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1 es in multiple neurodegenerative disorders ("synucleinopathies").
2  neuron toxicity, degeneration and death in "synucleinopathies".
3 may also benefit PD patients and others with synucleinopathy.
4 short-term development of clinically defined synucleinopathy.
5 er, before and after their conversion into a synucleinopathy.
6 led t test; P = .04) and more frequent alpha-synucleinopathy.
7 D are at very high risk of neurodegenerative synucleinopathy.
8 ell uptake and propagation for tauopathy and synucleinopathy.
9 nting with dementia in the context of a pure synucleinopathy.
10  generation, could be major players in alpha-synucleinopathy.
11 uld contribute to neurodegeneration in alpha-synucleinopathy.
12 mers in mouse and human brain with the alpha-synucleinopathy.
13 ration in Parkinson's disease (PD) and alpha-synucleinopathy.
14  value, and likelihood ratio 1.54 to predict synucleinopathy.
15 ntifies IRBD patients at short-term risk for synucleinopathy.
16 gh risk of phenoconverting to a manifest CNS synucleinopathy.
17 ng TDP-43 proteinopathy, tauopathy and alpha-synucleinopathy.
18 ce of parkinsonism and determine the type of synucleinopathy.
19 mortem brain tissue from patients with alpha-synucleinopathy.
20 e further evaluated in a Drosophila model of synucleinopathy.
21 n situ studies of human specimens with alpha-synucleinopathy.
22 neurodegenerative mechanism underlying alpha-synucleinopathy.
23 mouse model of PD delayed the progression of synucleinopathy.
24  these features of clinical heterogeneity in synucleinopathies.
25 pha-synuclein (alpha-syn) and jointly termed synucleinopathies.
26 ostasis, thereby reducing the progression of synucleinopathies.
27 autonomia in Parkinson's disease and related synucleinopathies.
28  cause Parkinson's disease and other chronic synucleinopathies.
29 resents an important therapeutic strategy in synucleinopathies.
30 peutic convergence point for a wide range of synucleinopathies.
31  beneficial as treatments for PD and related synucleinopathies.
32 group of neurological disorders described as synucleinopathies.
33  at this higher order has yet to be shown in synucleinopathies.
34 monomeric alpha-syn in PD and in other alpha-synucleinopathies.
35 ve drugs for the treatment of PD and related synucleinopathies.
36 are the pathogenic species in PD and related synucleinopathies.
37 w therapeutic target to combat the spread of synucleinopathies.
38  other neurodegenerative disorders, known as synucleinopathies.
39 n development of Parkinson disease and other synucleinopathies.
40 ipation in Parkinson disease and other alpha-synucleinopathies.
41 each other's aggregation via an interface in synucleinopathies.
42 different clinico-pathological traits within synucleinopathies.
43 d are thus a novel therapeutic candidate for synucleinopathies.
44 y body inclusions in neurodegenerative alpha-synucleinopathies.
45 RNA miR-19b occurs in the prodromal stage of synucleinopathies.
46  have immediate therapeutic implications for synucleinopathies.
47 ies for disease modification in PD and other synucleinopathies.
48 ders including Parkinson's disease and other synucleinopathies.
49 increase the risk of developing PD and other synucleinopathies.
50 for the treatment of the yet incurable alpha-synucleinopathies.
51 ng of alpha-syn biology and the treatment of synucleinopathies.
52 te the interaction between GBA mutations and synucleinopathies.
53 ound in Parkinson's disease brains and other synucleinopathies.
54 therapeutic value of sirtuin 2 inhibition in synucleinopathies.
55 sions in Parkinson's disease and other alpha-synucleinopathies.
56 is a promising strategy for the treatment of synucleinopathies.
57 ted to the onset of multiple diseases termed synucleinopathies.
58  in neurons in Parkinson's disease and other synucleinopathies.
59 athogenesis of Parkinson's disease and other synucleinopathies.
60 rogression of aSyn pathology in PD and other synucleinopathies.
61 topathology of Parkinson disease and related synucleinopathies.
62  a hallmark of Parkinson's disease and other synucleinopathies.
