Stories about: beta-thalassemia

Sickle cell disease and the thalassemias: The advantages of staying forever young

Flipping a single molecular switch could turn off the mutation that causes sickle cell diseae. Stuart Orkin has already done it in mice. (CDC PHIL)

What if we really could turn our bodies’ clocks back? In some cases, that could be a really good thing. Take sickle cell disease. A scourge of tens of thousands worldwide, it stems from a genetic defect in hemoglobin, the oxygen-carrying protein in red blood cells.

Normally, our bodies can produce two forms of hemoglobin: adult hemoglobin, the form susceptible to the sickle cell mutation; and fetal hemoglobin, which is largely produced during development and for a short time after birth. Our bodies finish making the switch from fetal to adult hemoglobin production by about four to six months old – the same time frame when children with the sickle cell mutation first start to show symptoms of the disease.

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