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Alzheimer disease (AD) is characterized by a buildup of amyloid-β (Aβ) plaques. One way to prevent synthesis of Aβ is to stimulate production of proteins called α-secretases.
In a study from the Massachusetts Institute of Technology, mice that overproduce Aβ (and that develop pathological and cognitive changes like those seen in AD) were mated with mice that overproduce SIRT1, a molecule that stimulates production of an α-secretase and that counters oxidative and metabolic stressors and slows aging (JW Gen Med Sep 23 2003). The resulting offspring had fewer Aβ plaques than the parent AD mice and were protected from developing learning and memory deficits. In contrast, when AD mice were mated with mice that did not express the gene for SIRT1,…