ライフサイエンスコーパス: alpha-synuclein

1 levels of glucocerebrosidase and oligomeric alpha-synuclein.

2 y lipoprotein receptor-related protein 2 and alpha-synuclein.

3 st, it has a direct proaggregatory effect on alpha-synuclein.

4 A53T-SNCA) mice overexpressing mutated human alpha-synuclein.

5 the mechanism observed for amyloid-beta and alpha-synuclein.

6 as paralleled in mice overexpressing mutated alpha-synuclein.

7 erminus affect the aggregation propensity of alpha-synuclein.

8 parkinsonism demonstrated elevated levels of alpha-synuclein.

9 kdown increased the lysosomal degradation of alpha-synuclein.

10 by a peptide derived from residues 36-55 of alpha-synuclein.

11 nd nitric oxide (NO), in response to LPS and alpha-synuclein.

12 rent length fibrilized slower than wild-type alpha-synuclein.

13 f Lewy body inclusions containing aggregated alpha-synuclein.

14 efined set of peptides that are derived from alpha-synuclein, a protein aggregated in Parkinson's dis

15 cellular uptake of aggregates consisting of alpha-synuclein, a protein forming amyloid aggregates in

16 ditionally, the presence of PD-related human alpha-synuclein A53T mutant or dopamine transporter (DAT

17 crotubule disruption or co-transfection with alpha-synuclein A53T, a PD-associated mutation, caused T

18 activity was associated with increased total alpha-synuclein accumulation in both these models.

19 was identified in a screen as a modulator of alpha-synuclein accumulation in vivo.

20 alpha-Synuclein accumulation is a pathological hallmark

21 zymatic activity, lysosomal dysfunction, and alpha-synuclein accumulation.

22 Our study identifies alpha-synuclein acetylation as a key regulatory mechanis

23 in vitro and in vivo modulates the levels of alpha-synuclein acetylation, its aggregation, and autoph

24 ere and point to a possible relation between alpha-synuclein aggregates and insulin resistance.

25 ltiple system atrophy is the accumulation of alpha-synuclein aggregates in oligodendrocytes, forming

26 s mainly in the form of small phosphorylated alpha-synuclein aggregates that are associated with chan

27 synuclein, observing a dramatic reduction of alpha-synuclein aggregation and an almost complete elimi

28 Genetics and neuropathology strongly link alpha-synuclein aggregation and neurotoxicity to the pat

29 tion as a key regulatory mechanism governing alpha-synuclein aggregation and toxicity, demonstrating

30 Second, SUMOylation facilitates alpha-synuclein aggregation by blocking its ubiquitin-de

31 ylation of alpha-synuclein by PIAS2 promotes alpha-synuclein aggregation by two mutually reinforcing

32 Finally, a gradient of phosphorylated alpha-synuclein aggregation in synapses (pre > pre + pos

33 and antiviral activity, dramatically affects alpha-synuclein aggregation in vitro and in vivo.

34 phingosine, sphingosine-1-phosphate) promote alpha-synuclein aggregation in vitro, glucosylsphingosin

35 y such alpha-synuclein sequence extension on alpha-synuclein aggregation propensity are, however, not

36 t to deliver an antibody designed to inhibit alpha-synuclein aggregation, and show that it can lead t

37 Besides alpha-synuclein aggregation, mitochondrial dysfunction a

38 deletion of the gene encoding c-Abl reduced alpha-synuclein aggregation, neuropathology, and neurobe

39 ive c-Abl in hA53Talpha-syn mice accelerated alpha-synuclein aggregation, neuropathology, and neurobe

40 nds exhibited significant protection against alpha-synuclein aggregation-induced cytotoxicity in SH-S

41 s plays a critical role in the regulation of alpha-synuclein aggregation.

42 early-onset locomotor deficits, and abundant alpha-synuclein aggregation.

43 features of PD: dopaminergic cell death and alpha-synuclein aggregation.

