Association studies have previously implicated the EphB2 receptor in Alzheimer’s disease. As a member of a large family of tyrosine kinase receptors that regulate diverse biological functions, its role in the condition remained unknown. Cissé et al. now show that amyloid-β oligomers interact with EphB2 and trigger its degradation. EphB2 regulates NMDA-type glutamate receptors, and its depletion in normal mice reduces NMDAR currents and impairs long-term potentiation, both of which are important for memory formation. Increasing EphB2 levels in a mouse model of Alzheimer’s disease improves memory, suggesting that increasing EphB2 levels or function could be of therapeutic value in Alzheimer’s disease.
- Reversing EphB2 depletion rescues cognitive functions in Alzheimer model (Article p47, doi: 10.1038/nature09635)
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