神经科学
5-羟色胺能
多巴胺
多巴胺能
运动障碍
左旋多巴
黑质
帕金森病
心理学
医学
血清素
内科学
疾病
受体
作者
Sergio Vegas‐Suárez,Elena Paredes-Rodriguez,Asier Aristieta,José Vicente Lafuente,Cristina Miguélez,Luisa Ugedo
出处
期刊:International Review of Neurobiology
日期:2019-01-01
卷期号:: 259-279
被引量:18
标识
DOI:10.1016/bs.irn.2019.06.013
摘要
Parkinson's disease (PD) is characterized by the degeneration of dopaminergic neurons in the substantia nigra, the depletion of striatal dopamine and the presence of Lewy aggregates containing alpha-synuclein. Clinically, there are motor impairments involving cardinal movement symptoms, bradykinesia, resting tremor, muscle rigidity, and postural abnormalities, along with non-motor symptoms such as sleep, behavior and mood disorders. The current treatment for PD focuses on restoring dopaminergic neurotransmission by l-3,4-dihydroxyphenylalanine (levodopa), which loses therapeutic efficacy and induces disabling abnormal involuntary movements known as levodopa-induced dyskinesia (LID) after several years. Evidence indicates that the pathophysiology of both PD and LID disorders is also associated with the dysfunctional activity of the serotonergic (5-HT) neurons that may be responsible for motor and non-motor disturbances. The main population of 5-HT neurons is located in the dorsal raphe nuclei (DRN), which provides extensive innervation to almost the entire neuroaxis and controls multiple functions in the brain. The degeneration of DRN 5-HT neurons occurs in early PD. These neurons can also take exogenous levodopa to transform it into dopamine, which may disturb neuron activity. This review will provide an overview of the underlying mechanisms responsible for 5-HT dysfunction and its clinical relevance in PD and dyskinesia.
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