ライフサイエンスコーパス: alpha-synuclein

1 activity has been linked to accumulation of alpha-synuclein.

2 e in vitro assembly of the Parkinson protein alpha-synuclein.

3 on two major pathological proteins: tau and alpha-synuclein.

4 ns are those that contain Sarkosyl-insoluble alpha-synuclein.

5 ne, maneb, paraquat, or preformed fibrils of alpha-synuclein.

6 icroglia in the clearance of neuron-released alpha-synuclein.

7 at we observe for H50Q compared to wild-type alpha-synuclein.

8 ions and their global structural effects on alpha-synuclein.

9 pace of the intrinsically disordered protein alpha-synuclein.

10 ses including prion protein (PrPC), tau, and alpha-synuclein.

11 e activity does not result in aggregation of alpha-synuclein.

12 n of proline 128 in the C-terminal domain of alpha-synuclein.

13 the architecture of amyloid fibrils of human alpha-synuclein.

14 on membrane-catalyzed amyloid aggregation of alpha-synuclein, a protein implicated in Parkinson's dis

15 d in cytotoxic accumulation of overexpressed alpha-synuclein, a protein known to aggregate in Parkins

16 tribution of impaired autophagy machinery to alpha-synuclein accumulation and the degeneration of dop

17 Parkinson's disease is characterized by alpha-synuclein accumulation that frequently associates

18 dent motor function abnormalities as well as alpha-synuclein accumulation, impaired autophagy and dop

19 ding SNc DA neuron loss, motor deficits, and alpha-synuclein accumulation.

20 , whereas the SSVEP facilitated detection of alpha-synuclein across reflects all stages of PD model p

21 Moreover, filament-forming alpha-synuclein activated HRI-dependent responses, which

22 Neuronal alpha-synuclein activates microglia, which in turn engul

23 dramatically suppressed the transmission of alpha-synuclein after stereotaxic injection of preformed

24 In addition, alpha-synuclein aggregates appeared in infected cell pop

25 estigate the structure and morphology of the alpha-synuclein aggregates generated by RT-QuIC.

26 ique that has previously been used to detect alpha-synuclein aggregates in samples of cerebrospinal f

27 A, and found that the characteristics of the alpha-synuclein aggregates in the cerebrospinal fluid co

28 quitination can induce structural changes in alpha-synuclein aggregates in vitro.

29 n-associated pathology in mice injected with alpha-synuclein aggregates into the striatum or substant

30 ever, it remains uncertain where the initial alpha-synuclein aggregates originate.

31 rent strains of recombinant or brain-derived alpha-synuclein aggregates produces clinically and patho

32 These findings suggest that alpha-synuclein aggregates that are associated with Park

33 ntrol patients with Parkinson's disease, and alpha-synuclein aggregates were detected in neurons that

34 uclein staining was observed at 4 years, and alpha-synuclein aggregates were not observed until 14-16

35 en postulated to stem from unique strains of alpha-synuclein aggregates, akin to what occurs in prion

36 d by the presence of abnormal, intraneuronal alpha-synuclein aggregates, which may propagate from cel

37 ibrils, and we observed marked reductions in alpha-synuclein aggregation and neurotoxicity, thus vali

38 l to investigate the contribution of glia to alpha-synuclein aggregation and spread.

39 omers that formed during the early stages of alpha-synuclein aggregation are thought to be the main t

40 ular and structural mechanisms of inhibiting alpha-synuclein aggregation by novel analogs of nordihyd

41 In microfluidic devices CLR01 reduced alpha-synuclein aggregation in cell somas when axonal te

42 f patients worldwide and is characterized by alpha-synuclein aggregation in dopamine neurons.

43 n CD11b+ exosomes, which were able to induce alpha-synuclein aggregation in neurons, further supporti

44 Aberrant alpha-synuclein aggregation is strongly associated with

45 Various known inhibitors of alpha-synuclein aggregation were used to validate the AS

46 quitination at residue 6, 23, or 96 inhibits alpha-synuclein aggregation, only modification at residu

47 em atrophy (MSA) for their ability to induce alpha-synuclein aggregation.

