[1] Lin SC, Lin KJ, Hsiao IT, et al.In vivo detection of monoaminergic degeneration in early Parkinson disease by (18)F-9-fluoropropyl-(+)-dihydrotetrabenzazine PET[J]. J Nucl Med,2014,55(1):73-79.
[2] Perlmutter JS, Norris SA.Neuroimaging biomarkers for Parkinson disease: facts and fantasy[J]. Ann Neurol,2014, 76(6):769-783.
[3] Lee CS, Samii A, Sossi V, et al.In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease[J]. Ann Neurol,2000,47(4):493-503.
[4] Ginovart N, Galineau L, Willeit M, et al.Binding characteristics and sensitivity to endogenous dopamine of [11C]-(+)-PHNO, a new agonist radiotracer for imaging the high-affinity state of D2 receptors in vivo using positron emission tomography[J]. J Neurochem,2006,97(4):1089-1103.
[5] Nandhagopal R, Kuramoto L, Schulzer M, et al.Longitudinal evolution of compensatory changes in striatal dopamine processing in Parkinson's disease[J]. Brain,2011,134(Pt 11):3290-3298.
[6] Remy P, Doder M, Lees A, et al.Depression in Parkinson's disease: loss of dopamine and noradrenaline innervation in the limbic system[J]. Brain,2005,128(Pt 6):1314-1322.
[7] Politis M, Wu K, Loane C, et al.Staging of serotonergic dysfunction in Parkinson's disease: an in vivo 11C-DASB PET study[J]. Neurobiol Dis,2010,40(1):216-221.
[8] Bohnen NI, Kaufer DI, Ivanco LS, et al.Cortical choli-nergic function is more severely affected in parkinsonian dementia than in Alzheimer disease: an in vivo positron emission tomographic study[J]. Arch Neurol,2003,60(12):1745-1748.
[9] Bohnen NI, Müller ML, Koeppe RA, et al.History of falls in Parkinson disease is associated with reduced cholinergic activity[J]. Neurology,2009,73(20):1670-1676.
[10] Gjerløff T, Fedorova T, Knudsen K, et al.Imaging acetylcholinesterase density in peripheral organs in Parkinson's disease with 11C-donepezil PET[J]. Brain,2015,138(Pt 3):653-663.
[11] Niethammer M, Eidelberg D.Metabolic brain networks in translational neurology: concepts and applications[J]. Ann Neurol,2012,72(5):635-647.
[12] Shah M, Seibyl J, Cartier A, et al.Molecular imaging insights into neurodegeneration: focus on α-synuclein radiotracers[J]. J Nucl Med,2014,55(9):1397-1400.
[13] Bagchi DP, Yu L, Perlmutter JS, et al.Binding of the radioligand SIL23 to α-synuclein fibrils in Parkinson di-sease brain tissue establishes feasibility and screening approaches for developing a Parkinson disease imaging agent[J]. PLoS One,2013,8(2):e55031.
[14] Petrou M, Dwamena BA, Foerster BR, et al.Amyloid deposition in Parkinson's disease and cognitive impairment: a systematic review[J]. Mov Disord,2015,30(7):928-935.
[15] Villemagne VL, Fodero-Tavoletti MT, Masters CL, et al.Tau imaging: early progress and future directions[J]. Lancet Neurol,2015,14(1):114-124.
[16] Compta Y, Parkkinen L, Kempster P, et al.The significance of α-synuclein, amyloid-β and tau pathologies in Parkinson's disease progression and related dementia[J]. Neurodegener Dis,2014,13(2-3):154-156.
[17] Hirsch EC, Hunot S.Neuroinflammation in Parkinson's disease: a target for neuroprotection?[J]. Lancet Neurol,2009,8(4):382-397.
[18] Ouchi Y, Yoshikawa E, Sekine Y, et al.Microglial activation and dopamine terminal loss in early Parkinson's disease[J]. Ann Neurol,2005,57(2):168-175.
[19] 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]. Neurobiol Dis,2006,21(2):404-412.
[20] Adams JR, van Netten H, Schulzer M, et al. PET in LRRK2 mutations: comparison to sporadic Parkinson's di-sease and evidence for presymptomatic compensation[J]. Brain,2005,128(Pt 12):2777-2785.
[21] Stoessl AJ.Positron emission tomography in premotor Parkinson's disease[J]. Parkinsonism Relat Disord,2007, 13(Suppl 3):S421-S424.
[22] Sakakibara R, Tateno F, Kishi M, et al.MIBG myocardial scintigraphy in pre-motor Parkinson's disease: a review[J]. Parkinsonism Relat Disord,2014,20(3):267-273.
[23] Nandhagopal R, Kuramoto L, Schulzer M, et al. Longitudinal progression of sporadic Parkinson's disease: a multi-tracer positron emission tomography study[J]. Brain.2009 Nov,132(Pt 11):2970-2979.
[24] de la Fuente-Fernández R, Schulzer M, Kuramoto L, et al. Age-specific progression of nigrostriatal dysfunction in Parkinson's disease[J]. Ann Neurol,2011,69(5):803-810.
[25] Stoessl AJ.Central pharmacokinetics of levodopa: Lessons from imaging studies[J]. Mov Disord,2015,30(1):73-79.
[26] Politis M, Wu K, Loane C, et al.Serotonergic mechanisms responsible for levodopa-induced dyskinesias in Parkinson's disease patients[J]. J Clin Invest,2014,124(3):1340-1349.
[27] Ahmed I, Bose SK, Pavese N, et al.Glutamate NMDA receptor dysregulation in Parkinson's disease with dyskinesias[J]. Brain,2011,134(Pt 4):979-986.
[28] Ramlackhansingh AF, Bose SK, Ahmed I, et al.Adenosine 2A receptor availability in dyskinetic and nondyskinetic patients with Parkinson disease[J]. Neurology,2011, 76(21):1811-1816.
