Purpose: Presbycusis, age-related hearing loss, is believed to involve neural changes in the central nervous system, which is associated with an increased risk of cognitive impairment. The goal of this study was to determine if presbycusis disrupted spontaneous neural activity in specific brain areas involved in auditory processing, attention and cognitive function using resting-state functional magnetic resonance imaging (fMRI) approach.Methods: Hearing and resting-state fMRI measurements were obtained from 22 presbycusis patients and 23 age-, sex- and education-matched healthy controls. To identify changes in spontaneous neural activity associated with age-related hearing loss, we compared the amplitude of low-frequency fluctuations (ALFF) and regional homogeneity (ReHo) of fMRI signals in presbycusis patients vs. controls and then determined if these changes were linked to clinical measures of presbycusis.Results: Compared with healthy controls, presbycusis patients manifested decreased spontaneous activity mainly in the superior temporal gyrus (STG), parahippocampal gyrus (PHG), precuneus and inferior parietal lobule (IPL) as well as increased neural activity in the middle frontal gyrus (MFG), cuneus and postcentral gyrus (PoCG). A significant negative correlation was observed between ALFF/ReHo activity in the STG and average hearing thresholds in presbycusis patients. Increased ALFF/ReHo activity in the MFG was positively correlated with impaired Trail-Making Test B (TMT-B) scores, indicative of impaired cognitive function involving the frontal lobe.Conclusions: Presbycusis patients have disrupted spontaneous neural activity reflected by ALFF and ReHo measurements in several brain regions; these changes are associated with specific cognitive performance and speech/language processing. These findings mainly emphasize the crucial role of aberrant resting-state ALFF/ReHo patterns in presbycusis patients and will lead to a better understanding of the neuropathological mechanisms underlying presbycusis.

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Purpose Amide proton transfer (APT) MRI is promising to serve as a surrogate metabolic imaging biomarker of acute stroke. Although the magnetization transfer ratio asymmetry (MTRasym) has been used commonly, the origin of pH‐weighted MRI effect remains an area of investigation, including contributions from APT, semisolid MT contrast asymmetry, and nuclear Overhauser enhancement effects. Our study aimed to determine the origin of pH‐weighted MTRasym contrast following acute stroke. Methods Multiparametric MRI, including T1, T2, diffusion and Z‐spectrum, were performed in rats after middle cerebral artery occlusion. We analyzed the conventional Z‐spectrum )(IΔωI0 and the apparent exchange spectrum )(Rex)(normalΔnormalω, being the difference between the relaxation‐scaled inverse Z‐spectrum and the intrinsic spinlock relaxation rate )(R10.166667em·0.166667emcos2normalθ0.166667em·0.166667emnormalI0normalI)(normalΔnormalω-R1ρ)(normalΔnormalω. The ischemia‐induced change was calculated as the spectral difference between the diffusion lesion and the contralateral normal area. Results The conventional Z‐spectrum signal change at −3.5 ppm dominates that at +3.5 ppm (−1.16 ± 0.39% vs. 0.76 ± 0.26%, P < .01) following acute stroke. In comparison, the magnitude of ΔRex change at 3.5 ppm becomes significantly larger than that at −3.5 ppm (−2.80 ± 0.40% vs. −0.94 ± 0.80%, P < .001), with their SNR being 7.0 and 1.2, respectively. We extended the magnetization transfer and relaxation normalized APT concept to the apparent exchange–dependent relaxation image, documenting an enhanced pH contrast between the ischemic lesion and the intact tissue, over that of MTRasym. Conclusion Our study shows that after the relaxation‐effect correction, the APT effect is the dominant contributing factor to pH‐weighted MTRasym following acute stroke.