44 in (Abeta42), a decapeptide Abeta(14-23) and alpha-synuclein; all three systems demonstrate a dramati

45 Alpha synuclein (alpha-syn) is a central player in neuro

46 of evidence support the causal link between alpha-synuclein (alpha-syn) accumulation in the brain an

47 gical hallmark of MSA is the accumulation of alpha-synuclein (alpha-syn) aggregates in affected oligo

48 ct cell-to-cell transmission of proteopathic alpha-synuclein (alpha-syn) aggregates is thought to und

49 alpha-Synuclein (alpha-syn) aggregation is a key event i

50 other toxic protein aggregates such as tau, alpha-synuclein (alpha-Syn) and islet amyloid polypeptid

51 characterized by progressive accumulation of alpha-synuclein (alpha-syn) and jointly termed synuclein

52 Although trace levels of phosphorylated alpha-synuclein (alpha-syn) are detectable in normal bra

53 the Parkinson's disease (PD)-related protein alpha-synuclein (alpha-SYN) can propagate from cell to c

54 otion that prion-like spreading of misfolded alpha-synuclein (alpha-SYN) causes Parkinson's disease (

55 The accumulation of alpha-synuclein (alpha-syn) fibrils in neuronal inclusio

56 otor disorder associated with aggregation of alpha-synuclein (alpha-syn) in the substantia-nigra (SN)

57 Alpha-synuclein (alpha-SYN) is a central molecule in Par

58 alpha-synuclein (alpha-SYN) is a major pathologic contri

59 Alpha-synuclein (alpha-syn) is involved in both familial

60 Cell-to-cell spreading of misfolded alpha-synuclein (alpha-syn) is suggested to contribute t

61 LBs are protein-rich inclusions, in which alpha-synuclein (alpha-syn) is the most abundant protein

62 Although a causative role of alpha-synuclein (alpha-syn) is well established in Parki

63 Synaptic protein alpha-synuclein (alpha-SYN) modulates neurotransmission

64 uman astrocytes actively transfer aggregated alpha-synuclein (alpha-SYN) to healthy astrocytes via di

65 ased calcineurin activity is associated with alpha-synuclein (alpha-syn) toxicity, a protein implicat

66 OAG-4 by characterizing its interaction with alpha-synuclein (alpha-Syn).

67 sion of misfolded preformed fibrils (PFF) of alpha-synuclein (alpha-syn).

68 pc) and widespread aggregates of the protein alpha-synuclein (alpha-syn).

69 To decipher the seeding mechanisms of alpha-synuclein (alphaS) aggregates in human cells, we v

70 alpha-Synuclein (alphaS) forms round cytoplasmic inclusi

71 The intrinsically disordered human protein alpha-Synuclein (alphaS) has a prominent role in Parkins

72 To examine the pathogenic role of alpha-synuclein (alphaS) in Parkinson's Disease, we have

73 The misfolding and accumulation of alpha-synuclein (alphaS) inclusions are found in a numbe

74 Although the self-assembly of alpha-synuclein (alphaS) into oligomers and amyloid fibr

75 Misfolded alpha-synuclein (alphaS) is hypothesized to spread throu

76 alpha-Synuclein (alphaS) is the primary protein associat

77 The protein alpha-synuclein (alphaS) self-assembles into small oligo

78 es express the Lewy body constituent protein alpha-synuclein (alphaS), we not only find that this pro

79 defined by inclusions containing aggregated alpha-synuclein (alphaS).

80 alpha-Synuclein (alphaSyn) is the major gene linked to s

81 rders, such as amyloid-beta (Abeta), tau, or alpha-synuclein (alphaSyn) might be the major deleteriou

82 nscriptional networks and protect cells from alpha-synuclein (alphaSyn) toxicity.

83 Increasing dopamine synthesis or alpha-synuclein amounts in mouse midbrain neurons recapi

84 ion, we analyzed the interaction between the alpha-synuclein amyloid fibrils and heparan sulfate and

85 pH-sensitive probe, that internalization of alpha-synuclein amyloid fibrils in neuroblastoma cells i

86 ase (PD) is associated with the formation of alpha-synuclein amyloid fibrils.

87 lore the relationship between salivary total alpha-synuclein and alpha-synuclein SNP variants levels.

