Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Metabolism. 2013 Jan;62 Suppl 1:S27-9. doi: 10.1016/j.metabol.2012.08.025. Epub 2012 Sep 20.
Patients exhibiting the classic manifestations of parkinsonism - tremors, rigidity, postural instability, slowed movements and, sometimes, sleep disturbances and depression - may also display severe cognitive disturbances. All of these particular motoric and behavioral symptoms may arise from Parkinson's disease [PD] per se, but they can also characterize Lewy Body dementia [LBD] or concurrent Parkinson's and Alzheimer's diseases [PD & AD]. Abnormalities of both movement and cognition are also observed in numerous other neurologic diseases, for example Huntington's Disease and the frontotemporal dementia. Distinguishing among these diseases in an individual patient is important in "personalizing" his or her mode of treatment, since an agent that is often highly effective in one of the diagnoses (e.g., L-dopa or muscarinic antagonists in PD) might be ineffective or even damaging in one of the others. That such personalization, based on genetic, biochemical, and imaging-based biomarkers, is feasible is suggested by the numerous genetic abnormalities already discovered in patients with parkinsonism, Alzheimer's disease and Huntington's disease (HD) and by the variety of regional and temporal patterns that these diseases can produce, as shown using imaging techniques.
表现出典型帕金森病特征的患者 - 震颤、僵直、姿势不稳、运动迟缓，有时还伴有睡眠障碍和抑郁 - 也可能出现严重的认知障碍。所有这些特定的运动和行为症状可能源于帕金森病 [PD] 本身，但也可能是路易体痴呆 [LBD] 或同时患有帕金森病和阿尔茨海默病 [PD & AD] 的特征。在许多其他神经疾病中也观察到运动和认知的异常，例如亨廷顿病和额颞叶痴呆。在个体患者中区分这些疾病很重要，因为在一种诊断中通常非常有效的药物（例如，PD 中的左旋多巴或毒蕈碱拮抗剂）在其他诊断中可能无效甚至有害。已经在帕金森病、阿尔茨海默病和亨廷顿病患者中发现了许多遗传异常，并且这些疾病可以使用成像技术显示出多种区域和时间模式，这表明基于遗传、生化和成像生物标志物的个性化治疗是可行的。