48 al protein homeostasis plays a major role in alpha-synuclein aggregation.

49 n antiinfluenza drug, prevented H1N1-induced alpha-synuclein aggregation.

50 ease is characterised neuropathologically by alpha-synuclein aggregation.

51 alpha-Synuclein (alpha-Syn) accumulation is a pathologic

52 ain dopaminergic neurons and accumulation of alpha-synuclein (alpha-Syn) aggregates.

53 sed of intracellular inclusions of misfolded alpha-synuclein (alpha-syn) among other proteins.

54 al Lewy body (LB) inclusions with aggregated alpha-synuclein (alpha-Syn) as the major component.

55 , obtained by coinjection of preformed human alpha-synuclein (alpha-syn) fibrils and adeno-associated

56 eding of Parkinson's disease (PD)-associated alpha-synuclein (alpha-syn) fibrils, in part, due to lac

57 The function of alpha-synuclein (alpha-syn) has been long debated, and t

58 ell-to-cell transmission of misfolding-prone alpha-synuclein (alpha-Syn) has emerged as a key patholo

59 tration, separation, and characterization of alpha-synuclein (alpha-syn) in blood at the intact prote

60 ve been reported to contain higher levels of alpha-synuclein (alpha-syn) in Parkinson's disease patie

61 the accumulation of misfolded and aggregated alpha-synuclein (alpha-syn) into intraneuronal inclusion

62 alpha-Synuclein (alpha-Syn) is a protein implicated in t

63 The aggregation of the protein alpha-synuclein (alpha-Syn) leads to different synuclein

64 agy lysosomal pathway resulting in increased alpha-synuclein (alpha-syn) levels.

65 n overlap of Abeta plaques, tau tangles, and alpha-synuclein (alpha-syn) pathologies in the brains of

66 progress, the temporal relationship between alpha-synuclein (alpha-syn) pathology and the functional

67 human pathology led Braak to postulate that alpha-synuclein (alpha-syn) pathology could spread from

68 In the pure autonomic failure (PAF), alpha-synuclein (alpha-Syn) pathology is confined within

69 einopathies in humans.SIGNIFICANCE STATEMENT alpha-Synuclein (alpha-syn) pathology plays a critical r

70 re we examined the temporal relation between alpha-synuclein (alpha-syn) T cell reactivity and PD.

71 often focuses on the ability of the protein alpha-synuclein (alpha-syn) to form oligomers and amyloi

72 Parkinson's disease is associated with alpha-synuclein (alpha-syn), a cytosolic protein enriche

73 ivity was amplified by the overexpression of alpha-Synuclein (alpha-Syn), a pathological protein in P

74 iseases, including mutant huntingtin (mHTT), alpha-synuclein (alpha-syn), tau, and others, raising th

75 alpha-Synuclein (alpha-syn), the hallmark pathological a

76 alpha-Synuclein (alpha-syn)-induced neurotoxicity has be

77 haracterized by pathological accumulation of alpha-synuclein (alpha-syn).

78 Alpha synuclein (alphaS) oligomers are a key component o

79 Cell-to-cell transmission of toxic forms of alpha-Synuclein (alphaS) is thought to underlie disease

80 Aggregation of alpha-Synuclein (alphaS) is widely regarded as a key fac

81 The aggregation of alpha-synuclein (alphaS), a protein abundant at presynap

82 A key therapeutic target in PD is alpha-synuclein (alphaS), which is both genetically impl

83 Aggregation of alpha-synuclein (alphaSN) is an important histological f

84 Alpha synuclein (alphaSyn) is shown here to interact dir

85 eterogeneous aggregates of the human protein alpha-synuclein (alphaSyn) are abundantly found in Lewy

86 mplicated the ubiquitous presynaptic protein alpha-synuclein (alphaSyn) in its pathogenesis.

