gene do not work correctly, it leads to the symptoms described above. 

Pycnodysostosis

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What is Pycnodysostosis?

Pycnodysostosis is an autosomal recessive disorder that affects the bones.  Signs and symptoms begin at birth and include short stature, fragile bones, repeated bone fractures, abnormal fingernails, curved spine, absent or abnormal collarbone, distinctive facial features, abnormal teeth, and abnormally developed skull and jawbone.  Adults are typically less than five feet tall.  Currently, there is no cure or specific treatment for this disorder; however, growth hormone replacement may help increase height.

What causes Pycnodysostosis?

Pycnodysostosis is caused by a gene change, or mutation, in both copies of the CTSK gene pair. These mutations cause the genes to not work properly or not work at all. Normal function of the CTSK genes is important for bone health. When both copies of the CTSK genes do not work correctly, it leads to the symptoms described above. 

Pyruvate Dehydrogenase Deficiency, PDHB-Related

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What is Pyruvate Dehydrogenase Deficiency, PDHB-Related?

Pyruvate Dehydrogenase Deficiency, PDHB-Related is a rare autosomal recessive disorder that causes lactic acid to build up in the body. Too much lactic acid in the blood is toxic and lead to problems with movement and brain function as well as episodes of nausea, vomiting, breathing problems, and abnormal heartbeat. Signs and symptoms usually begin sometime between birth and early childhood, vary from person to person, and range from mild to severe. In addition to the above episodes, symptoms may include poor coordination and unsteadiness, poor muscle control, and intellectual disability that worsen over time. Some people with this condition also have physical differences including brain abnormalities, facial changes, small hands and feet, and short lower limbs. In the most severe cases, a baby shows symptoms before or shortly after birth and early death occurs. Currently there is no cure for this condition. Treatment may include daily supplements to attempt to lessen the symptoms. Lifespan is usually shortened, although children who have symptoms that start later often live into adulthood.

What causes Pyruvate Dehydrogenase Deficiency, PDHB-Related?

Pyruvate Dehydrogenase Deficiency, PDHB-Related is caused by a gene change, or mutation, in both copies of the PDHB gene pair. These mutations cause the genes to not work properly or not work at all. When both copies of this gene do not work correctly, it leads to the symptoms described above.

Pyruvate Dehydrogenase Deficiency, X-Linked

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What is Pyruvate Dehydrogenase Deficiency, X-Linked?

Pyruvate Dehydrogenase Deficiency, X-Linked is a rare X-linked inherited disorder that causes lactic acid to build up in the body.  This causes problems with movement and brain function. Symptoms vary from person to person and range from mild to severe.  Some people with Pyruvate Dehydrogenase Deficiency, X-Linked have poor coordination and unsteadiness while others have both poor muscle control and intellectual disability that progresses over time.  In the most severe cases of Pyruvate Dehydrogenase Deficiency, X-Linked, a baby shows symptoms before or shortly after birth and early death occurs. Some people with Pyruvate Dehydrogenase Deficiency, X-Linked also have physical differences including facial changes, small hands and feet, and short lower limbs. Males with Pyruvate Dehydrogenase Deficiency, X-Linked are more likely to be severely affected and show symptoms as newborns. Females with this disorder typically have milder symptoms that begin after the newborn period. Currently there is no cure for this disorder but treatment with specific supplements may help reduce symptoms in some individuals.

What causes Pyruvate Dehydrogenase Deficiency, X-Linked?

Pyruvate Dehydrogenase Deficiency, X-Linked is caused by a change, or mutation, in the PDHA1 gene.  This mutation causes the gene to not work correctly or not work at all, causing the symptoms described above.

Renal Tubular Acidosis and Deafness, ATP6V1B1-Related

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What is Renal Tubular Acidosis and Deafness, ATP6V1B1-Related?

Renal Tubular Acidosis and Deafness, ATP6V1B1-Related is an autosomal recessive disorder that causes kidney problems and hearing loss.  In this condition, the kidneys cannot clear the body of certain waste products, leading to a buildup of acidic substances in the blood.  As a result, the blood becomes too acidic causing a condition known as metabolic acidosis.  Symptoms of metabolic acidosis include dehydration, nausea, and vomiting.  Over time this disorder can lead to growth delay, kidney stones, and weakened bones (rickets).  Hearing loss usually occurs sometime in childhood or early adulthood and worsens over time.  Treatment to reduce the amount of acid in the blood can help lessen some of the symptoms but currently there is no cure for this disorder.

What causes Renal Tubular Acidosis and Deafness, ATP6V1B1-Related?

Renal Tubular Acidosis and Deafness, ATP6V1B1-Related is caused by a gene change, or mutation, in both copies of the ATP6V1B1 gene pair. These mutations cause the genes to not work properly or not work at all. The ATP6V1B1 gene is important for the normal function of the kidneys and inner ear. When both copies of the ATP6V1B1 gene do not work correctly, it leads to the symptoms described above. 

Retinitis Pigmentosa 25

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What is Retinitis Pigmentosa 25?

Retinitis Pigmentosa 25 is autosomal recessive.  It is one of a group of inherited eye disorders in which the retina, the area at the back of the eye that allows you to see, gradually stops working.  Retinitis Pigmentosa 25 causes progressive vision loss.  The age at which symptoms begin and the severity of the condition varies from person to person.  The first symptom is usually loss of night vision. Over time, loss of peripheral vision (tunnel vision) develops.  Then, loss of central vision occurs.  RP affects only the vision.  Currently there is no cure or specific treatment to prevent the vision loss. 

What causes Retinitis Pigmentosa 25?

Retinitis Pigmentosa can be caused by mutations in one of a number of different genes with different inheritance patterns.  Retinitis Pigmentosa 25 is caused by a gene change, or mutation, in both copies of the EYS gene pair.  These mutations cause the genes to not work properly or not work at all.  When both copies of this gene do not work correctly, it results in the progressive vision loss described above.

Retinitis Pigmentosa 26

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What is Retinitis Pigmentosa 26?

Retinitis Pigmentosa 26 is autosomal recessive.  It is one of a group of inherited eye disorders in which the retina, the area at the back of the eye that allows you to see, gradually stops working.  Retinitis Pigmentosa 26 causes progressive vision loss.  The age at which symptoms begin and the severity of the condition varies from person to person. The first symptom is usually loss of night vision.  Over time, loss of peripheral vision (tunnel vision) develops. Then, loss of central vision occurs.  Retinitis Pigmentosa 26 affects only the vision. Currently there is no cure or specific treatment to prevent the vision loss. 

What causes Retinitis Pigmentosa 26?

Retinitis Pigmentosa can be caused by mutations in one of a number of different genes with different inheritance patterns. Retinitis Pigmentosa 26 is caused by a gene change, or mutation, in both copies of the CERKL gene pair.  These mutations cause the genes to not work properly or not work at all.  When both copies of this gene do not work correctly, it results in the progressive vision loss described above.

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