63 may underlie the tremendous heterogeneity of synucleinopathies.
64 ould be a viable target for the treatment of synucleinopathies.
65 egrade alpha-synuclein in PD and other alpha-synucleinopathies.
66 c pathology as one of the earliest events in synucleinopathies.
67 strategy for the treatment of PD and related synucleinopathies.
68 ng and may modulate the progression of alpha-synucleinopathies.
69 rking memory performance improvements in the synucleinopathies.
70 generative disease and particularly with the synucleinopathies.
71 nal dysfunction and toxicity in PD and other synucleinopathies.
72 treatment of Parkinson's disease and related synucleinopathies.
73  from alphaSyn-overexpressing mice and human synucleinopathies.
74 d with Parkinson's disease and several other synucleinopathies.
75 nderlie the progression of neurodegenerative synucleinopathies.
76  an effective therapy for PD and other alpha-synucleinopathies.
77  in Parkinson's disease (PD) and other alpha-synucleinopathies.
78 hat contribute to neurodegeneration in alpha-synucleinopathies.
79 sses might contribute to the pathogenesis of synucleinopathies.
80 ic hallmark of Parkinson's disease and other synucleinopathies.
81 nd may induce a cascade of events leading to synucleinopathies.
82 utic strategy in Parkinson disease and other synucleinopathies.
83  contributes to the pathogenesis of sporadic synucleinopathies.
84 t a therapeutic strategy for GBA1-associated synucleinopathies.
85 inson's disease and related disorders called synucleinopathies.
86 genesis of Parkinson disease and other alpha-synucleinopathies.
87 ecific therapeutic approach for PD and other synucleinopathies.
88 ]) are common features of sleep in the alpha-synucleinopathies.
89 or slowing the progression of PD and related synucleinopathies.
90  a therapeutic target for PD and other alpha-synucleinopathies.
91 our understanding of disease pathogenesis in synucleinopathies.
92 strategy to lessen alpha-synuclein burden in synucleinopathies.
93 ment of Parkinson's disease as well as other synucleinopathies.
94 pects of neurodegeneration in PD and related synucleinopathies.
95 cesses seen in Parkinson's disease and other synucleinopathies.
96 modifying therapies for PD, DLB, and related synucleinopathies.
97 ed aggregation of alpha-Syn in various alpha-synucleinopathies.
98  neurodegenerative disease, particularly the synucleinopathies.
99 or LB PD, DLB, and related neurodegenerative synucleinopathies.
100 alpha-syn inclusions in PD and related alpha-synucleinopathies.
101 s for PD and related neurodegenerative alpha-synucleinopathies.
102 ent of targeted therapies for PD and related synucleinopathies.
103 e disorders, including tauopathies and alpha-synucleinopathies.
104 nesis of Parkinson's disease and other alpha-synucleinopathies.
105 ognomonic protein inclusions in PD and other synucleinopathies.
106 mation of inclusions in PD and related alpha synucleinopathies.
107 ative disorders, collectively referred to as synucleinopathies.
108 d related neurodegenerative disorders termed synucleinopathies.
109  of Parkinson's disease (PD) and other alpha-synucleinopathies.
110 and pathological features of tauopathies and synucleinopathies.
111 nificant factor in the pathogenesis of alpha-synucleinopathies.
112 sis of Parkinson's disease and related alpha-synucleinopathies.
113 cating a treatment strategy for PD and other synucleinopathies.
114 al other neurodegenerative diseases known as synucleinopathies.
115  motor symptoms and dementia symptoms across synucleinopathies.
116 e and genotyped for variants associated with synucleinopathies.
117 re, MSA is included in the category of alpha-synucleinopathies.
118 GCS) inhibition as a potential treatment for synucleinopathies.
119 onal distribution of aggregates in different synucleinopathies.
120 disease course and survival in patients with synucleinopathies.
121 slow the progression of PD and related alpha-synucleinopathies.
122 rs could be a novel therapeutic strategy for synucleinopathies.
123 it evades sHsp chaperone action in the alpha-synucleinopathies.
124 thogenesis and developing new treatments for synucleinopathies.