88 rains, and it is accompanied by increases in alpha-synuclein and impairment of the autophagy-lysosoma

89 protein metal-complexes (like amyloid-beta, alpha-synuclein and prion-protein).

90 Thus, beta2AR is linked to transcription of alpha-synuclein and risk of PD in a ligand-specific fash

91 ing therapies targeting tau, amyloid-beta or alpha synuclein, and to stratify them by level of Alzhei

92 nce of Lewy bodies, depositions of insoluble alpha-synuclein, and other proteins that likely contribu

93 membrane binding, impaired the clearance of alpha-synuclein, and promoted the accumulation of toxic

94 other proteins, including amyloid-beta, tau, alpha-synuclein, and serum amyloid A, misfold into disti

95 the claim that pathological accumulation of alpha-synuclein, and subsequent synaptic disruption, occ

96 how that several proteins, including TDP-43, alpha-synuclein, and the microtubule-associated protein

97 tudy aggregates from other proteins, such as alpha-synuclein, and to probe the effects of complex bio

98 ) + rapamycin (RAP) induced both strong anti-alpha-synuclein antibody titers and regulatory T cells (

99 The toxic properties of alpha-synuclein are conserved from yeast to man, but the

100 suggests that the small soluble oligomers of alpha-synuclein are more toxic than the larger aggregate

101 ber mutations implicate excess production of alpha-synuclein as a possibly causative factor in Parkin

102 The analysis of the alpha-synuclein (aS) aggregation process, which is invol

103 alpha-Synuclein (aS) is a protein abundant in presynapti

104 otein plays a role in neuronal toxicities of alpha-synuclein (ASYN) in neurodegenerative disease such

105 alpha-Synuclein (aSyn) is the main driver of neurodegene

106 ed virus (AAV) 1/2-driven human mutated A53T alpha-synuclein (aSyn)-overexpressing PD rat model (AAV1

107 mally soluble intracellular proteins tau and alpha-synuclein become insoluble and filamentous.

108 r results demonstrate that whereas monomeric alpha-synuclein blocks the autocatalytic proliferation o

109 ition of MARKs led to increased pathological alpha-synuclein burden.

110 aptic changes in rats that overexpress human alpha-synuclein by local injection of viral-vectors in m

111 Our observations suggest that SUMOylation of alpha-synuclein by PIAS2 promotes alpha-synuclein aggreg

112 blem, the fusions of fluorescent proteins to alpha-synuclein C-terminus are often used in cellular an

113 models of disease that support the idea that alpha-synuclein can act as a prion.

114 ress these questions, we prepared mutants of alpha-synuclein carrying additional moieties of differen

115 llowing intraparenchymal injections of human alpha-synuclein carrying viral vectors, pathological acc

116 42-residue form of Abeta) fibrils, fibrillar alpha-synuclein catalyses the heterogeneous nucleation o

117 IFICANCE STATEMENT: Overexpression of mutant alpha-synuclein causes Parkinson's disease, presumably b

118 lity and non-cell-autonomous factors such as alpha-synuclein cell-to-cell propagation and neuroinflam

119 We then immunized mice with both chaperone/alpha-synuclein combinations using monomeric or oligomer

120 Exogenous application of low unfolded alpha-synuclein concentrations is able to increase the A

121 Furthermore, alpha-synuclein contributes to the fibrilization of amyl

122 els of alpha-synuclein in part by increasing alpha-synuclein degradation.

123 different E3 ubiquitin ligases and regulates alpha-synuclein degradation.

124 at NCEH-1 protects dopaminergic neurons from alpha-synuclein-dependent neurotoxicity in C. elegans vi

125 Between 19% and 25% of phosphorylated alpha-synuclein deposits were found in presynaptic termi

126 Intracellular alpha-synuclein deposits, known as Lewy bodies, have bee

127 eased phosphorylated and detergent-insoluble alpha-synuclein deposits.

