Magyar-Sumegi Zsofia Dina, Csendes Mark, Lendvai-Emmert Dominika, Sebestyen Gabriella, Tamas Viktoria, Bandi Szabolcs, Czigler Andras, Yabluchanskiy Andriy, Tarantini Stefano, Ungvari Zoltan, Czeiter Endre, Amrein Krisztina, Orsi Gergely, Perlaki Gabor, Buki Andras, Toth Peter
Department of Neurosurgery, Medical School, University of Pecs, Pecs, Hungary.
Department of Psychiatry and Psychotherapy, Medical School, University of Pecs, Pecs, Hungary.
Geroscience. 2025 May 14. doi: 10.1007/s11357-025-01683-w.
Severe traumatic brain injury (TBI) leads to chronic cognitive decline, imposing a significant societal burden. The regulation of cerebral blood flow (CBF) is critical for cognitive function, and acute disruptions in CBF regulation predict poor TBI outcomes. However, the long-term effects of TBI on CBF regulation and their association with cognitive function remain poorly understood. This study aimed to investigate whether severe TBI results in chronic CBF dysregulation and whether this contributes to long-term cognitive deficits. Additionally, we examined the role of TBI-induced insulin-like growth factor 1 (IGF-1) deficiency in cerebrovascular dysfunction. We assessed cognitive function, basal CBF (via phase contrast MRI), CBF autoregulation (via transcranial Doppler), and neurovascular coupling (NVC) in 33 TBI survivors (mean age 37.6 years, ~ 10 years post-injury) and 21 age-matched healthy controls. Serum IGF-1 levels were also measured. TBI survivors exhibited significant impairments in memory and executive function compared to controls. While basal CBF and autoregulation remained intact, NVC responses were chronically impaired and correlated with cognitive deficits. However, IGF-1 levels did not differ between groups and were not associated with NVC impairment or cognitive function. Our findings indicate that severe TBI results in chronic impairment of neurovascular coupling, which likely contributes to long-term cognitive deficits. These results highlight the need for further research to identify underlying neurovascular mechanisms and develop interventions to restore NVC and cognitive function in TBI survivors.
重度创伤性脑损伤（TBI）会导致慢性认知功能衰退，给社会带来沉重负担。脑血流量（CBF）的调节对认知功能至关重要，CBF调节的急性紊乱预示着TBI预后不良。然而，TBI对CBF调节的长期影响及其与认知功能的关联仍知之甚少。本研究旨在调查重度TBI是否会导致慢性CBF调节异常，以及这是否会导致长期认知缺陷。此外，我们研究了TBI诱导的胰岛素样生长因子1（IGF-1）缺乏在脑血管功能障碍中的作用。我们评估了33名TBI幸存者（平均年龄37.6岁，受伤后约10年）和21名年龄匹配的健康对照者的认知功能、基础CBF（通过相位对比MRI）、CBF自动调节（通过经颅多普勒）和神经血管耦合（NVC）。还测量了血清IGF-1水平。与对照组相比，TBI幸存者在记忆和执行功能方面表现出显著受损。虽然基础CBF和自动调节保持完好，但NVC反应长期受损，并与认知缺陷相关。然而，两组之间的IGF-1水平没有差异，并且与NVC损伤或认知功能无关。我们的研究结果表明，重度TBI会导致神经血管耦合的慢性损伤，这可能导致长期认知缺陷。这些结果凸显了进一步研究以确定潜在神经血管机制并开发干预措施以恢复TBI幸存者的NVC和认知功能的必要性。
