In mice, a total of 100 genes are known to affect albinism.All the genetic traits for albinism are recessive traits. This means that their influence is hidden when paired with stronger traits. For the recessive albino trait to be expressed in a mammal, the offspring must inherit a recessive gene from both parents.Albinism occurs throughout the animal kingdom. The condition is most commonly seen in birds, reptiles and amphibians, but more rarely seen in mammals and other taxa. It is often difficult to explain occasional occurrences, especially when only one documented incidence has occurred, such as only one albino gorilla and one albino koala. In mammals, albinism occurs once in every 10,000 births, but in birds, the rate is once in every 1,764 births.Some species, such as white peacocks, swans and geese, are not believed to be true albinos, as they do not have red eyes, rather, their colouration is suggested to be the expression of a white fur or feather gene, not a lack of melanin. Consequences
Melanin has several functions in most mammals and other animals; these are disrupted by albinism. Abnormal eye development and appearance
Melanin functions in the normal development of various parts of the eye, including the iris, retina, eye muscles, and optic nerve. The absence of melanin results in abnormal development of eyes and leads to problems with focusing, and depth perception.
Schizencephaly (from Greek  skhizein to split, and  enkephalos brain) is a rare birth defect characterized by abnormal clefts lined with grey matter that form the ependyma of the cerebral ventricles to the pia mater. These clefts can occur bilaterally or unilaterally. Common clinical features of this malformation include epilepsy, motor deficits, and psychomotor retardation. Presentation
Schizencephaly can be distinguished from porencephaly by the fact that in schizencephaly, the fluid-filled component is entirely lined by heterotopic grey matter, while a porencephalic cyst is lined mostly by white matter. Individuals with clefts in both hemispheres, or bilateral clefts, are often developmentally delayed and have delayed speech and language skills and corticospinal dysfunction. Individuals with smaller, unilateral clefts (clefts in one hemisphere) may be weak or paralyzed on one side of the body and may have average or near-average intelligence. Patients with schizencephaly may also have varying degrees of microcephaly, Cognitive impairment, hemiparesis (weakness or paralysis affecting one side of the body), or quadriparesis (weakness or paralysis affecting all four extremities), and may have reduced muscle tone (hypotonia). Most patients have seizures, and some may have hydrocephalus. Causes
In schizencephaly, the neurons border the edge of the cleft, implying a very early disruption of the usual grey matter migration during embryogenesis. The cause of the disruption is not known, but likely the cause may be either genetic or a physical insult, such as infection, infarction, hemorrhage, in utero stroke, exposure to a toxin, or mutation.