125  treatments of Parkinson's disease and other synucleinopathies.
126 allmarks of Parkinson disease (PD) and alpha-synucleinopathies.
127 l disease indicator for PD and related alpha-synucleinopathies.
128 eneration in Parkinson's disease and related synucleinopathies.
129 pathogens may contribute to the diversity of synucleinopathies.
130 tential therapeutics for GD, PD, and related synucleinopathies.
131 eases, collectively referred to as the alpha-synucleinopathies.
132 y diagnosis of Alzheimer's disease, 230 with synucleinopathies, 157 with TDP-43 proteinopathies, 144
133                     Of the 461 patients with synucleinopathies, 279 (60.5%) were men, and of the 452
134 0, 461 individuals received a diagnosis of a synucleinopathy (309 [67%] of Parkinson disease, 81 [17.
135            Of the 389 patients with presumed synucleinopathies (71.8%), 264 had Parkinson disease (48
136 roxyphenylglycol was also lower in the three synucleinopathies (8.82 +/- 0.44, 7.75 +/- 0.42, 5.82 +/
137                         Two murine models of synucleinopathy (a Gaucher-related synucleinopathy model
138 CIT putamen uptake greater than 25% predicts synucleinopathy after 3 years' follow-up.
139                  In the mouse model of alpha-synucleinopathy, alphaS oligomers initially form before
140 s in some of the most common tauopathies and synucleinopathies: Alzheimer's disease, progressive supr
141 low-up, 68.6% (n = 316) of the patients with synucleinopathies and 48.7% (n = 220) of the referent pa
142 patients with incident, clinically diagnosed synucleinopathies and age- and sex-matched referent part
143   alpha-Syn oligomers are a toxic species in synucleinopathies and are suspected to cause neuritic pa
144 difying therapeutic strategy for GBA-related synucleinopathies and conceivably for certain forms of s
145 heimer's disease neuropathology is common in synucleinopathies and confers a worse prognosis for each
146 nts with Parkinson's disease and other alpha-synucleinopathies and demonstrated that NUB1, as well as
147 between OH and cognitive impairment in alpha-synucleinopathies and discuss possible mechanisms and im
148  O-GlcNAcylation may slow the progression of synucleinopathies and further support a general function
149 ydrolase trafficking may prove beneficial in synucleinopathies and indicates that human midbrain dise
150 insight in the role of alphaSYN oligomers in synucleinopathies and opens new opportunities to evaluat
151 on may herald Parkinson's disease or related synucleinopathies and precede these neurodegenerative co
152            The frequency and distribution of synucleinopathies and tauopathies manifesting with parki
153 ted with the intracellular pathology in both synucleinopathies and tauopathies.
154 ed inhibitors in a SH-SY5Y cellular model of synucleinopathy and demonstrate a significant antiaggreg
155  epsilon status, presence of infarcts, alpha-synucleinopathy and neuronal loss in substantia nigra.
156 eutic and pathological implications for both synucleinopathy and Parkinson's disease, identifying con
157 nphilin-1 can diminish the severity of alpha-synucleinopathy and play a neuroprotective role against
158 ultiple system atrophy (MSA, a non-Lewy body synucleinopathy); and in normal controls.
159 between OH and cognitive impairment in alpha-synucleinopathies, and 'indirect-evidence studies' based
160 ein accumulation as occurs in PD and related synucleinopathies, and accumulation of lipofuscin deposi
161 rodegenerative diseases like prion diseases, synucleinopathies, and tauopathies that are collectively
162 ation in Parkinson's disease and other human synucleinopathies, and that small molecules that stabili
163 for Gaucher disease for the treatment of the synucleinopathies, and the role of lysosomal pathways in
164                                              Synucleinopathies are a group of neurodegenerative disor
165                                              Synucleinopathies are a group of progressive disorders c
166                                              Synucleinopathies are characterized by aggregation of th
167            Parkinson disease and other alpha-synucleinopathies are characterized by the deposition of
168 lpha-synuclein overexpression for idiopathic synucleinopathies are discussed.
