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1 es in multiple neurodegenerative disorders ("synucleinopathies").
2 mortem brain tissue from patients with alpha-synucleinopathy.
3 short-term development of clinically defined synucleinopathy.
4 value, and likelihood ratio 1.54 to predict synucleinopathy.
5 ntifies IRBD patients at short-term risk for synucleinopathy.
6 gh risk of phenoconverting to a manifest CNS synucleinopathy.
7 ng TDP-43 proteinopathy, tauopathy and alpha-synucleinopathy.
8 ce of parkinsonism and determine the type of synucleinopathy.
9 e further evaluated in a Drosophila model of synucleinopathy.
10 n situ studies of human specimens with alpha-synucleinopathy.
11 neurodegenerative mechanism underlying alpha-synucleinopathy.
12 mouse model of PD delayed the progression of synucleinopathy.
13 may also benefit PD patients and others with synucleinopathy.
14 er, before and after their conversion into a synucleinopathy.
15 led t test; P = .04) and more frequent alpha-synucleinopathy.
16 D are at very high risk of neurodegenerative synucleinopathy.
17 ell uptake and propagation for tauopathy and synucleinopathy.
18 nting with dementia in the context of a pure synucleinopathy.
19 y in the SNc in two distinct mouse models of synucleinopathy.
20 on in iRBD to more severe/dementing forms of synucleinopathy.
21 hy, as >80% will eventually convert to overt synucleinopathy.
22 l features of autonomic dysfunction in alpha-synucleinopathy.
23 pha-synuclein (alpha-Syn) leads to different synucleinopathies.
24 pha-synuclein (alpha-syn) and jointly termed synucleinopathies.
25 w therapeutic target to combat the spread of synucleinopathies.
26 ies for disease modification in PD and other synucleinopathies.
27 therapeutic value of sirtuin 2 inhibition in synucleinopathies.
28 nderlie the progression of neurodegenerative synucleinopathies.
29 our understanding of disease pathogenesis in synucleinopathies.
30 ent of targeted therapies for PD and related synucleinopathies.
31 ognomonic protein inclusions in PD and other synucleinopathies.
32 sis of Parkinson's disease and related alpha-synucleinopathies.
33 cating a treatment strategy for PD and other synucleinopathies.
34 al other neurodegenerative diseases known as synucleinopathies.
35 motor symptoms and dementia symptoms across synucleinopathies.
36 e and genotyped for variants associated with synucleinopathies.
37 re, MSA is included in the category of alpha-synucleinopathies.
38 associated with iRBD and with pRBD in overt synucleinopathies.
39 GCS) inhibition as a potential treatment for synucleinopathies.
40 onal distribution of aggregates in different synucleinopathies.
41 disease course and survival in patients with synucleinopathies.
42 slow the progression of PD and related alpha-synucleinopathies.
43 rs could be a novel therapeutic strategy for synucleinopathies.
44 it evades sHsp chaperone action in the alpha-synucleinopathies.
45 thogenesis and developing new treatments for synucleinopathies.
46 treatments of Parkinson's disease and other synucleinopathies.
47 allmarks of Parkinson disease (PD) and alpha-synucleinopathies.
48 on that may be applicable for PD and related synucleinopathies.
49 l disease indicator for PD and related alpha-synucleinopathies.
50 eneration in Parkinson's disease and related synucleinopathies.
51 therapeutic strategy for PD and other alpha-synucleinopathies.
52 pathogens may contribute to the diversity of synucleinopathies.
53 tential therapeutics for GD, PD, and related synucleinopathies.
54 eases, collectively referred to as the alpha-synucleinopathies.
55 g pathophysiologic mechanisms underlying the synucleinopathies.
56 ostasis, thereby reducing the progression of synucleinopathies.
57 autonomia in Parkinson's disease and related synucleinopathies.
58 cause Parkinson's disease and other chronic synucleinopathies.
