[1] Connolly B S, Lang A E. Pharmacological treatment of Parkinson disease: a review[J]. Jama, 2014, 311(16):1670. [2] Johnson M E, Bobrovskaya L. An update on the rotenone models of Parkinson's disease: Their ability to reproduce the features of clinical disease and model gene-environment interactions[J]. Neurotoxicology, 2015, 46:101. [3] Zhang S, Shao S Y, Song X Y, et al. Protective effects of Forsythia suspense, extract with antioxidant and anti-inflammatory properties in a model of rotenone induced neurotoxicity[J]. Neurotoxicology, 2015, 52:72-83. [4] Wang Y, Shi M, Chung K A, et al. Phosphorylated alpha-synuclein in Parkinson's disease[J]. Science Translational Medicine, 2012, 4(6): 1-27. [5] Sacino A N, Brooks M, McGarvey N H, et al. Induction of CNS alpha-synuclein pathology by fibrillar and non-amyloidogenic recombinant alpha-synuclein[J]. Acta neuropathologica communications 2013, 1: 38. [6] Tenreiro S, Eckermann K, Outeiro T F. Protein phosphorylation in neurodegeneration: friend or foe?[J]. Front Mol Neurosci, 2014, 7:42. [7] Ouchi Y, Yoshikawa E, Sekine Y, et al. Microglial activation and dopamine terminal loss in early Parkinson's disease[J]. Annals of Neurology, 2005, 57(2):168. [8] Gerhard A, Pavese N, Hotton G, et al. In vivo imaging of microglial activation with [11C](R)-PK11195 PET in idiopathic Parkinson's disease.[J]. Neurobiology of Disease, 2006, 21(2):404-412. [9] Soulet D, Rivest S. Microglia[J]. Current Biology Cb, 2008, 18(12):R506. [10] Zhang Q S, Heng Y, Yuan Y H, et al. Pathological-synuclein exacerbates the progression of Parkinson's disease through microglial activation[J]. Toxicology Letters, 2016, 265:30-37. [11] Blumdegen D, Müller T, Kuhn W, et al. Interleukin-1 beta and interleukin-6 are elevated in the cerebrospinal fluid of Alzheimer's and de novo Parkinson's disease patients.[J]. Neuroscience Letters, 1995, 202(1-2):17-20. [12] Mogi M, Harada M, Riederer P, et al. Tumor necrosis factor-alpha (TNF-alpha) increases both in the brain and in the cerebrospinal fluid from parkinsonian patients[J]. Neuroscience Letters, 1994, 165(1-2):208. [13] Gagne J J, Power M C. Anti-inflammatory drugs and risk of Parkinson disease: A meta-analysis[J]. Neurology, 2010, 74(12):995. [14] Manthripragada A D, Schernhammer A E S, Qiu A C D J, et al. Non-steroidal anti-inflammatory drug use and the risk of Parkinson's disease.[J]. Neuroepidemiology, 2011, 36(3):155-161. [15] Minghetti L. Cyclooxygenase-2 (COX-2) in inflammatory and degenerative brain diseases[J]. J Neuropathol Exp Neurol, 2004, 63(9):901. [16] Knott C, Stern G, Wilkin G P. Inflammatory Regulators in Parkinson's Disease: iNOS, Lipocortin-1, and Cyclooxygenases-1 and -2[J]. Molecular & Cellular Neuroscience, 2000, 16(6):724. [17] Sindhu K M, Banerjee R, Senthilkumar K S, et al. Rats with unilateral median forebrain bundle, but not striatal or nigral, lesions by the neurotoxins MPP+ or rotenone display differential sensitivity to amphetamine and apomorphine[J]. Pharmacology Biochemistry & Behavior, 2006, 84(2):321-329. [18] Sindhu K M, Saravanan K S, Mohanakumar K P. Behavioral differences in a rotenone-induced hemiparkinsonian rat model developed following intranigral or median forebrain bundle infusion[J]. Brain Research, 2005, 1051(1-2):25-34. |