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Neurologically, ALD/AMN can manifest with highly variable phenotypes, ranging from very aggressive and rapidly fatal inflammatory CNS demyelination in young boys to a more slowly progressive adult form either with cerebral white matter inflammatory lesions, or a more indolent progressive myelopathy and peripheral neuropathy (Moser, 1997)

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This iron overload deposits in vital organs such as the heart, liver, and endocrine glands, leading to complications including cardiac dysfunction, liver disease, diabetes, and hormonal disturbances

failure of tissues to respond to somatomedin, or failure of the liver to produce somatomedin