Central presbycusis is caused by degradation of the auditory centre during ageing. Its main characteristics are difficulties in understanding language and localizing sound. Presbycusis is an increasingly critical public health problem, but the underlying molecular mechanism has not been fully elucidated. Ferroptosis is a form of regulated cell death caused by iron-and reactive oxygen species-induced lipid peroxidation. Ferroptosis is related to many pathological processes, but whether it participates in the degeneration of the auditory system remains unclear. To investigate this, we measured iron levels in a simulated ageing model established by the addition of D-galactose (D-gal). We found, for the first time, that iron accumulated within cells and that the ultrastructural features of ferroptosis appeared in the auditory cortex with ageing. These changes were accompanied by upregulation of iron regulatory protein 2 (IRP-2), which led to an increase in transferrin receptor 1 (TfR-1), thus increasing iron entry into cells and potentially leading to ferroptosis. In addition, the malondialdehyde (MDA) content and the occurrence of mitochondrial DNA common deletions (CDs) increased, neuron degeneration appeared, and glutathione (GSH) and superoxide dismutase (SOD) activity decreased. Furthermore, we found that treatment with the iron chelator deferoxamine (DFO) and knockdown of IRP-2 both relieved ferroptosis during the simulated ageing process, thus achieving a partial protective effect to delay ageing. In summary, we describe here the first discovery that age-related iron deposition and ferroptosis may be associated with auditory cortex neurodegeneration. Relieving ferroptosis might thus be a new intervention strategy for age-related hearing loss.

<b><i>Introduction:</i></b> Spontaneous cerebrospinal fluid rhinorrhea (SCSFR) is the most common type of cerebrospinal fluid leakage and may cause serious cerebral complications. The aim of this research was to investigate the relationship between the degree of pneumatization variants of the paranasal sinus and skull base and the incidence of SCSFR. <b><i>Methods:</i></b> In total, 131 patients with SCSFR were analyzed, and 50 patients suffering from the nasal septal deviation were selected as controls. The pneumatization of the paranasal sinus and skull base was observed by CT scan. <b><i>Results:</i></b> Among the 137 fistulas, 55 (40.15%) were found in the ethmoid sinus. The incidences of Onodi cells (27.27 vs. 8%) and type 3 lateral recess of the sphenoid sinus (LRSS, 70.37 vs. 22%) in the SCSFR subgroups were significantly higher than those in the control group (<i>p</i> &lt; 0.05). Moreover, the occurrence of SCSFR was linearly correlated with the classification of Onodi cells and LRSS (<i>p</i> &lt; 0.05). There was no significant difference in the incidence of frontal cells, anterior clinoid process pneumatization, and posterior clinoid process pneumatization between the SCSFR patients and the controls. <b><i>Conclusion:</i></b> The most common site of SCSFR is the ethmoid sinus. The excessive pneumatization of the Onodi cell and LRSS increases the risk for the occurrence of SCSFR in the ethmoid sinus and sphenoid sinus, respectively. The possible association between the paranasal sinus ontogeny and SCSFR pathophysiology needs further studies.