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Alzheimer's disease (AD)

AMP-activated protein kinase (AMPK); b-amyloid 42 (Ab42); calcium calmodulin-dependent protein kinase kinase 2 (CAMKK2)

Mouse and cell culture studies suggest inhibiting the CAMKK2/AMPK pathway could help prevent Ab42 toxicity in AD. In cultured mouse hippocampal neurons, knockout or pharmacological inhibition of Camkk2 decreased Ab42 oligomer-induced synaptotoxicity compared with no knockout or inhibition. In cell culture studies in neurons, the Ab42 oligomers induced AMPK-mediated phosphorylation of microtubule-associated protein-t (MAPT; TAU; FTDP-17). In mice overexpressing Ab42 in the hippocampus, inhibiting Camkk2/Ampk signaling decreased the loss of dendritic spines compared with no inhibition. Next steps include validating the long-term protective effects of blocking CAMKK2/AMPK signaling on additional measures of AD histopathology.

SciBX 6(17); doi:10.1038/scibx.2013.418
Published online May 2, 2013

Unpatented; licensing status not applicable

Mairet-Coello, G. et al. Neuron; published online April 10, 2013;
Contact: Franck Polleux, The Scripps Research Institute, La Jolla, Calif.