#1

Accumulation of F-actin drives brain aging and limits healthspan in Drosophila . Nature Communications , 2024; 15 (1) DOI: 10.1038/s41467-024-53389-w

  • a neat paper where they used Rapa and also gene therapy to lower F-actin accumulation in the brain.

." By tweaking a few specific genes in aging fruit flies’ neurons, the researchers prevented F-actin buildup, maintained cellular recycling and extended the healthy lifespan of fruit flies by approximately 30%."

“Their first clue of a correlation: Flies on a restricted diet both lived longer and had less F-actin buildup in their brains. Their second clue: When treated with a drug known to extend lifespan, called rapamycin, there was also less F-actin in the brains of aged flies.”

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#2

AI Overview

Glucagon-like peptide-1 (GLP-1) and F-actin are related in a number of ways, including:

  • F-actin determines docking dynamics

F-actin determines how GLP-1 granules dock over time when secretion is stimulated.

  • GLP-1 restores F-actin dynamics

GLP-1 can partially restore F-actin dynamics and the number of fusion events in cells that have been exposed to glucotoxicity.

  • GLP-1 depolymerizes F-actin

GLP-1 can depolymerize the F-actin cytoskeleton by inhibiting the RhoA-ROCK signaling pathway.

  • F-actin remodeling regulates insulin release

Remodeling of F-actin is necessary for the normal pattern of insulin secretion in response to nutrients.

Here are some other details about GLP-1 and F-actin:

  • GLP-1 production: The intestinal L-cells produce GLP-1.

  • F-actin remodeling: Cortical F-actin remodeling is linked to the SNARE exocytosis machinery.

  • ARRB2 and F-actin depolymerization: ARRB2 is essential for F-actin depolymerization in response to GIP stimulation.

  • FAK and Paxillin: FAK and Paxillin are activated in response to GLP-1 and GIP

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#3

Would this indicate that GLP agonists help F-actin remodeling?