169                         Clinically diagnosed synucleinopathies are much more common than tauopathies.
170                                              Synucleinopathies are neurodegenerative diseases associa
171 nson's disease and related neurodegenerative synucleinopathies are still largely unclear, but environ
172 n accumulations and their relevance to human synucleinopathies are unknown.
173  system atrophy, collectively referred to as synucleinopathies, are associated with a diverse group o
174  a novel drug target that can be explored in synucleinopathies as well as in other neurodegenerative
175 al SNCA and suggest that PDC be considered a synucleinopathy as well as a tauopathy.
176  body disorders with autopsy-confirmed alpha synucleinopathy (as of Oct 1, 2015) who were previously
177             In mice expressing a human alpha-synucleinopathy-associated mutation (hA53Talpha-syn mice
178 by alpha-synuclein impedes understanding the synucleinopathies at the molecular level.
179  we describe a new Drosophila model of alpha-synucleinopathy based on widespread expression of wild-t
180 model of LB disease and in LBs of postmortem synucleinopathy brains.
181 ions of Parkinson's disease (PD) and related synucleinopathies, but the pathogenesis and neurodegener
182 p a severe movement disorder, paralysis, and synucleinopathy, but the mechanisms are not understood.
183 iver of neurodegenerative diseases known as "synucleinopathies," but the mechanisms underlying this t
184 candidate to achieve disease modification in synucleinopathies by limiting alpha-syn accumulation.
185 odies, and multiple system atrophy are alpha-synucleinopathies characterized by filamentous alpha-syn
186                Parkinson's disease (PD) is a synucleinopathy characterized by a preferential loss of
187 survival and causes of death of persons with synucleinopathies compared with the general population h
188  patients with the Parkinson disease-related synucleinopathy dementia with Lewy bodies showed less ph
189                            Patients with any synucleinopathy died a median of 2 years earlier than re
190 in dementia with Lewy bodies and other alpha-synucleinopathies, direct evidence for the precise synap
191 lysosomal enzyme glucocerebrosidase, and the synucleinopathies directly resulted from the clinical re
192 e kinase 2 (PLK2), an enzyme up-regulated in synucleinopathy-diseased brains, interacts with, phospho
193 lating many features observed in the various synucleinopathy disorders.
194 ase pathogenesis, available animal models of synucleinopathy do not replicate the full range of cellu
195 opulations differ in when they exhibit alpha-synucleinopathies during PD pathogenesis, they could als
196 ing that DMV neurons display extensive alpha-synucleinopathies earlier than SN dopamine neurons while
197                      Finally, cases of alpha-synucleinopathy exhibit increases in the total soluble a
198  cognitive impairment in patients with alpha-synucleinopathies exists, but the underlying mechanisms
199 cocerebrosidase activity in murine models of synucleinopathy (expressing wild type Gba1) affected alp
200                                              Synucleinopathies feature cerebrospinal fluid neurochemi
201 a localized fashion in human tauopathies and synucleinopathies, followed by seed-dependent propagatio
202 ened the cerebella of 12 patients with alpha-synucleinopathies for neuropathological changes.
203 ated patients with DAT deficit who developed synucleinopathy from patients with DAT deficit that rema
204 e as a random effect, we observed that alpha-synucleinopathies, frontotemporal lobar degeneration due
205 resymptomatic mouse model of Gaucher-related synucleinopathy (Gba1(D409V/D409V)) and ameliorate the a
206                                  These alpha-synucleinopathies have in common parkinsonism and non-mo
207 ng protein 43 immunoreactive deposits, alpha-synucleinopathies, hippocampal sclerosis and prion disea
208 at consistently induced specific patterns of synucleinopathies in mice.
209 system, Parkinson's disease (PD) begins as a synucleinopathy in nondopaminergic structures of the low
210 l analysis showed increased risk of incident synucleinopathy in patients with abnormal DAT-SPECT than
211 d have prospect in the amelioration of alpha-synucleinopathy in PD and other Lewy body diseases.
212 t generally seen to be associated with alpha-synucleinopathy in vivo.
213 resentative of a group of disorders known as synucleinopathies, in which misfolding and aggregation o
214 ggregation as a mediator of neurotoxicity in synucleinopathies including MSA.
