Potential new therapeutic target for Alzheimer’s Disease:

Cissé and coworkers provide evidence that increasing the tyrosine kinase receptor EphB2 can reverse memory deficits in a mouse model of Alzheimer’s Disease. It is widely known that Amyloid-? peptide oligomers may cause cognitive deficits in Alzheimer’s disease by impairing neuronal NMDA receptor function. Amyloid-? oligomers were shown to decrease levels of EphB2, a tyrosine kinase receptor which regulates NMDA receptor function. Increasing EphB2 levels in a mouse model of Alzheimer’s (human amyloid precursor protein transgenic mice), reversed memory impairments. EphB2 is a potential therapeutic target in Alzheimer’s disease.
Cissé M et al.: Reversing EphB2 depletion rescues cognitive functions in Alzheimer model. Nature 469: 47-51 (2011).
http://www.ncbi.nlm.nih.gov/pubmed/21113149