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Fig. 9 | Acta Neuropathologica Communications

Fig. 9

From: Lipid microdomain modification sustains neuronal viability in models of Alzheimer’s disease

Fig. 9

GCS inhibition increases neuronal viability in AD and increases the levels of functional IR on the neuronal cell surface. The proposed mechanism suggests that GCS-derived gangliosides facilitate ADDL-mediated internalization of surface IR via caveolin-1-containing caveolae. Low levels of caveolin-1 in GCS-deficient neurons lead to increased levels of IR at the neuronal surface. IR sensitivity and signaling are maintained in GCS-deficient neurons despite exposure to ADDLs. This contributes to the increased neuronal viability observed in AD models in vivo, where neurons harbor a genetic GCS deletion or in vitro, when they are treated with the specific GCS inhibitor GENZ

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