215 bodies (LBs) and Lewy neurites (LNs), define synucleinopathies including Parkinson's disease (PD) and
216 n leading to motor and cognitive deficits in synucleinopathies including Parkinson's disease (PD) and
217 unds, which might yield clinical benefit for synucleinopathies including Parkinson's disease, Lewy bo
218 3) alpha-synuclein inclusion ratings in four synucleinopathies including Parkinson's disease, Parkins
219 erapeutic strategies for treating pathologic synucleinopathies including PD.
220 ein is a key molecule in the pathogenesis of synucleinopathy including dementia with Lewy bodies, Par
221 nt role in oxidative stress, cell death, and synucleinopathies, including Parkinson disease.
222 nical and pathophysiological overlap seen in synucleinopathies, including Parkinson's disease, dement
223  a toxic aggregating protein associated with synucleinopathies, including Parkinson's disease.
224 ins of patients with neurodegenerative alpha-synucleinopathies, including Parkinson's disease.
225 egy for GBA1-related and non-GBA1-associated synucleinopathies, including PD.
226 a1(D409V/D409V)) exhibits characteristics of synucleinopathies, including progressive accumulation of
227 uggesting that this pathological hallmark of synucleinopathies is an epiphenomenon.
228 ice isoforms affect vesicular trafficking in synucleinopathies is warranted.
229  of phospho-eIF2alpha, indicating that alpha-synucleinopathy is associated with abnormal UPR that cou
230 osited in brain tissue from individuals with synucleinopathy is extensively phosphorylated at Ser-129
231 nstem involvement accompanying mesencephalic synucleinopathy is often observed.
232                                The brainstem synucleinopathy is postulated to progress rostrally to a
233 STN DBS can be protective in other models of synucleinopathy is unknown.
234 se, and other human disorders known as alpha-synucleinopathies, is well established.
235  to cause Parkinson disease as well as other synucleinopathies like dementia with LBs.
236 evelopment of therapeutic strategies against synucleinopathies like Parkinson disease.
237 ovel therapeutic target for the treatment of synucleinopathies like PD.
238 urotoxicity in Parkinson disease and related synucleinopathies may result from an imbalance between t
239                                        Thus, synucleinopathies may result from disruptions in basic c
240 Similar changes are present in a mouse alpha-synucleinopathy model and in postmortem brain tissue fro
241 models of synucleinopathy (a Gaucher-related synucleinopathy model, Gba(D409V/D409V) and a A53T-alpha
242 triggering neuroprotective Treg responses in synucleinopathy models, and the combined vaccine is more
243 lglycol in Parkinson's disease and two other synucleinopathies, multiple system atrophy and pure auto
244 of alpha-synuclein in brain is a hallmark of synucleinopathies, neurodegenerative diseases that inclu
245 ne of many neurodegenerative diseases termed synucleinopathies, neuropathologically defined by inclus
246 ularly in dementia with Lewy bodies and when synucleinopathy occurs in the absence of neurological ma
247 t of a manifest central nervous system (CNS) synucleinopathy (odds ratio = 7.1).
248 ctors, imaging changes associated with alpha-synucleinopathy, or physical findings of parkinsonism.
249 ommon genetic risk factor for developing the synucleinopathies Parkinson disease (PD) and dementia wi
250 gests a link between Gaucher disease and the synucleinopathies Parkinson disease and dementia with Le
251                          To test whether the synucleinopathies Parkinson's disease and multiple syste
252 28.7%) subjects developed clinically defined synucleinopathy (Parkinson's disease in 11, dementia wit
253      These findings implicate MARKs early in synucleinopathy pathogenesis and as potential therapeuti
254 d catechols were assayed in 146 subjects-108 synucleinopathy patients (34 Parkinson's disease, 54 mul
255 ed human midbrain dopamine (DA) neurons from synucleinopathy patients with different PD-linked mutati
256  In Parkinson's disease (PD) and other alpha-synucleinopathies, prefibrillar alpha-synuclein (alphaS)
257 and alpha-synDelta6 and may be protective of synucleinopathy progression.
