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Some develop optic atrophy, which is the degeneration atrophy of the nerves that carry information from the eyes to the brain. Many of the neurological symptoms of triple A syndrome worsen over time.


People with triple A syndrome frequently develop a thickening of the outer layer of skin hyperkeratosis on the palms of their hands and the soles of their feet. Other skin abnormalities may also be present in people with this condition. Alacrima is usually the first noticeable sign of triple A syndrome , as it becomes apparent early in life that affected children produce little or no tears while crying.

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They develop Addison disease and achalasia during childhood or adolescence, and most of the neurologic features of triple A syndrome begin during adulthood. The signs and symptoms of this condition vary among affected individuals, even among members of the same family.

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Triple A syndrome is a rare condition, although its exact prevalence is unknown. Within cells, ALADIN is found in the nuclear envelope, the structure that surrounds the nucleus and separates it from the rest of the cell. Mutations in the AAAS gene change the structure of ALADIN in different ways; however, almost all mutations prevent this protein from reaching its proper location in the nuclear envelope.

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DNA damage that is not repaired can cause the cell to become unstable and lead to cell death. Although the nervous system is particularly vulnerable to DNA damage, it remains unknown exactly how mutations in the AAAS gene lead to the signs and symptoms of triple A syndrome. The genetic cause of the disorder is unknown in these individuals.

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