128 alpha-Synuclein disease mutants are more SUMOylated comp

129 Alterations in alpha-synuclein dosage lead to familial Parkinson's dise

130 teins or the Amyloid-beta42 peptide, but not alpha-Synuclein, enhances Cdk5-dependent phosphorylation

131 of total and phosphorylated (S129) monomeric alpha-synuclein, evidence of amyloid oligomers and incre

132 nstrating that different structural forms of alpha-synuclein exert different effects on Abeta aggrega

133 nalysis in our new model to demonstrate that alpha-synuclein expression promotes reorganization of th

134 reduced striatal dopamine content, disrupted alpha-synuclein expression, deficits in motor function,

135 egenerative processes triggered by increased alpha-synuclein expression.

136 his, we manipulated both dopamine levels and alpha-synuclein expression.

137 Following alpha-synuclein fibril treatment, neurons deficient in T

138 We also show that alpha-synuclein fibril uptake in an oligodendrocyte-like

139 We also discuss whether different strains of alpha-synuclein fibrils can underlie differences in cell

140 In this study, two morphologically different alpha-synuclein fibrils, one helical and the other ribbo

141 ted in increased susceptibility to exogenous alpha-synuclein fibrils.

142 ed mutations (A30P, E46K, G51D, and A53T) on alpha-synuclein fibrils.

143 ue for characterizing structural features of alpha-synuclein fibrils.

144 ation, and find that this compound displaces alpha-synuclein from the surfaces of such vesicles, ther

145 renoreceptor (beta2AR) is a regulator of the alpha-synuclein gene (SNCA).

146 yrosine cross-links in peptides of Abeta and alpha-synuclein generated in vitro by enzymatic peroxida

147 In vivo imaging studies of alpha-synuclein-GFP transgenic mice using two-photon mic

148 cell models expressing mutant huntingtin and alpha-synuclein, given that both of these proteins cause

149 plish this goal, we overexpressed human A53T-alpha- synuclein (hA53T-alpha-syn) in the rat nigrostria

150 Animals overexpressing alpha-synuclein had progressive motor impairment and, 12

151 The protein alpha-synuclein has a central role in the pathogenesis o

152 The complex interplay between Abeta and alpha-synuclein has led to seemingly contradictory resul

153 ich is the exact opposite of the effect that alpha-synuclein has on dopaminergic neurons, where its a

154 populated during the aggregation process of alpha-synuclein have been linked to neuronal impairment

155 -terminal truncations of monomeric wild-type alpha-synuclein (henceforth WT-alphaS) have been shown t

156 nd mesoscopic self-assembly of amyloid-beta, alpha synuclein, human islet amyloid polypeptide and pri

157 enous THSer(P)-31 was detected in VMAT2- and alpha-synuclein-immunoprecipitated mouse brain samples.

158 ts to analyse the presence of phosphorylated alpha-synuclein immunoreactivity at the synapse and thei

159 The cellular origin of alpha-synuclein in GCI and a 'prion hypothesis' are disc

160 s disease (PD) patients accumulate misfolded alpha-synuclein in LBs, the diagnostic signatures of PD.

161 metabolism and location of mutant LRRK2 and alpha-synuclein in living neurons at the single-cell lev

162 Although the exact role of alpha-synuclein in neural transmission is not completely

163 esicular monoamine transporter 2 (VMAT2) and alpha-synuclein in neuroblastoma cells, and endogenous T

164 In conclusion, pathological alpha-synuclein in nigro-striatal axonal terminals leads

165 Nrf2 decreased steady-state levels of alpha-synuclein in part by increasing alpha-synuclein de

166 se in PIAS2 expression along with SUMOylated alpha-synuclein in PD brains, providing a causal mechani

167 ementia with Lewy bodies show aggregation of alpha-synuclein in precerebellar brainstem structures.

168 nuclein mobility and enhances aggregation of alpha-synuclein in primary cultured neurons and in dopam

169 these mice also exhibited an accumulation of alpha-synuclein in the brain, along with increased conve

170 ce with GZ667161 reduced membrane-associated alpha-synuclein in the CNS and ameliorated cognitive def

171 oxide induced a profound increase in soluble alpha-synuclein in the CNS and exacerbated cognitive and

172 igated the effect of overexpression of human alpha-synuclein in the substantia nigra of aged (18 to 2

173 may increase the progression of pathological alpha-synuclein inclusions after the initial formation o

174 In Parkinson's disease, intracellular alpha-synuclein inclusions form in neurons.

175 u neurofibrillary tangles, neuritic plaques, alpha-synuclein inclusions, and other pathological chang

176 ngosine promotes pathological aggregation of alpha-synuclein, increasing PD risk in GD patients and c

177 dings suggest new therapeutic approaches for alpha-synuclein induced neurodegeneration.

