Calderón-Garcidueñas Lilian, González-González Luis O, Kulesza Randy J, Fech Tatiana M, Pérez-Guillé Gabriela, Luna Miguel Angel Jiménez-Bravo, Soriano-Rosales Rosa Eugenia, Solorio Edelmira, Miramontes-Higuera José de Jesús, Gómez-Maqueo Chew Aline, Bernal-Morúa Alexia F, Mukherjee Partha S, Torres-Jardón Ricardo, Mills Paul C, Wilson Wayne J, Pérez-Guillé Beatriz, D'Angiulli Amedeo
The University of Montana, Missoula, MT 59812, USA; Universidad del Valle de México, Mexico.
Instituto Nacional de Pediatría, Mexico City 04530, Mexico.
Environ Res. 2017 Oct;158:324-332. doi: 10.1016/j.envres.2017.06.026. Epub 2017 Jun 30.
Delayed central conduction times in the auditory brainstem have been observed in Mexico City (MC) healthy children exposed to fine particulate matter (PM) and ozone (O) above the current United States Environmental Protection Agency (US-EPA) standards. MC children have α synuclein brainstem accumulation and medial superior olivary complex (MSO) dysmorphology. The present study used a dog model to investigate the potential effects of air pollution on the function and morphology of the auditory brainstem.
Twenty-four dogs living in clean air v MC, average age 37.1 ± 26.3 months, underwent brainstem auditory evoked potential (BAEP) measurements. Eight dogs (4 MC, 4 Controls) were analysed for auditory brainstem morphology and histopathology.
MC dogs showed ventral cochlear nuclei hypotrophy and MSO dysmorphology with a significant decrease in cell body size, decreased neuronal packing density with regions in the nucleus devoid of neurons and marked gliosis. MC dogs showed significant delayed BAEP absolute wave I, III and V latencies compared to controls.
MC dogs show auditory nuclei dysmorphology and BAEPs consistent with an alteration of the generator sites of the auditory brainstem response waveform. This study puts forward the usefulness of BAEPs to study auditory brainstem neurodegenerative changes associated with air pollution in dogs. Recognition of the role of non-invasive BAEPs in urban dogs is warranted to elucidate novel neurodegenerative pathways link to air pollution and a promising early diagnostic strategy for Alzheimer's Disease.
在墨西哥城(MC),暴露于高于美国环境保护局(US-EPA)现行标准的细颗粒物(PM)和臭氧(O)环境中的健康儿童,已观察到其听觉脑干的中枢传导时间延迟。MC儿童存在α突触核蛋白在脑干的蓄积以及内侧上橄榄复合体(MSO)形态异常。本研究使用犬模型来探究空气污染对听觉脑干功能和形态的潜在影响。
24只生活在清洁空气环境(对照MC)中的犬,平均年龄37.1±26.3个月,接受脑干听觉诱发电位(BAEP)测量。对8只犬(4只MC犬,4只对照犬)进行听觉脑干形态学和组织病理学分析。
MC犬表现出蜗腹侧核萎缩和MSO形态异常,细胞体大小显著减小,神经元堆积密度降低,核内部分区域无神经元且有明显的胶质增生。与对照犬相比,MC犬的BAEP绝对波I、III和V潜伏期显著延迟。
MC犬表现出听觉核形态异常和BAEP变化,这与听觉脑干反应波形的起源部位改变一致。本研究提出了BAEP在研究与犬空气污染相关的听觉脑干神经退行性变化中的有用性。认识到无创BAEP在城市犬中的作用,对于阐明与空气污染相关的新神经退行性途径以及作为阿尔茨海默病有前景的早期诊断策略是必要的。