Abstract
Patients with trisomy 21 not only have developmental delays in early childhood but also have premature Alzheimer-like changes in early adulthood. Postmortem studies of infants with trisomy 21 have shown loss of neurons and structural abnormalities of the brain during late gestation and early postnatal life. Two enzymes encoded on chromosome 21 — copper/zinc superoxide dismutase and cystathionine β-synthase — might be involved with this neuronal damage. Increased activity of …
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