Page 72 - Read Online
P. 72
Page 140 Chalatsa et al. Neuroimmunol Neuroinflammation 2020;7:132-40 I http://dx.doi.org/10.20517/2347-8659.2020.01
70. Shi M, Liu C, Cook TJ, Bullock KM, Zhao Y, et al. Plasma exosomal α-synuclein is likely CNS-derived and increased in Parkinson’s
disease. Acta Neuropathol 2014;128:639-50.
71. Shi M, Kovac A, Korff A, Cook TJ, Ginghina C, et al. CNS tau efflux via exosomes is likely increased in Parkinson’s disease but not in
Alzheimer’s disease. Alzheimers Dement 2016;12:1125-31.
72. Tomlinson PR, Zheng Y, Fischer R, Heidasch R, Gardiner C, et al. Identification of distinct circulating exosomes in Parkinson’s disease.
Ann Clin Transl Neurol 2015;2:353-61.
73. Papadopoulos VE, Nikolopoulou G, Antoniadou I, Karachaliou A, Arianoglou G, et al. Modulation of β-glucocerebrosidase increases
α-synuclein secretion and exosome release in mouse models of Parkinson’s disease. Hum Mol Genet 2018;27:1696-710.
74. Parnetti L, Paciotti S, Eusebi P, Dardis A, Zampieri S, et al. Cerebrospinal fluid β-glucocerebrosidase activity is reduced in parkinson’s
disease patients. Mov Disord 2017;32:1423-31.
75. Cerri S, Ghezzi C, Sampieri M, Siani F, Avenali M, et al. The exosomal/total α-synuclein ratio in plasma is associated with
glucocerebrosidase activity and correlates with measures of disease severity in PD patients. Front Cell Neurosci 2018;12:125.
76. Gui YX, Liu H, Zhang LS, Lv W, Hu XY. Altered microRNA profiles in cerebrospinal fluid exosome in Parkinson disease and Alzheimer
disease. Oncotarget 2015;6:37043-53.
77. Peelaerts W, Bousset L, Van der Perren A, Moskalyuk A, Pulizzi R, et al. alpha-Synuclein strains cause distinct synucleinopathies after
local and systemic administration. Nature 2015;522:340-4.
78. Lee SJ, Masliah E. Neurodegeneration: aggregates feel the strain. Nature 2015;522:296-7.
79. De Toro J, Herschlik L, Waldner C, Mongini C. Emerging roles of exosomes in normal and pathological conditions: new insights for
diagnosis and therapeutic applications. Front Immunol.2015;6:203.