Abstract
Background and ObjectiveHearing loss (HL) is one of the modifiable risk factors for Alzheimer's disease (AD). However, the underlying mechanism behind HL in AD remains elusive. A possible mechanism is cognitive load hypothesis, which postulates that over-processing of degraded auditory signals in the auditory cortex leads to deficits in other cognitive functions. Given mild cognitive impairment (MCI) is a prodromal stage of AD, untangling the association between HL and MCI might provide insights for potential mechanism behind HL.MethodsWe included 85 cognitively normal (CN) subjects with no hearing loss (NHL), 24 CN with HL, 103 mild cognitive impairment (MCI) patients with NHL, and 23 MCI with HL from the ADNI database. All subjects underwent resting-state functional MRI and neuropsychological scale assessments. Fractional amplitude of low-frequency fluctuation (fALFF) was used to reflect spontaneous brain activity. The mixed-effects analysis was applied to explore the interactive effects between HL and cognitive status (GRF corrected, voxel p-value <0.005, cluster p-value < 0.05, two-tailed). Then, the FDG data was included to further reflect the regional neuronal abnormalities. Finally, Pearson correlation analysis was performed between imaging metrics and cognitive scores to explore the clinical significance (Bonferroni corrected, p < 0.05).ResultsThe interactive effects primarily located in the left superior temporal gyrus (STG) and bilateral inferior temporal gyrus (ITG). Post-hoc analysis showed that NC with HL had lower fALFF in bilateral ITG compared to NC with NHL. NC with HL had higher fALFF in the left STG and decreased fALFF in bilateral ITG compared to MCI with HL. In addition, NC with HL had lower fALFF in the right ITG compared to MCI with NHL. Correlation analysis revealed that fALFF was associated with MMSE and ADNI-VS, while SUVR was associated with MMSE, MoCA, ADNI-EF and ADNI-Lan.ConclusionHL showed different effects on NC and MCI stages. NC had increased spontaneous brain activity in auditory cortex while decreased activity in the ITG. Such pattern altered with disease stage changing and manifested as decreased activity in auditory cortex along with increased activity in ITG in MCI. This suggested that the cognitive load hypothesis may be the underlying mechanism behind HL.
Highlights
Alzheimer’s disease (AD) is the most primary cause of dementia, which is clinically characterized by progressive cognitive decline (Scheltens et al, 2021)
The database was launched by the National Institute on Aging (NIA), the Food and Drug Administration (FDA), and the National Institute of Biomedical Imaging and Bioengineering (NIBIB), aiming to explore whether serial magnetic resonance imaging (MRI), positron emission tomography (PET), biological markers, and other neuropsychological assessment can be used for early detecting and tracking AD
The fractional amplitude of low-frequency fluctuation (fALFF) in the right inferior temporal gyrus (ITG) was negatively correlated with Alzheimer’s Disease Neuroimaging Initiative (ADNI) -VS (r = −0.143, p < 0.05)
Summary
Alzheimer’s disease (AD) is the most primary cause of dementia, which is clinically characterized by progressive cognitive decline (Scheltens et al, 2021). As a transitional stage between normal aging and AD, mild cognitive impairment (MCI) is an appropriate period for early diagnosis and prevention of AD. Several studies have indicated the relationship between HL and cognitive decline, and the role of HL as an increased risk for dementia (Deal et al, 2017; Thomson et al, 2017; Wei et al, 2017; Zheng et al, 2017). A longitudinal study of 836 subjects found that elders with HL had an higher risk of developing dementia and a faster decline of cognition (Gurgel et al, 2014). Given mild cognitive impairment (MCI) is a prodromal stage of AD, untangling the association between HL and MCI might provide insights for potential mechanism behind HL
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