PIP2 depletion and altered endocytosis caused by expression of Alzheimer's disease‐protective variant PLCγ2 R522
Emily Maguire, Georgina Menzies, Tom J. Phillips, Michael Sasner, Harriet M. Williams, Magdalena A. Czubala, Neil D. Evans, Emma L. Cope, Rebecca Sims, Gareth R. Howell, Emyr Lloyd‐Evans, Julie Williams, Nicholas D. Allen, Philip R. Taylor
Abstract
levels in vivo. Furthermore, it was associated with impaired phagocytosis and enhanced endocytosis. PLCγ2 acts downstream of other AD-related factors, such as TREM2 and CSF1R, and alterations in its activity directly impact cell function. The inherent druggability of enzymes such as PLCγ2 raises the prospect of PLCγ2 manipulation as a future therapeutic approach in AD.
Topics & Concepts
BiologyCell biologyTREM2EndocytosisMicrogliaCellGeneticsImmunologyInflammationNeuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsTryptophan and brain disorders