研究解析老年性耳聋发生机制

Core Insights - The research highlights the irreversible progressive hearing loss characteristic of presbycusis, which not only severely impairs auditory function but also potentially leads to social barriers, cognitive decline, and increased risk of Alzheimer's disease [1] - A collaborative team has successfully mapped the cellular and molecular features of cochlear aging in primates, identifying the downregulation of the transmembrane transport protein SLC35F1 as a core molecular marker and driver of cochlear aging [1][2] - The study demonstrates the protective effects of metformin on the cochlea, providing a new target for the prevention and treatment of presbycusis [1][3] Group 1: Research Findings - The research team overcame technical challenges in dissecting and isolating primate cochlear tissue, leading to a comprehensive analysis of key biological features associated with cochlear aging [2] - Core pathological changes identified include loss of hair cells, accelerated aging of spiral neurons, increased inflammatory damage, atrophy of the stria vascularis, and dysfunction of transmembrane transport [2] - The specific downregulation of SLC35F1 in hair cells was confirmed as a significant molecular marker of cochlear aging, providing crucial insights into its molecular mechanisms [2] Group 2: Therapeutic Implications - Previous studies indicated that metformin, a treatment for type 2 diabetes, has significant anti-aging effects in elderly primates, prompting further investigation into its protective role in aging cochlea [3] - A 3.3-year treatment with clinical doses of metformin resulted in notable rejuvenation of cochlear tissue in aged crabs-eating macaques, with reduced hair cell loss and vascular atrophy [3] - Transcriptomic analysis revealed that metformin exerts protective effects through dual mechanisms: downregulating inflammation-related genes and upregulating key functional genes related to sound perception and neural signaling [3]