Optogenetic regulation of phosphatidylinositides in cellular and mouse models of Alzheimer’s disease

Major disappointments in late‐stage clinical trials have made it clear that additional therapeutic targets beyond amyloid β‐peptide (Aβ) and tau are urgently required for Alzheimer’s disease (AD). Phosphatidylinositol 4,5‐biphosphate [PI(4,5)P2] has previously been established as an important signaling lipid at the synapse and in a mouse model of Alzheimer’s disease. We hypothesize that the level of PI(4,5)P2 in the plasma membrane may be an early and critical determinant of AD associated molecular and behavioral deficits in cellular and mouse models of the disease.