A protein which aggravates Alzheimer's Disease
Following these observations, the researchers decided to begin an in vitro study of cultured mouse neurons in which they over-expressed the ITPKB protein. The results did not disappoint the researchers: a large number of these neurons died and the cell culture supernanant provided evidence of highly increased production of amyloid peptide. 'However, these two things are precisely the particularities of Alzheimer's Disease', specifies Schurmans. Over-expression does not trigger, but aggravates the diseaseWhat is the effect of ITPKB over-expression in vivo? 'We have created mice which over-express the ITPKB enzyme specifically in the neurons of the hippocampus and the cerebral cortex, i.e. where changes are found in patients affected by Alzheimer's Disease', indicates the researcher. However, this experiment did not yield any particular observations. 'This means that the over-expression of ITPKB alone is insufficient to trigger Alzheimer's Disease and lead to the formation of senile plaques as well as neuron apoptosis', continues Schurmans. 'This enzyme probably does not play a major role in the disease, but may play a regulating role'.
(1) V. Stygelbout, K. Leroy, V. Pouillon, K. Ando, E. D’Amico,Y. Jia, H. R. Luo, C. Duyckaerts, C. Erneux, S. Schurmans and J.-P. Brion. Inositol trisphosphate 3-kinase B is increased in human Alzheimer brain and exacerbates mouse Alzheimer pathology. Brain. 2014 Jan 8. |
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