Skip to main content
Fig. 11 | Acta Neuropathologica Communications

Fig. 11

From: Protein farnesylation is upregulated in Alzheimer’s human brains and neuron-specific suppression of farnesyltransferase mitigates pathogenic processes in Alzheimer’s model mice

Fig. 11

Schematic illustration of FT upregulation pathways leading to AD and reversal by FT deletion or inhibition. Aberrant upregulation of FT/protein farnesylation increases the membrane association of farnesylated proteins, including Ras and Rheb, and their interactions with downstream effectors, leading to hyperactivation of mTORC1 signaling and AD. Deletion or inhibition of FT results in the reduced membrane association of Ras and Rheb and reverses the pathogenic activation of the signaling pathway

Back to article page