年龄相关性听力损失中结构连接性降低与感觉剥夺理论相符

文献信息

中文摘要

背景： 年龄相关性听力损失（ARHL）可能通过结构退化和大脑重组导致认知下降，正如感觉剥夺理论所假设的那样。这些过程可以通过拓扑变化来表征，例如脑区之间结构连接的增强和减弱。更强的连接与重组更相关，因为重组被认为通过招募额外的脑网络作为代偿机制来支持言语加工。我们研究了与ARHL相关的连接性变化，以增进对感觉剥夺理论的理解。方法：类似于言语加工的偏侧化，我们假设与ARHL相关的结构重组在左半球最为明显。我们使用1.5特斯拉弥散加权MRI和结构T1图像，对来自基于人群的鹿特丹研究的2402名参与者（中位年龄=66.1岁，女性=54.7%）评估了全脑结构连接性。进行了纯音测听，并针对较好耳确定了不同频率范围的纯音平均值（PTA），包括PTAlow（250-1000 Hz）和PTAall（250-8000 Hz），以反映ARHL。结果：ARHL主要与涉及额叶和皮层下灰质区域的较弱连接相关。与我们的假设相反，未观察到连接性改变的偏侧化。PTAlow和PTAall产生了最强的关联，可能由低频听力阈值驱动。调整心血管危险因素后关联减弱，尤其是PTAlow。结论：总之，这些发现与感觉剥夺的神经效应所预期的代偿性结构重组相矛盾。虽然观察到的较弱连接与感觉剥夺理论相符，但结果也提示心血管健康是一个共同危险因素。

英文摘要

Age-related hearing loss (ARHL) may contribute to cognitive decline through structural degeneration and brain reorganization, as posited by the sensory deprivation theory. These processes can be characterized by topological changes, such as strengthening and weakening of structural connections between brain regions. Stronger connections are more relevant to reorganization, as reorganization is thought to support speech processing by recruiting additional brain networks as a compensatory mechanism. We investigated connectivity changes associated with ARHL to improve the understanding of the sensory deprivation theory. Similar to the lateralization of speech processing, we hypothesized that structural reorganization associated with ARHL would be most evident in the left hemisphere. We assessed whole-brain structural connectivity using 1.5 Tesla diffusion-weighted MRI and structural T1 images in 2402 participants (median age = 66.1 years, females = 54.7%) from the population-based Rotterdam Study. Pure-tone audiometry was performed, and pure-tone averages (PTAs), for different frequency ranges including PTAlow (250-1000 Hz) and PTAall (250-8000 Hz), were determined for the better-hearing ear to reflect ARHL. ARHL was primarily associated with weaker connections involving frontal and subcortical gray matter regions. Contrary to our hypothesis, no lateralization in the connectivity alterations was observed. PTAlow and PTAall yielded the strongest associations, likely driven by low-frequency hearing thresholds. Adjusting for cardiovascular risk factors attenuated associations, especially for PTAlow. In conclusion, the findings contradict the hypothesized compensatory structural reorganization expected from the neural effects of sensory deprivation. While the observed weaker connectivity aligns with the sensory deprivation theory, the results also suggest cardiovascular health as a common risk factor.