Lopez-Vilaret Karel M, Fernandez-Alvarez Marina, Bierbrauer Anne, Axmacher Nikolai, Cantero Jose L, Atienza Mercedes
Laboratory of Functional Neuroscience, Pablo de Olavide University, Seville, Spain.
CIBER de Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain.
Aging Dis. 2024 Nov 18;16(5):3154-3179. doi: 10.14336/AD.2024.0975.
Path integration (PI), which supports navigation without external spatial cues, is facilitated by grid cells in the entorhinal cortex. These cells are often impaired in individuals at risk for Alzheimer's disease (AD). However, other brain systems can compensate for this impairment, especially when spatial cues are available. From a graph-theoretical perspective, this compensatory mechanism might manifest through changes in network segregation, indicating shifts in distinct functional roles among specialized brain regions. This study explored whether similar compensatory mechanisms are active in APOE ε4 carriers and individuals with elevated insulin resistance, both susceptible to entorhinal cortex dysfunction. We applied a graph-theoretical segregation index to resting-state fMRI data from two cohorts (aged 50-75) to assess PI performance across virtual environments. Although insulin resistance did not directly impair PI performance, individuals with higher insulin resistance demonstrated better PI with less segregated brain networks, regardless of spatial cue availability. In contrast, the APOE effect was cue-dependent: ε4 heterozygotes outperformed ε3 homozygotes in the presence of local landmarks, linked to increased sensorimotor network segregation. When spatial cues were absent, ε4 carriers exhibited reduced PI performance due to lower segregation in the secondary visual network. Controlling cortical thickness and intracortical myelin variability mitigated these APOE effects on PI, with no similar adjustment made for insulin resistance. Our findings suggest that ε4 carriers depend on cortical integrity and spatial landmarks for successful navigation, while insulin-resistant individuals may rely on less efficient neural mechanisms for processing PI. These results highlight the importance of targeting insulin resistance to prevent cognitive decline, particularly in aging navigation and spatial cognition.
路径整合(PI)支持在没有外部空间线索的情况下进行导航,内嗅皮层中的网格细胞促进了这一过程。这些细胞在患阿尔茨海默病(AD)风险较高的个体中常常受损。然而,其他脑系统可以补偿这种损伤,尤其是在有空间线索可用时。从图论的角度来看,这种补偿机制可能通过网络分离的变化表现出来,这表明专门脑区之间不同功能作用的转变。本研究探讨了类似的补偿机制在APOEε4携带者和胰岛素抵抗升高的个体中是否活跃,这两类个体都易患内嗅皮层功能障碍。我们将图论分离指数应用于来自两个队列(年龄在50 - 75岁)的静息态功能磁共振成像数据,以评估虚拟环境中的路径整合表现。尽管胰岛素抵抗并未直接损害路径整合表现,但胰岛素抵抗较高的个体在脑网络分离较少的情况下表现出更好的路径整合,无论空间线索是否可用。相比之下,APOE的影响依赖于线索:在存在局部地标时,ε4杂合子的表现优于ε3纯合子,这与感觉运动网络分离增加有关。当没有空间线索时,ε4携带者由于次级视觉网络分离较低而表现出路径整合能力下降。控制皮层厚度和皮层内髓鞘变异性减轻了这些APOE对路径整合的影响,而对胰岛素抵抗没有进行类似的调整。我们的研究结果表明,ε4携带者成功导航依赖于皮层完整性和空间地标,而胰岛素抵抗个体可能依赖效率较低的神经机制来处理路径整合。这些结果凸显了针对胰岛素抵抗以预防认知衰退的重要性,特别是在衰老过程中的导航和空间认知方面。