178 levels in mice expressing human A53T mutant alpha-synuclein induced progressive nigrostriatal degene

179 uronal cultures and four candidates enhanced alpha-synuclein-induced neurodegeneration in Drosophila.

180 ition of intrinsically disordered, monomeric alpha-synuclein into beta-sheet-rich oligomers and fibri

181 transmission of TAR DNA-binding protein and alpha-synuclein, involved in amyotrophic lateral scleros

182 We suggest that prion-like behavior of alpha-synuclein is a key component in Parkinson's diseas

183 We found that alpha-synuclein is acetylated on lysines 6 and 10 and th

184 hallmarks of Parkinson's disease (PD), where alpha-synuclein is also a key player.

185 alpha-synuclein is an intrinsically disordered protein t

186 Although phosphorylated alpha-synuclein is believed to exert toxic effects at th

187 The self-assembly of alpha-synuclein is closely associated with Parkinson's d

188 tion of the amyloid-beta peptide (Abeta) and alpha-synuclein is commonly observed in a range of neuro

189 These results indicate that phosphorylated alpha-synuclein is found at the presynaptic terminals of

190 dysregulation of autophagy, suggesting that alpha-synuclein is highly beneficial to advanced melanom

191 We found that phosphorylated alpha-synuclein is present exclusively in dementia with

192 Ubiquitinated alpha-synuclein is targeted to proteasomal or lysosomal

193 ionally impacts neurodegeneration induced by alpha-synuclein is undefined.

194 racytoplasmic inclusions formed by misfolded alpha-synuclein known as Lewy bodies (LBs).

195 in leucine-rich repeat kinase 2 (LRRK2) and alpha-synuclein lead to Parkinson's disease (PD).

196 We report that PIAS2 promotes SUMOylation of alpha-synuclein, leading to a decrease in alpha-synuclei

197 Aggregation of neuronal protein alpha-synuclein leads to the formation of amyloid fibril

198 ein SUMOylation provide a strategy to reduce alpha-synuclein levels and possibly aggregation in PD.

199 SUMO E1 inhibitor, ginkgolic acid, decreases alpha-synuclein levels by relieving the inhibition exert

200 ostic value of salivary total and oligomeric alpha-synuclein levels in PD.

201 We aimed to achieve alpha-synuclein levels sufficient to induce terminal pat

202 our analysis,No difference in salivary total alpha-synuclein levels was found between PD patients and

203 074 was correlated with lower salivary total alpha-synuclein levels, while G allele of rs894278 was a

204 effects on insulin resistance and monomeric alpha-synuclein load in the striatum, as well as surviva

205 e major Parkinson's disease-related proteins-alpha-synuclein, LRRK2, and Parkin-alpha-synuclein might

206 Overall, soluble alpha-synuclein maintains lipid interactions following t

207 n combinations using monomeric or oligomeric alpha-synuclein (MalphaSyn or OalphaSyn, respectively),

208 the notion that pathological phosphorylated alpha-synuclein may disrupt the structure and function o

209 proteins-alpha-synuclein, LRRK2, and Parkin-alpha-synuclein might be a major link.

210 alpha-Synuclein misfolding and aggregation is a hallmark

211 We consider potential triggers of the alpha-synuclein misfolding and why the aggregates escape

212 ow that expression of G2019S-LRRK2 increases alpha-synuclein mobility and enhances aggregation of alp

213 e are at least two steps of incorporation of alpha-synuclein monomers into the amyloid fibril: namely

214 is a lack of reproducible methods to compare alpha-synuclein multimer abundance between complex biolo

215 e to study the molecular factors influencing alpha-synuclein multimerization.

