Fernández-Espejo Emilio, Rodriguez de Fonseca Fernando, Suárez Juan, Martín de Pablos Ángel
Reial Acadèmia de Medicina de Catalunya, 08010 Barcelona, Spain; Red Andaluza de Investigación Clínica y Traslacional en Neurología (Neuro-RECA), Laboratorio de Medicina Regenerativa, Hospital Regional Universitario, 29010 Málaga, Spain.
Unidad de Gestión Clínica de Salud Mental, Hospital Regional Universitario, Instituto de Investigación Biomédica de Málaga (IBIMA), 29010 Málaga, Spain; Red Andaluza de Investigación Clínica y Traslacional en Neurología (Neuro-RECA), Laboratorio de Medicina Regenerativa, Hospital Regional Universitario, 29010 Málaga, Spain.
Brain Res. 2021 Mar 5;1761:147411. doi: 10.1016/j.brainres.2021.147411.
Lactoperoxidase (LPO) is proposed to play a role in the pathogenesis of Parkinson's disease (PD). This enzyme has been reported to be enhanced in the cerebrospinal fluid (CSF) in parkinsonian patients. The objective was to look at the relationship of LPO in the CSF and serum with clinical features of idiopathic PD. LPO concentration was analyzed through ELISA techniques. Correlation of CSF or serum LPO and MDS-UPDRS, dopaminergic medication, and other clinical parameters was examined. The findings revealed that LPO concentration in the CSF, not serum, was found to be elevated in patients with PD relative to controls (p < 0.001). CSF LPO concentration negatively correlated with MDS-UPDRS part-IV score (p < .0001), a rating scale that allows evaluating motor complications. CSF LPO level inversely correlated with the dose intensity of the dopaminergic medication regimen, as evaluated with levodopa equivalent dose or LED (mg/day; p < .0001). LED value positively correlated with MDS-UPDRS part-IV score (p < .0001). To sum up, the findings indicate that CSF LPO is found to be elevated in the CSF of PD patients, and this enzyme holds promise as potential biomarker for diagnosis of PD. Increasing the dose intensity of the dopaminergic medication regimen attenuates the elevation in LPO levels in the CSF, and it facilitates the development of motor complications in patients. The pathophysiological mechanisms that seem to be responsible for LPO increase would include dopamine deficiency, oxidative stress, and less likely, microbial infection.
乳过氧化物酶(LPO)被认为在帕金森病(PD)的发病机制中起作用。据报道,帕金森病患者脑脊液(CSF)中的这种酶水平会升高。目的是研究CSF和血清中LPO与特发性PD临床特征之间的关系。通过酶联免疫吸附测定(ELISA)技术分析LPO浓度。检测CSF或血清LPO与运动障碍协会统一帕金森病评定量表(MDS-UPDRS)、多巴胺能药物及其他临床参数之间的相关性。研究结果显示,与对照组相比,PD患者CSF中的LPO浓度升高,而血清中的LPO浓度未升高(p < 0.001)。CSF中LPO浓度与MDS-UPDRS第四部分评分呈负相关(p < 0.0001),MDS-UPDRS第四部分评分是用于评估运动并发症的量表。CSF中LPO水平与多巴胺能药物治疗方案的剂量强度呈负相关,以左旋多巴等效剂量(LED,mg/天)评估时,二者相关性显著(p < 0.0001)。LED值与MDS-UPDRS第四部分评分呈正相关(p < 0.0001)。综上所述,研究结果表明,PD患者CSF中的LPO水平升高,这种酶有望成为诊断PD的潜在生物标志物。增加多巴胺能药物治疗方案的剂量强度可减弱CSF中LPO水平的升高,并促使患者出现运动并发症。导致LPO升高的病理生理机制可能包括多巴胺缺乏、氧化应激,微生物感染的可能性较小。