Department of Aerospace and Mechanical Engineering, University of Notre Dame, Notre Dame, IN, 46556, USA.
Biomech Model Mechanobiol. 2024 Dec;23(6):2229-2241. doi: 10.1007/s10237-024-01890-y. Epub 2024 Sep 19.
The brain glymphatic system is currently being explored in the context of many neurological disorders and diseases, including traumatic brain injury, Alzheimer's disease, and ischemic stroke. However, little is known about the impact of brain tumors on glymphatic function. Mechanical forces generated during tumor development and growth may be responsible for compromised glymphatic transport pathways, reducing waste clearance and cerebrospinal fluid (CSF) transport in the brain parenchyma. One such force is solid stress, i.e., growth-induced forces from cell hyperproliferation and excess matrix deposition. Because there are no prior studies assessing the impact of tumor-derived solid stress on glymphatic system structure and performance in the brain parenchyma, this study serves to fill an important gap in the field. We adapted a previously developed Electrical Analog Model using MATLAB Simulink for glymphatic transport coupled with Finite Element Analysis for tumor mechanical stresses and strains in COMSOL. This allowed simulation of the impact of tumor mechanical force generation on fluid transport within brain parenchymal glymphatic units-which include perivascular spaces, astrocytic networks, interstitial spaces, and capillary basement membranes. We conducted a parametric analysis to compare the contributions of tumor size, tumor proximity, and ratio of glymphatic subunits to the stress and strain experienced by the glymphatic unit and corresponding reduction in flow rate of CSF. Mechanical stresses intensify with proximity to the tumor and increasing tumor size, highlighting the vulnerability of nearby glymphatic units to tumor-derived forces. Our stress and strain profiles reveal compressive deformation of these surrounding glymphatics and demonstrate that varying the relative contributions of astrocytes vs. interstitial spaces impact the resulting glymphatic structure significantly under tumor mechanical forces. Increased tumor size and proximity caused increased stress and strain across all glymphatic subunits, as does decreased astrocyte composition. Indeed, our model reveals an inverse correlation between extent of astrocyte contribution to the composition of the glymphatic unit and the resulting mechanical stress. This increased mechanical strain across the glymphatic unit decreases the venous efflux rate of CSF, dependent on the degree of strain and the specific glymphatic subunit of interest. For example, a 20% mechanical strain on capillary basement membranes does not significantly decrease venous efflux (2% decrease in flow rates), while the same magnitude of strain on astrocyte networks and interstitial spaces decreases efflux flow rates by 7% and 22%, respectively. Our simulations reveal that solid stress from growing brain tumors directly reduces glymphatic fluid transport, independently from biochemical effects from cancer cells. Understanding these pathophysiological implications is crucial for developing targeted interventions aimed at restoring effective waste clearance mechanisms in the brain. This study opens potential avenues for future experimental research in brain tumor-related glymphatic dysfunction.
脑淋巴系统目前正在许多神经退行性疾病和疾病的背景下进行研究,包括创伤性脑损伤、阿尔茨海默病和缺血性中风。然而,对于脑肿瘤对淋巴功能的影响知之甚少。肿瘤发展和生长过程中产生的机械力可能导致淋巴转运途径受损,从而减少脑实质中的废物清除和脑脊液(CSF)转运。其中一种力是固有力,即细胞过度增殖和基质过度沉积引起的生长诱导力。由于没有先前的研究评估肿瘤衍生的固有力对脑实质中淋巴系统结构和功能的影响,因此本研究填补了该领域的一个重要空白。我们使用 MATLAB Simulink 中的先前开发的电气模拟模型来模拟与有限元分析结合的肿瘤机械应力和 COMSOL 中的脑实质淋巴系统中的流体运输。这允许模拟肿瘤机械力产生对脑实质淋巴单位内流体运输的影响,这些单位包括血管周围空间、星形胶质细胞网络、细胞间隙和毛细血管基底膜。我们进行了参数分析,以比较肿瘤大小、肿瘤接近度和淋巴单位比例对淋巴单位的影响,以及相应的 CSF 流动速率降低。随着肿瘤的接近度和肿瘤大小的增加,机械应力会加剧,突出了附近淋巴单位对肿瘤衍生力的脆弱性。我们的应力和应变曲线揭示了这些周围淋巴的压缩变形,并表明在肿瘤机械力下,星形胶质细胞与细胞间隙的相对贡献的变化会显著影响最终的淋巴结构。肿瘤大小和接近度的增加会导致所有淋巴单位的应力和应变增加,星形胶质细胞组成的减少也是如此。事实上,我们的模型揭示了星形胶质细胞对淋巴单位组成的贡献程度与产生的机械应力之间存在反比关系。淋巴单位的机械应变增加会降低 CSF 的静脉流出率,这取决于应变程度和感兴趣的特定淋巴单位。例如,毛细血管基底膜的 20%机械应变不会显著降低静脉流出率(流量降低 2%),而星形胶质细胞网络和细胞间隙的相同大小的应变分别降低流出率 7%和 22%。我们的模拟表明,来自生长中的脑肿瘤的固有力直接降低了淋巴液的流体转运,而与癌细胞的生化效应无关。了解这些病理生理学意义对于开发旨在恢复大脑中有效废物清除机制的靶向干预措施至关重要。这项研究为脑肿瘤相关淋巴功能障碍的未来实验研究开辟了潜在途径。