Department Organs of Sense, ENT Section, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy; Department of Surgical Science, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.
Department Organs of Sense, ENT Section, 'Sapienza' University of Rome, Viale del Policlinico 155, 00100, Rome, Italy.
Autoimmun Rev. 2016 Oct;15(10):1005-11. doi: 10.1016/j.autrev.2016.07.022. Epub 2016 Aug 4.
Parkinson's disease is a neurodegenerative disease that causes the death of dopaminergic neurons in the substantia nigra. The resulting dopamine deficiency in the basal ganglia leads to a movement disorder that is characterized by classical parkinsonian motor symptoms. Parkinson's disease is recognized as the most common neurodegenerative disorder after Alzheimer's disease. PD ethiopathogenesis remains to be elucidated and has been connected to genetic, environmental and immunologic conditions. The past decade has provided evidence for a significant role of the immune system in PD pathogenesis, either through inflammation or an autoimmune response. Several autoantibodies directed at antigens associated with PD pathogenesis have been identified in PD patients. This immune activation may be the cause of, rather than a response to, the observed neuronal loss. Parkinsonian motor symptoms include bradykinesia, muscular rigidity and resting tremor. The non-motor features include olfactory dysfunction, cognitive impairment, psychiatric symptoms and autonomic dysfunction. Microscopically, the specific degeneration of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies, which are brain deposits containing a substantial amount of α-synuclein, have been recognized. The progression of Parkinson's disease is characterized by a worsening of motor features; however, as the disease progresses, there is an emergence of complications related to long-term symptomatic treatment. The available therapies for Parkinson's disease only treat the symptoms of the disease. A major goal of Parkinson's disease research is the development of disease-modifying drugs that slow or stop the neurodegenerative process. Drugs that enhance the intracerebral dopamine concentrations or stimulate dopamine receptors remain the mainstay treatment for motor symptoms. Immunomodulatory therapeutic strategies aiming to attenuate PD neurodegeneration have become an attractive option and warrant further investigation.
帕金森病是一种神经退行性疾病，导致黑质中多巴胺能神经元死亡。基底节中多巴胺的缺乏导致运动障碍，其特征是典型的帕金森运动症状。帕金森病是继阿尔茨海默病之后最常见的神经退行性疾病。PD 的发病机制仍有待阐明，并与遗传、环境和免疫条件有关。过去十年的研究为免疫系统在 PD 发病机制中的重要作用提供了证据，无论是通过炎症还是自身免疫反应。在帕金森病患者中已经鉴定出几种针对与帕金森病发病机制相关抗原的自身抗体。这种免疫激活可能是观察到的神经元丢失的原因，而不是对其的反应。帕金森运动症状包括运动迟缓、肌肉僵硬和静止性震颤。非运动症状包括嗅觉功能障碍、认知障碍、精神症状和自主神经功能障碍。从显微镜下可以看到，黑质中多巴胺能神经元的特定退化和路易体的存在，路易体是含有大量α-突触核蛋白的脑沉积物。帕金森病的进展特征是运动特征的恶化；然而，随着疾病的进展，出现了与长期对症治疗相关的并发症。目前用于治疗帕金森病的方法只能治疗疾病的症状。帕金森病研究的一个主要目标是开发能够减缓或阻止神经退行性过程的疾病修饰药物。提高脑内多巴胺浓度或刺激多巴胺受体的药物仍然是治疗运动症状的主要方法。旨在减轻 PD 神经退行性变的免疫调节治疗策略已成为一种有吸引力的选择，并值得进一步研究。
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