Endophilin I expression is increased in the brains of Alzheimer's disease patients
Ren Y, Xu HW, Davey F, Taylor M, Aiton J, Coote P, Fang F, Yao J, Chen JX, Yan SD, Gunn-Moore FJ
J Biol Chem
Cells used in publication:
Neuron, cortical, mouse
Tissue Origin: brain
Alzheimer's patients have increased levels of both the 42 beta amyloid-beta-peptide (Abeta) and Amyloid Binding Alcohol Dehydrogenase (ABAD) which is an intracellular binding site for Abeta. The over-expression of Abeta and ABAD in transgenic mice has shown that the binding of Abeta to ABAD results in amplified neuronal stress and impairment of learning and memory. From a proteomic analysis of the brains from these animals we have identified for the first time that the protein endophilin I increases in Alzheimer's diseased brain. The increase in endophilin I levels in neurons is linked to an increase in the activation of the stress kinase c-Jun N-terminal kinase with the subsequent death of the neurons. We also demonstrate in living animals that the expression level of endophilin I is an indicator for the interaction of ABAD and Abeta as its expression levels return to normal if this interaction is perturbed. Therefore this identifies endophilin I as a new indicator of the progression of Alzheimer's disease.
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