Core Viewpoint - The research indicates that aging brain neurons produce excessive WDFY1 protein, which is transferred to bones via extracellular vesicles, leading to bone-fat imbalance and osteoporosis [2][5][6]. Group 1: Research Findings - Aging brain neurons, particularly in the hippocampus and cerebral cortex, generate excessive WDFY1 protein [5]. - Increased expression of the Wdfy1 gene in the brain accelerates bone aging, while inhibiting Wdfy1 expression or knocking it out in neurons improves bone health [5]. - WDFY1 interacts with the Retromer complex, promoting the recycling of cathepsin D and peroxiredoxin 2 from endosomes to the Golgi apparatus, which inhibits osteogenesis and promotes fat generation [5]. Group 2: Implications - The study reveals that extracellular vesicles from aging brain neurons transfer WDFY1 protein to bones, acting as a messenger that triggers bone-fat imbalance and leads to bone loss [6].