87 alpha-Synuclein (alphasyn) is an abundant brain neuronal

88 Aggregation of human alpha-synuclein (alphaSyn) is linked to Parkinson's dise

89 alpha-Synuclein (alphasyn) is the primary component of p

90 In mice overexpressing the human amyloid alpha-synuclein (alphaSyn), we reveal that colonization

91 oteins such as actin, tropomyosin, CDK2, and alpha-synuclein (alphaSyn).

92 aracterized by the accumulation of insoluble alpha-synuclein (alphaSyn).

93 onally upregulated in response to aggregated alpha-synuclein (alphaSynAgg) stimulation in primary mic

94 that UBE2W can modify the N-terminus of both alpha-synuclein and a tau tetra-repeat domain with a sin

95 unds were screened for their ability to bind alpha-synuclein and amyloid beta fibrils in vitro.

96 n (Hsp27, HSPB1) during amyloid formation by alpha-synuclein and apolipoprotein C-II.

97 clein promotes the accumulation of misfolded alpha-synuclein and causes midbrain dopaminergic neuron

98 Combined neuron-derived exosomal alpha-synuclein and clusterin measurement predicted Park

99 ute H1N1 infection leads to the formation of alpha-synuclein and Disrupted-in-Schizophrenia 1 (DISC1)

100 nges mediated by the increased expression of alpha-synuclein and especially when full overexpression

101 lex displays a contact between alanine 53 of alpha-synuclein and glutamine 111 in the catalytic pocke

102 hown dysregulated extracellular transport of alpha-synuclein and growth factors in the extracellular

103 ific phorbol esters, such as PEP005, reduced alpha-synuclein and phosphorylated protein kinase Calpha

104 etric assay of two internal exosome markers (alpha-synuclein and syntenin-1) from neuronal exosomes.

105 Mutant forms of alpha-synuclein and tau linked to familial Parkinson's d

106 olved in neurodegenerative disorders such as alpha-synuclein and tau, might also play a role in CD.

107 oaches, including immunotherapy that targets alpha-synuclein and the targeting of immune mediators su

108 This study demonstrated a critical role of alpha-synuclein and toxins interactions in producing gut

109 tivation domain of the tumor suppressor p53, alpha-synuclein, and folded ubiquitin.

110 beta peptide, the islet amyloid polypeptide, alpha-synuclein, and the hungingtin protein.

111 g element as it is functionalised with anti-(alpha-synuclein) antibodies using a dual strategy: i) an

112 Hereditary mutations in alpha-synuclein are linked to both Parkinson's disease a

113 Deposits of amyloid fibrils of alpha-synuclein are the histological hallmarks of Parkin

114 The experiments, tested on alpha-synuclein, are then used to investigate how alpha-

115 alpha-Synuclein (AS) is an intrinsically disordered prot

116 ntibodies directed against aggregated, toxic alpha-synuclein.as well as anti-aggregation or protein c

117 Finally, CLR01 reduced alpha-synuclein-associated pathology in mice injected wi

118 Alpha-synuclein (aSyn) is a central player in Parkinson'

119 alpha-synuclein (aSyn) is a major player in Parkinson's

120 intrinsically disordered protein, monomeric alpha-synuclein (aSyn) occupies a large conformational s

121 is among the first brain regions affected by alpha-synuclein (asyn) pathology, yet how asyn affects t

122 LBs are primarily composed of misfolded alpha-synuclein (aSyn), and neurofibrillary tangles are

123 The imprinted electrode can detect alpha-synuclein at fg/mL levels, and was therefore used

124 study effects of metal ion interaction with alpha-synuclein at the molecular level, observing change

125 ion and asymmetric membrane deformation upon alpha-synuclein binding to phosphatidylglycerol vesicles

126 synuclein fibril structure is fundamental to alpha-synuclein biology.

127 in motor defects and a decreased oligomeric alpha-synuclein burden.

