Researchers at Tiangong University and Shandong Provincial Hospital have identified a neurobiological link between age-related hearing loss, known as presbycusis, and cognitive decline, pinpointing a ratio measuring brain network integration as a potential early indicator of dementia risk.
The study, published in eNeuro, centers on the Functional-Structural Ratio (FSR), which assesses how well brain regions responsible for sound, speech, memory, and decision-making remain connected within functional networks. As hearing deteriorates, the research demonstrates a corresponding decline in both the physical structure and the electrical communication within these critical brain areas.
Specifically, the study highlighted the putamen and fusiform gyrus – areas involved in processing sound and speech – and the precuneus and medial superior frontal gyrus – regions crucial for memory and decision-making – as becoming increasingly disconnected in individuals experiencing presbycusis. These reduced connections directly correlated with poorer performance on both hearing threshold tests and assessments of memory and executive function, according to the research team led by Ning Li.
“The most important takeaway is that preserving hearing health may protect brain integrity,” said Li. “Due to the fact that changes in the FSR correlate with both hearing loss and cognitive decline, this ratio could eventually serve as a biomarker—a tool for doctors to identify who is at the highest risk for dementia simply by looking at their brain scans.”
The findings build upon decades of observed correlation between hearing loss and cognitive impairment, but represent a significant step toward understanding the underlying biological mechanisms. Previous research has established that presbycusis is a common condition among geriatric populations, often linked to factors such as noise exposure, smoking, medication, hypertension, and family history. However, the precise “bridge” connecting hearing loss to dementia has remained elusive.
Scientists have also explored the role of mitochondrial dysfunction in both presbycusis and Alzheimer’s disease, suggesting potential shared pathways involving the SIRT1-PGC1α and LKB1 (or CaMKKβ)-AMPK signaling pathways. These pathways are believed to contribute to the preservation of cerebral neuron function and maintenance of the blood-brain barrier. Altered expression levels of these pathways have been observed in both mouse models of hearing loss and Alzheimer’s disease.
The research suggests that the coordinated decline in brain structure and function associated with hearing loss may contribute to the symptoms of cognitive decline. The FSR, as a potential biomarker, could offer a new avenue for early detection and intervention, though further research is needed to validate its predictive power and clinical utility.
