Albinism affects approximately 1 in 20,000 individuals. Although the most obvious symptom is a deficiency in pigmentation, many more serious conditions accompany the disorder. It produces abnormal crossings of the temporal fibers in the optic chiasm, nystagmus, photophobia, variable visual acuity and, frequently, strabismus. The main subdivisions of albinism include oculocutaneous, ocular, and albinoidism. Albinoidism is the absence of pigment in localized areas; the pigment in the skin, hair, and eyes is less than normal but does not affect the individual as severely as the oculocutaneous or ocular types.

Albinism is a genetic trait characterized by the lack of pigmentation, but albinos typically contain normal numbers of melanocytes in their skin. Cellular pigmentation is dependent upon a cell's ability to manufacture and sequester the pigment melanin. This is accomplished within organelles called melanosomes that reside inside cells called melanocytes. The melanocytes that originate in the neural crest provide pigment for the skin (including eyelids), hair, uvea, conjunctiva, stroma of the iris, ciliary body and choroids. The melanoctyes that supply pigment for the retinal pigment epithelium (RPE) are derived from neuroectoderm. The melanocytes of albinos are generally unable to express pigmentation because they lack the enzyme tyrosinase, which is involved in the conversion of the amino acid tyrosine to melanin. (http://www.albinism.org/)

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