128 rontotemporal dementia with parkinsonism and alpha-synuclein by increasing their secretion.

129 alpha-Synuclein can also contribute to disease propagati

130 Seeds of alpha-synuclein can induce the assembly of monomeric pro

131 odels have indicated that fibrillar forms of alpha-synuclein can initiate the propagation of endogeno

132 r similar proteopathic seeds, such as tau or alpha-synuclein, can also be transferred iatrogenically.

133 that VAMP8 could be used to increase tau and alpha-synuclein clearance to prevent their intracellular

134 Hsp104 homologs that selectively antagonized alpha-synuclein condensation and toxicity in yeast and d

135 thiolate-linked diubiquitin and an ubiquitin-alpha-synuclein conjugate.

136 c insights into the molecular details of the alpha-synuclein/CypA interaction.

137 lts indicate that the presynaptic effects of alpha-synuclein depend on specific patterns of neuronal

138 rrant protein accumulation, such as Abeta or alpha-synuclein deposition.

139 ime to disease onset, morphology of cerebral alpha-synuclein deposits and the conformational properti

140 NDGA analog-pretreated alpha-synuclein did not aggregate even without NDGA-anal

141 and co-localized with thioflavin S and with alpha-synuclein during rotenone-induced stress.

142 Increased alpha-synuclein egress in serum neuronal exosomes preced

143 approach for the difficult-to-target protein alpha-synuclein encoded by the SNCA gene.

144 A misfolded alpha-synuclein-enriched brain fraction from frontal cor

145 up and 105 in the validation group, exosomal alpha-synuclein exhibited a consistent performance (AUC=

146 Thus, pathogenic alpha-synuclein exhibits key hallmarks of prion strains,

147 alpha-Synuclein exists in multiple structural forms, inc

148 the effect of these hereditary mutations on alpha-synuclein fibril structure is fundamental to alpha

149 Indeed, PARL-activated Skd3 solubilizes alpha-synuclein fibrils connected to Parkinson's disease

150 o-electron microscopy (cryo-EM) structure of alpha-synuclein fibrils containing the hereditary E46K m

151 of myelin debris, amyloid-beta oligomers and alpha-synuclein fibrils in vivo.

152 ort two new polymorphic atomic structures of alpha-synuclein fibrils termed polymorphs 2a and 2b, at

153 s intraneuronal deposits composed in part of alpha-synuclein fibrils.

154 We conclude that alpha-synuclein filaments are the main driving force for

155 with tau assemblies(4-9), the structures of alpha-synuclein filaments extracted from the brains of i

156 wo-dimensional class averaging, we show that alpha-synuclein filaments from the brains of individuals

157 However, the structures of alpha-synuclein filaments from the human brain are unkno

158 We then injected these different alpha-synuclein forms into the mouse striatum to determi

159 ed HEK 293T cells to identify the species of alpha-synuclein from the brains of homozygous, symptomat

160 ent area for the propagation of pathological alpha-synuclein from the periphery to the brain.

161 104 MD variant, Hsp104-RYD, which suppresses alpha-synuclein, fused in sarcoma (FUS), and TDP-43 toxi

162 However, in the context of extant misfolded alpha-synuclein, GCase activity modulates neuronal susce

163 alpha-Synuclein has been identified as the major compone

164 tress has been implicated in PD and oxidized alpha-synuclein has been shown to assemble into soluble,

165 alpha-Synuclein has been shown to be O-GlcNAcylated at n

166 the formation of, filamentous inclusions of alpha-synuclein in brain cells(2,3).