258 he absence of neurological signs, have brain synucleinopathy ranging up to Braak stages 4 to 6 at pos
259             The concept that lower brainstem synucleinopathy represents "early PD" rests on the suppo
260 in, these diseases are called tauopathies or synucleinopathies, respectively.
261  Alzheimer's disease, tauopathies, and alpha-synucleinopathies, respectively.
262           Parkinson disease (PD) is an alpha-synucleinopathy resulting in the preferential loss of hi
263 eveloping Parkinson's disease (PD) and other synucleinopathies, resulting in a lower age of onset and
264 ms for the gene's association with increased synucleinopathy risk.
265 n GBA1 mutation carrier status and increased synucleinopathy risk.
266 rs for Alzheimer's disease neuropathology in synucleinopathies should help to identify the most appro
267  Alzheimer's disease and patients with alpha-synucleinopathy showed relatively lower burdens of their
268 of active immunotherapy for the treatment of synucleinopathies.SIGNIFICANCE STATEMENT We show that a
269  into possible disease mechanisms underlying synucleinopathies since the formation of alpha-syn fibri
270 ry urgency and frequency are common in alpha-synucleinopathies such as Parkinson disease, Lewy body d
271 sociated with an enhanced risk of developing synucleinopathies such as Parkinson's disease (PD) and d
272                    The molecular hallmark of synucleinopathies such as Parkinson's disease, dementia
273 catecholamine deficiency characterizes alpha-synucleinopathies such as Parkinson's disease.
274 nclusions more commonly found in other alpha-synucleinopathies such as Parkinson's disease.
275 ase-modifying therapeutic strategy for alpha-synucleinopathies such as PD.
276 is usually comorbid with or a precursor to a synucleinopathy such as Parkinson's disease (PD).
277  behavior disorder is intricately related to synucleinopathies, such as dementia with Lewy bodies, bu
278 hies, such as frontotemporal dementia; alpha-synucleinopathies, such as Parkinson's disease or dement
279 tional vaccine approach for the treatment of synucleinopathies, such as Parkinson's disease, dementia
280 rs including Parkinson's disease and related synucleinopathies that are characterized by accumulation
281           Pathologic inclusions define alpha-synucleinopathies that include Parkinson's disease (PD).
282 g evidence argues that prions feature in the synucleinopathies that include Parkinson's disease, Lewy
283 isease (PD), and its accumulation results in synucleinopathies that include PD, dementia with Lewy bo
284 enesis of Parkinson's disease (PD) and other synucleinopathies that leads to disruption in neuronal f
285 er, outside of that context, the patterns of synucleinopathy that Braak described are often not obser
286  Multiple system atrophy is a sporadic alpha-synucleinopathy that typically affects patients in their
287                           In tauopathies and synucleinopathies, the normally soluble intracellular pr
288  sex-adjusted risk of death for each type of synucleinopathy, the median time from diagnosis to death
289 apacity in human midbrain dopamine models of synucleinopathies through disrupting hydrolase trafficki
290 assessing risk factors for neurodegenerative synucleinopathy to patients with idiopathic RBD.
291                        The incidence rate of synucleinopathies was 21.0 per 100 000 person-years over
292                                         This synucleinopathy was fully developed already 10 days afte
293 y body disorder with autopsy-confirmed alpha synucleinopathy, we identified 49 (23%) patients with no
294 nsgenic (A53TalphaS Tg) mouse model of alpha-synucleinopathy, we show that disease onset in the alpha
295  aggregates in Parkinson disease and related synucleinopathies, were selectively elevated in neurons
296 s, our data point to a prion-like cascade in synucleinopathies whereby cell-cell transmission and pro
297 s, including Parkinson's disease and related synucleinopathies, which are characterized by the accumu
298 ementia due to Alzheimer's disease and alpha-synucleinopathies, which suggests that these disorders s
299 defects in neuronal autophagy prior to alpha-synucleinopathy, which was associated with accumulation
300 ile, synchronized rapid-onset model of alpha-synucleinopathy will be highly valuable in testing disea

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