216 Caenorhabditis elegans models, expression of alpha-synuclein mutated at the site of interaction with

217 s syntaxin-1, Munc18-1, or SNAP-25, modulate alpha-synuclein neuropathy and/or are dysregulated in Al

218 In protecting from alpha-synuclein neurotoxicity, NCEH-1 also stimulates ch

219 a neuroprotective mechanism that attenuates alpha-synuclein neurotoxicity, thereby pointing toward r

220 C-terminus significantly changed the rate of alpha-synuclein nucleation, but did not markedly affect

221 Caenorhabditis elegans strain overexpressing alpha-synuclein, observing a dramatic reduction of alpha

222 pathological accumulation of phosphorylated alpha-synuclein occurred within the transduced neurons.

223 almost completely suppresses the toxicity of alpha-synuclein oligomers in human neuroblastoma cells b

224 hat promotes strong membrane interactions by alpha-synuclein oligomers suppressed their toxicity in n

225 undamental characteristics that enable toxic alpha-synuclein oligomers to perturb biological membrane

226 T mice increased levels of potentially toxic alpha-synuclein oligomers, resulting in conformationally

227 Because this detrimental effect of alpha-synuclein on neurons can be rescued by the small m

228 within neurons containing elevated levels of alpha-synuclein or Lewy bodies.

229 Amyloid-beta, tau, and alpha-synuclein, or more specifically their soluble olig

230 einopathy model, Gba(D409V/D409V) and a A53T-alpha-synuclein overexpressing model harboring wild-type

231 alpha-Synuclein overexpression (ASOX) drives the formati

232 ulating this endogenous adaptive response to alpha-synuclein overexpression could lead to novel strat

233 oxidative load in response to chronic mutant alpha-synuclein overexpression.

234 eurodegenerative disease-associated proteins alpha-Synuclein, Parkin, and Huntingtin (Htt).

235 n linear regression analysis, but staging of alpha-synuclein pathologic changes was unrelated.

236 However, the extent of alpha-synuclein pathology (e.g., Lewy bodies) is not dir

237 urofibrillary tangles burden, in addition to alpha-synuclein pathology and amyloid plaque pathology,

238 in inclusions after the initial formation of alpha-synuclein pathology by increasing a pool of alpha-

239 vely investigate the synaptic phosphorylated alpha-synuclein pathology in dementia with Lewy bodies.

240 human alpha-syn fibrils to trigger Lewy-like alpha-synuclein pathology in the affected DA neurons is

241 ies in the neocortex, others have pointed to alpha-synuclein pathology in the hippocampus.

242 The mechanism of alpha-synuclein pathology is not fully understood and is

243 TN DBS in a parkinsonian model that displays alpha-synuclein pathology using unilateral, intranigral

244 aracterized human cases of DLB, finding that alpha-synuclein pathology was highest in two hippocampal

245 also associated with the induction of nigral alpha-synuclein pathology, persistent loss of dopaminerg

246 Inhibition of MARKs dramatically exacerbated alpha-synuclein pathology.

247 cosylceramide accumulations colocalized with alpha-synuclein pathology.

248 roteins in a primary neuron culture model of alpha-synuclein pathology.

249 h of which are composed mainly of aggregated alpha-synuclein phosphorylated at Ser129.

250 clozapine clears protein aggregates, such as alpha-synuclein, PolyQ protein, and alpha-1-antitrypsin

251 afted neurons were serine 129-phosphorylated alpha-synuclein positive in the left and right putamen,

252 In addition, ubiquitin- and alpha-synuclein-positive inclusions were seen, some with

253 Furthermore, phosphorylated alpha-synuclein-positive structures were also found in o

254 We report an essential role for the protein alpha-synuclein present in dopaminergic nigral afferents

255 Our conclusion is that alpha-synuclein probably acts as a prion in human diseas

256 nged antagonism of GCS in the CNS can affect alpha-synuclein processing and improve behavioral outcom

257 o seemingly contradictory results on whether alpha-synuclein promotes or inhibits Abeta aggregation.

258 Our data, presented here, demonstrate that alpha-synuclein promotes the survival of primary and met

259 evels by relieving the inhibition exerted on alpha-synuclein proteasomal degradation.