167 Parkinson's disease (PD)-associated protein alpha-synuclein in cells and interacts with alpha-synucl

168 o the structure of the PD-associated protein alpha-synuclein in complex with the most abundant cellul

169 Aggregates of alpha-synuclein in distinct synucleinopathies have been

170 Removal of alpha-synuclein in human cells leads to increased DNA do

171 of the OTU family, is enriched together with alpha-synuclein in LBs from individuals with PD and is a

172 Felodipine can clear mutant alpha-synuclein in mouse brains at plasma concentrations

173 Assembled alpha-synuclein in nerve cells and glial cells is the de

174 The egress of alpha-synuclein in neuronally derived exosomes predates

175 s amyloid-beta and tau in Alzheimer disease, alpha-synuclein in Parkinson disease, and TAR DNA-bindin

176 ization of prosaposin, and an aggregation of alpha-synuclein in patient-derived skin fibroblasts or i

177 both pathogenic and non-pathogenic forms of alpha-synuclein in primary hippocampal, cortical, and mi

178 ed with the disease-associated variant pS129-alpha-synuclein in rotenone-exposed mouse brains.

179 mL levels, and was therefore used to measure alpha-synuclein in the culture medium of human brain org

180 i(-/-) mice showed accumulation of misfolded alpha-synuclein in the lateral collateral pathway, a reg

181 that allows for the detection of amounts of alpha-synuclein in the range from 0.25 pM to 25 nM.

182 igate how virally-mediated overexpression of alpha-synuclein in the substantia nigra pars compacta im

183 presence of distinct conformers of assembled alpha-synuclein in these different samples.

184 iated with the misfolding and aggregation of alpha-synuclein, including Parkinson's disease, dementia

185 Nigral neurons with alpha-synuclein inclusions exhibited a phenotypic downre

186 using cryo-electron microscopy, we show that alpha-synuclein inclusions from the brains of individual

187 linical need to be able to image filamentous alpha-synuclein inclusions in the human brain.

188 sly account for tau neurofibrillary tangles, alpha-synuclein inclusions, neuritic plaques, inclusions

189 ion of DDR1 in a mouse model challenged with alpha-synuclein increases autophagy and reduces inflamma

190 ese insights into structural consequences of alpha-synuclein interaction with lipid vesicles highligh

191 fold because the E46-K80 salt bridge diverts alpha-synuclein into a kinetic trap-a shallower, more ac

192 Aggregation of the neuronal protein alpha-synuclein into amyloid fibrils plays a central rol

193 in activates microglia, which in turn engulf alpha-synuclein into autophagosomes for degradation via

194 The aggregation of alpha-synuclein is a critical event in the pathogenesis

195 Aggregation of alpha-synuclein is a defining molecular feature of Parki

196 Accumulation of neuronal alpha-synuclein is a prominent feature in Parkinson's di

197 has not been investigated whether pathologic alpha-synuclein is a specific trigger for excessive infl

198 alpha-Synuclein is an intrinsically disordered protein t

199 alpha-Synuclein is expressed at high levels at presynapt

200 We report that, in vivo, alpha-synuclein is responsible for the facilitation of d

201 The quantification of alpha-synuclein level across 40 clinical samples resolve

202 omatic mice transgenic for human mutant A53T alpha-synuclein (line M83) that seed aggregation.

203 system atrophy, with hereditary mutations in alpha-synuclein linked to the first two of these conditi

204 argets certain proteins for degradation, and alpha-synuclein may be ubiquitinated and recycled in the

205 ding the Parkinson's disease causing protein alpha-synuclein, may be one such cause.

206 key molecular pathogenic mechanisms include alpha-synuclein misfolding and aggregation, mitochondria

207 mprove our understanding of the mechanism of alpha-synuclein misfolding and the structures of the agg

208 cyclophilin A lowers the energy barrier for alpha-synuclein misfolding, while isomerase-binding to a

209 dies showed Synucleozid directly targets the alpha-synuclein mRNA 5' UTR at the designed site.

210 Homozygous alpha-synuclein mutant (SNCA) mice that overexpress huma

211 We also tested whether 4E-BP1 could prevent alpha-synuclein neurotoxicity by treating 4E-BP1-overexp

212 rodegenerative disorders but, in contrast to alpha-synuclein, no data are available about its express

213 Interestingly, the reduction in alpha-synuclein occurred through proteasomal degradation

214 sease patients, we confirmed the presence of alpha-synuclein oligomer in CD11b+ exosomes, which were

215 lso effective in monitoring the formation of alpha-synuclein oligomers at different times.

