ArticleCell reports2025
Control of aging-associated neurodegeneration via hypothalamic extracellular vesicles containing parathymosin.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
8 authors.
Funding
Abstract
Aging-associated neurodegeneration underlies various neurological diseases; however, the neurocrine basis remains poorly understood. Here, we investigate the role of parathymosin (PTMS), a secretory protein with nuclear functions that has recently been identified as a circulating factor in the brain. The results show that loss of PTMS is sufficient to cause severe, age-dependent neurodegeneration and reduced lifespan, whereas hypothalamic PTMS gain of function counteracts aging-associated brain disorders and extends lifespan. PTMS is present in hypothalamic extracellular vesicles (EVs), particularly in subpopulations released by hypothalamic neural stem/progenitor cells (htNSCs). These htNSC-derived EVs carry small nuclear and nucleolar RNAs in a PTMS-associated manner to protect recipient neurons from DNA damage. Therapeutically, these htNSC-derived EVs provide a strong effect against neurodegenerative disorders associated with PTMS deficiency in mouse models, including Alzheimer's disease (AD)-like phenotypes in the 5xFAD model. In conclusion, PTMS possesses anti-neurodegenerative properties, and PTMS-containing hypothalamic EVs are significant in combating aging-associated neurodegenerative diseases.
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