Fig. 3: β-arrestins in frontotemporal dementia. | Experimental & Molecular Medicine

Fig. 3: β-arrestins in frontotemporal dementia.

From: The multifaceted functions of β-arrestins and their therapeutic potential in neurodegenerative diseases

Fig. 3

In healthy neurons, β-arrestin monomers regulate the internalization, desensitization, and recycling of GPCRs. Additionally, P62/SQSTM1-mediated autophagy remains intact due to the successful self-interaction of P62, which is required for its localization to the autophagosome formation site, resulting in efficient removal of damaged organelles and misfolded proteins. Tau is able to bind to and stabilize microtubules. However, in FTLD-Tau, β-arrestin oligomers accumulate and prevent P62/SQSTM1 self-interaction, leading to autophagy impairment. β-arrestin1 also competes with tau for microtubule binding, inducing microtubule destabilization and tau accumulation. Created with BioRender.com.

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