Departamento de Farmacologia, Centro de Ciências Biológicas, Hospital Universitário, Universidade Federal de Santa Catarina, UFSC, Florianópolis-SC, Brazil.
J Alzheimers Dis. 2010;20 Suppl 1:S205-20. doi: 10.3233/JAD-2010-091459.
Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of the population older than 60 years. Classically, PD is considered to be a motor system disease and its diagnosis is based on the presence of a set of cardinal motor signs (rigidity, bradykinesia, rest tremor) that are consequence of a pronounced death of dopaminergic neurons in the substantia nigra pars compacta. Nowadays there is considerable evidence showing that non-dopaminergic degeneration also occurs in other brain areas which seems to be responsible for the deficits in olfactory, emotional and memory functions that precede the classical motor symptoms in PD. The present review attempts to examine results reported in epidemiological, clinical and animal studies to provide a comprehensive picture of the antiparkinsonian potential of caffeine. Convergent epidemiological and pre-clinical data suggest that caffeine may confer neuroprotection against the underlying dopaminergic neuron degeneration, and influence the onset and progression of PD. The available data also suggest that caffeine can improve the motor deficits of PD and that adenosine A2A receptor antagonists such as istradefylline reduces OFF time and dyskinesia associated with standard 'dopamine replacement' treatments. Finally, recent experimental findings have indicated the potential of caffeine in the management of non-motor symptoms of PD, which do not improve with the current dopaminergic drugs. Altogether, the studies reviewed provide strong evidence that caffeine may represent a promising therapeutic tool in PD, thus being the first compound to restore both motor and non-motor early symptoms of PD together with its neuroprotective potential.
帕金森病（PD）是影响 60 岁以上人群约 1%的第二大常见神经退行性疾病。经典地，PD 被认为是一种运动系统疾病，其诊断基于一组主要运动体征（僵硬、运动迟缓、静止性震颤）的存在，这些体征是由于黑质致密部多巴胺能神经元的明显死亡所致。如今，有相当多的证据表明，非多巴胺能变性也发生在其他脑区，这似乎是导致 PD 中经典运动症状之前出现嗅觉、情绪和记忆功能缺陷的原因。本综述试图检查流行病学、临床和动物研究中报告的结果，以提供咖啡因抗帕金森作用的全面图景。趋同的流行病学和临床前数据表明，咖啡因可能对潜在的多巴胺能神经元变性提供神经保护作用，并影响 PD 的发病和进展。现有数据还表明，咖啡因可以改善 PD 的运动障碍，而腺苷 A2A 受体拮抗剂，如伊曲茶碱，可减少与标准“多巴胺替代”治疗相关的关期和运动障碍。最后，最近的实验发现表明咖啡因在管理 PD 的非运动症状方面具有潜力，这些症状不能通过目前的多巴胺能药物改善。总之，综述研究提供了有力的证据表明，咖啡因可能是 PD 治疗的一种有前途的工具，因为它是第一种能够恢复 PD 的运动和非运动早期症状及其神经保护潜力的化合物。