260 ligomerization and accumulation of the human alpha-synuclein protein is a key pathological hallmark o

261 pseudotype 2/5 to overexpress wildtype human alpha-synuclein (rAAV2/5 alpha-syn).

262 e delivery system with encapsulated antigen (alpha-synuclein) + rapamycin (RAP) induced both strong a

263 affected primarily the N-terminal region of alpha-synuclein, reducing membrane binding, impaired the

264 This was associated with an increase in alpha-synuclein release from the cells.

265 evidence of amyloid oligomers and increased alpha-synuclein release.

266 generative disease, however, the function of alpha-synuclein remains unknown.

267 s disease neuropathology increased, cerebral alpha-synuclein scores were higher, and the interval bet

268 x, cerebral neuritic plaque scores, cerebral alpha-synuclein scores, presence of cerebrovascular dise

269 The effects induced by such alpha-synuclein sequence extension on alpha-synuclein ag

270 ease (PD) resulting from triplication of the alpha-synuclein (SNCA) gene locus allows unprecedented o

271 had the genetic information of two positive alpha-synuclein (SNCA) loci.

272 cer element that regulates the expression of alpha-synuclein (SNCA), a key gene implicated in the pat

273 p between salivary total alpha-synuclein and alpha-synuclein SNP variants levels.

274 ngosine triggers the formation of oligomeric alpha-synuclein species capable of templating in human c

275 al mechanism underlying the up-regulation of alpha-synuclein SUMOylation in the disease.

276 Therefore, inhibitors of alpha-synuclein SUMOylation provide a strategy to reduce

277 he concentrations of monomeric and fibrillar alpha-synuclein that determines the outcome of the Abeta

278 -synuclein pathology by increasing a pool of alpha-synuclein that is more susceptible to forming incl

279 ght into the interplay between sirtuin 2 and alpha-synuclein, the major component of the pathognomoni

280 al cytoplasmic inclusion (GCI) consisting of alpha-synuclein; therefore, MSA is included in the categ

281 Recent studies of factors contributing to alpha-synuclein toxicity and its disruption of downstrea

282 s disease, which suggests a central role for alpha-synuclein toxicity in neurodegeneration.

283 ed post-translational modification, enhanced alpha-synuclein toxicity in vitro and in vivo, in Drosop

284 gly, mutants blocking acetylation exacerbate alpha-synuclein toxicity in vivo, in the substantia nigr

285 ed by the lack of dopaminergic cell death in alpha-synuclein transgenic mice.

286 vo studies were conducted in three different alpha-synuclein transgenic rodent models.

287 ex [Gba mutant (N370S, L444P, KO) crossed to alpha-synuclein transgenics], we show that Gba mutations

288 he accumulation of hippocampal aggregates of alpha-synuclein, ubiquitin, and tau, and improved the as

289 of alpha-synuclein, leading to a decrease in alpha-synuclein ubiquitination by SIAH and Nedd4 ubiquit

290 ross-linked residues in human hemoglobin and alpha-synuclein under oxidative conditions.

291 Salivary total alpha-synuclein was assayed using a highly sensitive Lum

292 einase-K resistant and Ser129-phosphorylated alpha-synuclein was observed in dopaminergic terminals,

293 ighly sensitive Luminex assay and oligomeric alpha-synuclein was quantified by the combination of Gel

294 rs, we demonstrated that normal clearance of alpha-synuclein was re-established, aggregation was redu

295 ized with small aggregates of phosphorylated alpha-synuclein were significantly larger than those tha

296 on widespread expression of wild-type human alpha-synuclein, which shows robust neurodegeneration, e

297 we provide evidence that the interaction of alpha-synuclein with spectrin initiates pathological alt

298 educed the cortical synaptic accumulation of alpha-synuclein within 1 h post-administration.

299 se (PD) is recognized by the accumulation of alpha-synuclein within neurons.

300 arkinson's disease abrogate this property of alpha-synuclein without impairing its ability to inhibit

301 ntrast to the current ascending theory where alpha-synuclein would propagate from neuron to neuron, w