Krasko Maryann N, Hoffmeister Jesse D, Schaen-Heacock Nicole E, Welsch Jacob M, Kelm-Nelson Cynthia A, Ciucci Michelle R
Department of Surgery, University of Wisconsin-Madison, Madison, WI 53792, USA.
Department of Communication Sciences and Disorders, University of Wisconsin-Madison, Madison, WI 53706, USA.
Brain Sci. 2021 Jul 13;11(7):925. doi: 10.3390/brainsci11070925.
Parkinson's disease (PD) is a progressive, degenerative disorder that affects 10 million people worldwide. More than 90% of individuals with PD develop hypokinetic dysarthria, a motor speech disorder that impairs vocal communication and quality of life. Despite the prevalence of vocal deficits in this population, very little is known about the pathological mechanisms underlying this aspect of disease. As such, effective treatment options are limited. Rat models have provided unique insights into the disease-specific mechanisms of vocal deficits in PD. This review summarizes recent studies investigating vocal deficits in 6-hydroxydopamine (6-OHDA), alpha-synuclein overexpression, , and rat models of PD. Model-specific changes to rat ultrasonic vocalization (USV), and the effects of exercise and pharmacologic interventions on USV production in these models are discussed.
帕金森病（PD）是一种渐进性退行性疾病，全球有1000万人受其影响。超过90%的帕金森病患者会出现运动性构音障碍，这是一种运动性言语障碍，会损害言语交流和生活质量。尽管该人群中存在普遍的发声缺陷，但对于疾病这一方面的病理机制却知之甚少。因此，有效的治疗选择有限。大鼠模型为深入了解帕金森病中发声缺陷的疾病特异性机制提供了独特的视角。本综述总结了最近关于6-羟基多巴胺（6-OHDA）、α-突触核蛋白过表达以及帕金森病大鼠模型中发声缺陷的研究。讨论了这些模型中大鼠超声波发声（USV）的模型特异性变化，以及运动和药物干预对USV产生的影响。
