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]

Core Viewpoint - The article discusses the significant public health challenge posed by age-related hearing loss, emphasizing the need for deeper understanding of the molecular mechanisms involved in cochlear aging, particularly in primates, to develop targeted treatment strategies [1][2]. Group 1: Research Findings - A collaborative research team published a study in Nature Aging, identifying SLC35F1 deficiency as a key molecular marker and driver of cochlear aging in primates [2][7]. - The study successfully mapped the cellular and molecular characteristics of cochlear aging, revealing critical pathological changes such as hair cell loss and accelerated aging of spiral neurons [4][7]. - The research utilized innovative techniques to dissect primate cochlear tissue and employed single-cell sequencing combined with deep learning to create a high-resolution molecular map of cochlear aging [4][6]. Group 2: Mechanism and Treatment - The study demonstrated that silencing SLC35F1 in hair cells leads to significant cell apoptosis, indicating its crucial role in maintaining hair cell homeostasis [6]. - Long-term administration of metformin showed a rejuvenating effect on aged cochlear tissue in primates, reducing hair cell loss and vascular degeneration, while also decreasing the proportion of aging neurons [6][7]. - Metformin was found to exert protective effects through dual mechanisms: downregulating inflammation-related genes and upregulating key functional genes related to sound perception and neural signaling [6][7]. Group 3: Implications for Future Research - The findings provide a comprehensive understanding of the aging process in primate cochlea, highlighting specific susceptible cell types and their aging drivers, which could lead to innovative targeted therapies for age-related hearing loss [7][8]. - The research lays a solid theoretical foundation for developing clinical intervention strategies aimed at preventing and treating age-related hearing loss [7].