[1] Lin C H, Chen M L, Tai Y C, et al. Reaffirmation of GAK, but not HLA-DRA, as a Parkinson's disease susceptibility gene in a Taiwanese population [J]. Am J Med Genet B Neuropsychiatr Genet, 2013, 162B (8): 841-846. [2] Mizuta I, Takafuji K, Ando Y, et al. YY1 binds to alpha-synuclein 3,-flanking region SNP and stimulates antisense noncoding RNA expression [J]. J Hum Genet, 2013, 58 (11): 711-719. [3] Brockmann K, Schulte C, Hauser A K, et al. SNCA: major genetic modifier of age at onset of Parkinson's disease [J]. Mov Disord, 2013, 28 (9): 1217-1221. [4] Chang C, Lang H, Geng N, et al. Exosomes of BV-2 cells induced by alpha-synuclein: important mediator of neurodegeneration in PD [J]. Neurosci Lett, 2013, 548: 190-195. [5] Shaltiel-Karyo R, Frenkel-Pinter M, Rockenstein E, et al. A blood-brain barrier (BBB) disrupter is also a potent alpha-synuclein (alpha-syn) aggregation inhibitor: a novel dual mechanism of mannitol for the treatment of Parkinson disease (PD) [J]. J Biol Chem, 2013, 288 (24): 17579-17588. [6] Schulz-Schaeffer W J. The synaptic pathology of α-synuclein aggregation in dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia [J]. Acta Neuropathol, 2010, 120 (2): 131-143. [7] Specht C G, Tigaret C M, Rast G F, et al. Subcellular localisation of recombinant alpha-and gamma-synuclein [J]. Mol Cell Neurosci, 2005, 28 (2):326-334. [8] Al-Wandi A, Ninkina N, Millership S, et al. Absence of alpha-synuclein affects dopamine metabolism and synaptic markers in the striatum of aging mice[J]. Neurobiol Aging, 2010, 31 (5):796-804. [9] Kirkitadze M D, Bitan G, Teplow D B. Paradigm shifts in Alzheimer's disease and other neurodegenerative disorders: the emerging role of oligomeric assemblies [J]. J Neurosci Res, 2002, 69 (5): 567-577. [10] Yu S, Li X, Liu G, et al. Extensive nuclear localization of alpha-synuclein in normal rat brain neurons revealed by a novel monoclonal antibody [J]. Neuroscience, 2007, 145 (2): 539-555. [11] 尹娜, 陈予东,李昕,等. 帕金森病患者血浆增强α-突触核蛋白寡聚体形成[J]. 首都医科大学学报. 2013(06) :840-843. [12] Liu G, Chen M, Mi N, et al. Increased oligomerization and phosphorylation of α-synuclein are associated with decreased activity of glucocerebrosidase and protein phosphatase 2A in aging monkey brains [J]. Neurobiol Aging, 2015, 36 (9): 2649-2659. [13] 杨斌,杨巍巍,李昕,等. α-突触核蛋白和硝基化α-突触核蛋白在不同年龄段食蟹猴结肠中的表达 [J]. 首都医科大学学报,2014,35(2): 214-218. [14] 李昕, 杨巍巍,李旭冉,等. 寡聚化α-突触核蛋白在不同年龄段食蟹猴消化道中的表达[J]. 首都医科大学学报,2014,35(5) :592-595. [15] 张明华, 杨巍巍,李昕,等. 缺血性卒中患者血浆磷酸化α-突触核蛋白水平及磷酸化形成比例的改变[J]. 中国脑血管病杂志,2014,11(9) :476-479. [16] Li W, Lesuisse C, Xu Y, et al. Stabilization of α-synuclein protein with aging and familial Parkinson's disease-linked A53T mutation [J]. J Neurosci, 2004, 24 (33): 7400-7409. [17] Chu Y, Kordower J H. Age-associated increases of α-synuclein in monkeys and humans are associated with nigrostriatal dopamine depletion: is this the target for Parkinson's disease [J]. Neurobiology Dis, 2007, 25 (1): 134-149. [18] Xuan Q, Xu S L, Lu D H, et al. Increase expression of α-synuclein in aged human brain associated with neuromelanin accumulation [J]. J Neural Transm, 2011, 118 (11): 1575-1583. |