Specific cortical and subcortical grey matter regions are associated with insomnia severity.
Specific cortical and subcortical grey matter regions are associated with insomnia severity.
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DOI：
10.1371/journal.pone.0252076
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发表时间：
2021
期刊：
影响因子：
3.7
通讯作者：
Walsh CM
中科院分区：
文献类型：
--
作者：
Falgàs N;Illán-Gala I;Allen IE;Mumford P;Essanaa YM;Le MM;You M;Grinberg LT;Rosen HJ;Neylan TC;Kramer JH;Walsh CM
越来越多的人意识到睡眠障碍是痴呆症的一个危险因素。先前的病例对照研究表明，大脑灰质（GM）的变化，涉及皮层（即，前额叶区）和皮层下结构（即，壳核，丘脑）可能与失眠状态。然而，目前尚不清楚这些区域与可能有痴呆症风险的老年人失眠严重程度之间是否存在梯度关联。由于抑郁症状和睡眠呼吸暂停都可能与失眠相关的因素有关，可能影响大脑健康，并且经常出现在老年人群中，因此在研究失眠时将其包括在内非常重要。因此，我们的目标是调查健康老年人中与失眠严重程度相关的GM变化，同时考虑抑郁症和睡眠呼吸暂停的潜在影响。我们假设失眠的严重程度与1）负责调节睡眠和情绪的皮质区域（如眶额皮质）和2）皮质下区域（如壳核）相关。120名健康受试者（年龄74.8±5.7岁，55.7%为女性）从加州大学旧金山分校记忆与衰老中心的Hillblom健康衰老网络招募。所有参与者在神经系统评估、神经心理学评估和线人访谈后被确定为认知健康。参与者进行了3T脑部MRI检查，并完成了失眠严重程度指数（ISI）、老年抑郁量表（GDS）和柏林睡眠问卷（BA），以评估睡眠呼吸暂停。通过SPM 12中的CAT 12工具箱获得皮质厚度（CTh）和皮质下体积。我们使用经年龄、性别、惯用手和MRI扫描类型调整的多元回归研究了CTh和皮质下体积与ISI的相关性。还进行了通过GDS和BA调整的其他模型。ISI和GDS以轻度为主（分别为4.9±4.2和2.5±2.9），BA以低危为主（80%）。高ISI与右眶额区、右额中上级区和尾侧区、右颞顶交界区和左前扣带回皮质的CTh较低相关（p<0.001，未校正FWE）。经GDS校正后，右侧腹侧眶额交界处和颞顶交界处仍有显著性，左侧颞顶交界处变得有显著性（p<0.001，未校正FWE）。相反，BA没有表现出任何效果。FWE多重比较后，结果不再显著。关于皮层下区域，壳核体积越大，ISI越高（p<0.01）。我们的研究结果强调了失眠严重程度与大脑健康之间的关系，即使是相对轻微的失眠，也与抑郁症和睡眠呼吸暂停的可能性无关。这些结果扩展了先前的文献，表明特定GM区域（即眶额、岛叶和颞顶交界处）不仅与失眠的存在有关，而且与失眠的严重程度有关。此外，我们的研究结果表明皮质下结构（即，壳核）也参与其中。需要进行纵向研究，以澄清健康受试者中这些失眠相关的大脑变化如何与痴呆症风险增加相一致。
There is an increasing awareness that sleep disturbances are a risk factor for dementia. Prior case-control studies suggested that brain grey matter (GM) changes involving cortical (i.e, prefrontal areas) and subcortical structures (i.e, putamen, thalamus) could be associated with insomnia status. However, it remains unclear whether there is a gradient association between these regions and the severity of insomnia in older adults who could be at risk for dementia. Since depressive symptoms and sleep apnea can both feature insomnia-related factors, can impact brain health and are frequently present in older populations, it is important to include them when studying insomnia. Therefore, our goal was to investigate GM changes associated with insomnia severity in a cohort of healthy older adults, taking into account the potential effect of depression and sleep apnea as well. We hypothesized that insomnia severity is correlated with 1) cortical regions responsible for regulation of sleep and emotion, such as the orbitofrontal cortex and, 2) subcortical regions, such as the putamen. 120 healthy subjects (age 74.8±5.7 years old, 55.7% female) were recruited from the Hillblom Healthy Aging Network at the Memory and Aging Center, UCSF. All participants were determined to be cognitively healthy following a neurological evaluation, neuropsychological assessment and informant interview. Participants had a 3T brain MRI and completed the Insomnia Severity Index (ISI), Geriatric Depression Scale (GDS) and Berlin Sleep Questionnaire (BA) to assess sleep apnea. Cortical thickness (CTh) and subcortical volumes were obtained by the CAT12 toolbox within SPM12. We studied the correlation of CTh and subcortical volumes with ISI using multiple regressions adjusted by age, sex, handedness and MRI scan type. Additional models adjusting by GDS and BA were also performed. ISI and GDS were predominantly mild (4.9±4.2 and 2.5±2.9, respectively) and BA was mostly low risk (80%). Higher ISI correlated with lower CTh of the right orbitofrontal, right superior and caudal middle frontal areas, right temporo-parietal junction and left anterior cingulate cortex (p<0.001, uncorrected FWE). When adjusting by GDS, right ventral orbitofrontal and temporo-parietal junction remained significant, and left insula became significant (p<0.001, uncorrected FWE). Conversely, BA showed no effect. The results were no longer significant following FWE multiple comparisons. Regarding subcortical areas, higher putamen volumes were associated with higher ISI (p<0.01). Our findings highlight a relationship between insomnia severity and brain health, even with relatively mild insomnia, and independent of depression and likelihood of sleep apnea. The results extend the previous literature showing the association of specific GM areas (i.e, orbitofrontal, insular and temporo-parietal junction) not just with the presence of insomnia, but across the spectrum of severity itself. Moreover, our results suggest subcortical structures (i.e., putamen) are involved as well. Longitudinal studies are needed to clarify how these insomnia-related brain changes in healthy subjects align with an increased risk of dementia.
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