Like any well-oiled machine, a cell needs all of its parts to be kept in good condition. One faulty component can eventually cause a breakdown. In nerve cells of Alzheimer's disease patients, the faulty component is a protein called amyloid beta (Aβ). Aβ clumps together to form plaques that trigger a chain of events that destroy the cell. It may be possible to compensate for this fault by intervening somewhere else along this catastrophic cascade. Looking at the effects of Aβ in the developing eyes of the fruit fly provides some clues. Given Aβ (left) nerve cells (red) died, eyes were misshapen, and a protein called Crb (green) that's involved in nerve cell death appeared at higher levels. Tinkering with the genes of these flies revealed that activating another protein CBP, alongside Aβ rescues these defects (right). With more research, CBP may prove useful in treating Alzheimer's disease.
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