216 IR), we were able to reveal the structure of alpha-synuclein oligomers present at different stages of

217 investigation of structural organization of alpha-synuclein oligomers reported in this study is crit

218 alpha-synuclein in cells and interacts with alpha-synuclein oligomers.

219 somas when axonal terminals were exposed to alpha-synuclein oligomers.

220 Novel modules in the primary sequence of alpha-synuclein optimized for calcium sensing in highly

221 euronal cells can induce seeds of aggregated alpha-synuclein or DISC1 that may be able to initiate fu

222 ophagy in cells with accumulated mutant tau, alpha-synuclein, or huntingtin.

223 We then tested CLR01 in vivo in a humanized alpha-synuclein overexpressing mouse model; mice treated

224 key role for autophagy in clearing fibrillar alpha-synuclein pathologies in human neuronal cells.

225 tection deficits could be used to define how alpha-synuclein pathology affects other aspects of olfac

226 al exosomes contribute to the progression of alpha-synuclein pathology and therefore, they may serve

227 is unclear how mitochondrial impairment and alpha-synuclein pathology are coupled.

228 t extent microglia and their exosomes impact alpha-synuclein pathology has not been well delineated.

229 A brain-first (top-down) type, where alpha-synuclein pathology initially arises in the brain

230 lleagues suggested that early in the disease alpha-synuclein pathology is present in the dorsal motor

231 Although alpha-synuclein pathology is the hallmark of Parkinson d

232 nucleus and piriform cortex displayed a high alpha-synuclein pathology load.

233 e impairment including memory impairment and alpha-synuclein pathology, 148 consecutive patients with

234 activation contributes to the development of alpha-synuclein pathology, and supports the concept that

235 ed with mitochondrial stress, did not affect alpha-synuclein pathology.

236 n can initiate the propagation of endogenous alpha-synuclein pathology.

237 tegral role in the propagation and spread of alpha-synuclein pathology.

238 0 in the prevention and/or disaggregation of alpha-synuclein pathology.

239 ith activated microglia and the emergence of alpha-synuclein pathology.

240 In this work, three alpha-synuclein peptides were synthesized as templates f

241 at a single, transvascular administration of alpha-synuclein pff can lead to selective regional neuro

242 Here we show that the alpha-synuclein-PMCA assay can discriminate between samp

243 biological methods to analyse the product of alpha-synuclein-PMCA, and found that the characteristics

244 lein, which can be amplified and detected by alpha-synuclein-PMCA.

245 Astroglial alpha-synuclein-positive cytoplasmic accumulations have

246 In contrast, we find no evidence for alpha-synuclein-positive neuropathology in aged VPS35 KI

247 not generally recognize this modification on alpha-synuclein, potentially explaining why it remains u

248 Mechanistically, we report here that alpha-synuclein preformed fibrils impaired autophagy flu

249 aken together, our findings demonstrate that alpha-synuclein preformed fibrils induce a synucleinopat

250 Here, we bilaterally injected alpha-synuclein preformed fibrils into the olfactory bul

251 The alpha-synuclein preformed fibrils resulted in Lewy patho

252 reotaxic injection of exosomes isolated from alpha-synuclein preformed fibrils treated microglia into

253 ted the pathological features when exogenous alpha-synuclein preformed fibrils were injected into the

254 g 4E-BP1-overexpressing primary neurons with alpha-synuclein preformed fibrils, and we observed marke

255 We report here that when treated with human alpha-synuclein preformed fibrils, exosomes containing a

256 05 delivery to mouse striatum also decreased alpha-synuclein production in vivo.

