Topalis Anastasios, Bekiari Chrysanthi, Demiri Efterpi, Dionyssiou Dimitrios
From the Department of Plastic Surgery, Faculty of Medicine, School of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Laboratory of Anatomy, Histology and Embryology, Faculty of Veterinary Medicine, School of Health Sciences, Aristotle University, Thessaloniki, Greece.
Plast Reconstr Surg Glob Open. 2025 May 23;13(5):e6806. doi: 10.1097/GOX.0000000000006806. eCollection 2025 May.
Alzheimer disease (AD) is characterized by progressive cognitive function decline and neurodegeneration. Accumulation of amyloid-beta peptides forms plaques leading to brain inflammation and neuronal death. Glymphatic and meningeal lymphatic systems regulate brain fluid homeostasis and affect neurodegeneration by transferring amyloid-beta peptides from the brain to the cervical lymph nodes. We aimed to assess the feasibility of a novel operation in a rat model, to enhance the meningeal lymphatic system and consequently increase the clearance of amyloid-beta peptide.
Ten 12-month-old rats were divided into 2 groups. Group A (control) had no intervention. Group B underwent collagen scaffold implantation between the subdural space above the hippocampus and the right submandibular lymph node, to achieve guided lymphangiogenesis. Animals were weighed and examined for neurological, behavioral and cognitive tests preoperatively and 6 and 12 weeks postoperatively, including NeuroScale, modified open field, and novel object location recognition tests.
One animal of group B died 2 days postoperatively. The remaining rats had no complications, maintained or increased their weight, and showed no signs of infection or neurological impairment. Behavioral tests were in favor of group B at 12 weeks postoperative. Animals of group A had statistically significant decline in cognitive function over time. Animals of group B demonstrated the same or better cognitive function.
In this pilot study, we demonstrated the feasibility of the proposed surgical procedure, which resulted in positive cognitive function for the animals. We are now utilizing an AD rat model to evaluate the possible therapeutic effect of the procedure.
阿尔茨海默病(AD)的特征是进行性认知功能衰退和神经退行性变。β-淀粉样肽的积累形成斑块,导致脑部炎症和神经元死亡。类淋巴系统和脑膜淋巴系统调节脑液稳态,并通过将β-淀粉样肽从脑转移至颈淋巴结来影响神经退行性变。我们旨在评估在大鼠模型中一种新手术的可行性,以增强脑膜淋巴系统,从而增加β-淀粉样肽的清除。
将10只12月龄大鼠分为2组。A组(对照组)不进行干预。B组在海马上方的硬膜下间隙与右下颌下淋巴结之间植入胶原支架,以实现引导性淋巴管生成。术前以及术后6周和12周对动物进行称重,并进行神经学、行为学和认知测试,包括神经量表、改良旷场试验和新物体位置识别试验。
B组1只动物术后2天死亡。其余大鼠无并发症,体重维持或增加,且无感染或神经功能损害迹象。术后12周时行为测试结果有利于B组。随着时间推移,A组动物的认知功能有统计学意义的下降。B组动物表现出相同或更好的认知功能。
在这项初步研究中,我们证明了所提议手术程序的可行性,该程序对动物产生了积极的认知功能。我们现在正在利用AD大鼠模型评估该程序可能的治疗效果。