04.12.2012 - Scientists from VIB and KU Leuven have discovered a new target that could lay the foundations for a new approach to treat Alzheimer’s disease.
The research team, headed by Bart de Strooper from VIB, found that β-arrestin 2 blocks the plaque-form enzyme γ-secretase through interaction with the G protein–coupled receptors GPR3 and β2 -adrenergic receptor (Nature Medicine). Furthermore, they demonstrated that β-arrestin 2 was overexpressed in two independent cohorts of Alzheimer patients. Overexpression of the protein led to an increase in sticky amyloid-β (Aβ) peptides, called Aβ40 and Aβ42, which form the amyloid plaques that are associated with neurodegeneration. In contrast, genetic silencing of Arrb2, which encodes β-arrestin 2, reduced generation of Aβ in cell cultures and in knock-out mice for the Alzheimer regulator. The effect was mediated by direct binding to the Aph-1a subunit of the γ-secretase complex, which enzymatically generates the sticky Aβ peptides. Thus the scientists believe that inhibitors of β-arrestin 2 could block the generation of Aβ40 and Aβ42, in early stages of Alzheimer’s when no symptoms have yet emerged.
Currently there is no cure for the neurodegenerative disease. Many candidate drugs that target the γ-secretase complex fail because they also target proteins essential to life. The discovery from Leuven could form a target for a treatment against Alzheimer’s disease with fewer side effects and that suppresses the very first symptoms of the disease. β-arrestin 2 inhibition could be beneficial in prevention of the adverse side effects currently associated with γ-secretase inhibition. This study thus provides a previously unexplored avenue for the development of a treatment that can act at a very early stage of Alzheimer’s disease.
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