Researchers at GIGA have reported  that a majority of patients with Alzheimer’s disease overexpress the Inositol trisphosphate 3-kinase B (ITPKB) in the cerebral cortex and that neuronal ITPKB protein overexpression is associated with increased cell death, enhanced astrogliosis, production of amyloid-b-peptides and amyloid plaque formation as well as with increased tau phosphorylation in an Alzheimer’s disease mouse model.

In addition, they highlight that ITPKB and Ins(1,3,4,5)P4 are important regulators of Alzheimer’s disease pathology in vivo.

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