257 icroglial autophagy in mice expressing human alpha-synuclein promotes the accumulation of misfolded a

258 d after serial passaging, which implies that alpha-synuclein propagates via prion-like conformational

259 ntly inherited Parkinson's disease (PD), and alpha-synuclein protein aggregates in Lewy bodies and Le

260 OPD showed increased accumulation of soluble alpha-synuclein protein and phosphorylated protein kinas

261 isease (PD); however, the normal function of alpha-synuclein protein and the pathway that mediates it

262 Thus, reducing the expression of alpha-synuclein protein is expected to have therapeutic

263 ic studies revealed that Synucleozid reduces alpha-synuclein protein levels by decreasing the amount

264 clusterin was elevated in subjects with non-alpha-synuclein proteinopathies.

265 , lipid accumulation and increased insoluble alpha-synuclein relative to isogenic controls.

266 clein preformed fibrils, exosomes containing alpha-synuclein released by microglia are fully capable

267 tudinal sample analysis showed that exosomal alpha-synuclein remains stably elevated with Parkinson's

268 rier through posttranslational truncation of alpha-synuclein reverses the action of the proline isome

269 n and centrifugation steps, was subjected to alpha-synuclein/RT-QuIC analysis.

270 (2+), have recently been reported as key for alpha-synuclein's physiological function at the pre-syna

271 Structural variances of alpha-synuclein seeding kinetics and products in DLB and

272 rial protein import significantly aggravates alpha-synuclein seeding.

273 ) and Parkinson's disease (PD) brain-derived alpha-synuclein seeds by real-time quaking-induced conve

274 and spread following injection of aggregated alpha-synuclein seeds into brain, supporting a role for

275 ather is driven by the level of pathological alpha-synuclein seeds.

276 -synuclein, are then used to investigate how alpha-synuclein senses Ca(2+) concentration jumps associ

277 Alpha-synuclein SNCA has been implicated in the etiology

278 hepsin D (CTSD), which plays a major role in alpha-synuclein (SNCA) degradation and prosaposin (PSAP)

279 etected at 18 months, only diffuse monomeric alpha-synuclein staining was observed at 4 years, and al

280 r the first time, the existence of different alpha-synuclein strains in these groups.

281 the synucleinopathies is caused by distinct alpha-synuclein strains.

282 f Hsp110 is sufficient to prevent endogenous alpha-synuclein templating and spread following injectio

283 epresent different conformational strains of alpha-synuclein that can self-propagate and spread from

284 , we could show that the reduction of AB and alpha-synuclein toxicity in transgenic C. elegans models

285 Prokaryotic ClpG reduced TDP-43, FUS, and alpha-synuclein toxicity, whereas prokaryotic ClpB and h

286 on of exosome synthesis in microglia reduced alpha-synuclein transmission.

287 receptor, is necessary for the formation of alpha-synuclein/ubiquitin-positive puncta that are degra

288 n alpha-synculein clearance, suggesting that alpha-synuclein ubiquitnation is important for its clear

289 ve function of microglia in the clearance of alpha-synuclein via TLR4-NF-kappaB-p62 mediated synuclei

290 conductive polymers to enable recognition of alpha-synuclein via ultrasensitive electrochemical measu

291 fter a unilateral injection of vector, human alpha-synuclein was detected in the striatum and superio

292 Mean neuron-derived exosomal alpha-synuclein was increased by twofold in prodromal an

293 In contrast, alpha-synuclein was not detected at 18 months, only diff

294 Phosphorylated alpha-synuclein was observed in multiple brain regions c

295 spond to different conformational strains of alpha-synuclein, which can be amplified and detected by

296 ently demonstrated that the neuronal protein alpha-synuclein, which is critically involved in PD path

297 h early-onset PD, weakens the interaction of alpha-synuclein with CypA.

298 The interaction of the neuronal protein alpha-synuclein with lipid membranes appears crucial in

299 tigate the interaction kinetics of monomeric alpha-synuclein with surface-tethered vesicles composed

300 p that defines the supramolecular packing of alpha-synuclein within the fibrils.