59 resents an important therapeutic strategy in synucleinopathies.
60 peutic convergence point for a wide range of synucleinopathies.
61 conformers or strains characterize specific synucleinopathies.
62 beneficial as treatments for PD and related synucleinopathies.
63 group of neurological disorders described as synucleinopathies.
64 at this higher order has yet to be shown in synucleinopathies.
65 monomeric alpha-syn in PD and in other alpha-synucleinopathies.
66 ve drugs for the treatment of PD and related synucleinopathies.
67 are the pathogenic species in PD and related synucleinopathies.
68 other neurodegenerative disorders, known as synucleinopathies.
69 n development of Parkinson disease and other synucleinopathies.
70 ipation in Parkinson disease and other alpha-synucleinopathies.
71 each other's aggregation via an interface in synucleinopathies.
72 different clinico-pathological traits within synucleinopathies.
73 d are thus a novel therapeutic candidate for synucleinopathies.
74 f reactive samples between MSA and Lewy body synucleinopathies.
75 y body inclusions in neurodegenerative alpha-synucleinopathies.
76 RNA miR-19b occurs in the prodromal stage of synucleinopathies.
77 have immediate therapeutic implications for synucleinopathies.
78 ders including Parkinson's disease and other synucleinopathies.
79 increase the risk of developing PD and other synucleinopathies.
80 for the treatment of the yet incurable alpha-synucleinopathies.
81 ng of alpha-syn biology and the treatment of synucleinopathies.
82 te the interaction between GBA mutations and synucleinopathies.
83 ound in Parkinson's disease brains and other synucleinopathies.
84 sions in Parkinson's disease and other alpha-synucleinopathies.
85 is a promising strategy for the treatment of synucleinopathies.
86 ted to the onset of multiple diseases termed synucleinopathies.
87 in neurons in Parkinson's disease and other synucleinopathies.
88 athogenesis of Parkinson's disease and other synucleinopathies.
89 rogression of aSyn pathology in PD and other synucleinopathies.
90 topathology of Parkinson disease and related synucleinopathies.
91 a hallmark of Parkinson's disease and other synucleinopathies.
92 may underlie the tremendous heterogeneity of synucleinopathies.
93 ould be a viable target for the treatment of synucleinopathies.
94 egrade alpha-synuclein in PD and other alpha-synucleinopathies.
95 c pathology as one of the earliest events in synucleinopathies.
96 strategy for the treatment of PD and related synucleinopathies.
97 ng and may modulate the progression of alpha-synucleinopathies.
98 rking memory performance improvements in the synucleinopathies.
99 generative disease and particularly with the synucleinopathies.
100 nal dysfunction and toxicity in PD and other synucleinopathies.
101 treatment of Parkinson's disease and related synucleinopathies.
102 from alphaSyn-overexpressing mice and human synucleinopathies.
103 mplification and propagation of pathology in synucleinopathies.
104 feature of neurodegenerative diseases called synucleinopathies.
105 ts potential as a new therapeutic target for synucleinopathies.
106 other 5' risk variants across the different synucleinopathies.
107 asyn and, ultimately, in the pathogenesis of synucleinopathies.
108 the selective targeting observed among human synucleinopathies.
109 eveloped into a therapeutic for PD and other synucleinopathies.
110 sitioning this approach to treat human alpha-synucleinopathies.
111 SA not only from CON but also from Lewy body synucleinopathies.
112 glycation-associated cellular pathologies in synucleinopathies.
113 eatments for Parkinson's disease and related synucleinopathies.
114 cholinergic neurons to model PD and related synucleinopathies.
115 res with relevant clinical outcomes in alpha-synucleinopathies.
116 points to shared disease mechanisms in alpha-synucleinopathies.
117 for therapeutic intervention in PD and other synucleinopathies.
118 -synuclein ubiquitination in models of alpha-synucleinopathies.
119 n, which may be applicable to other types of synucleinopathies.
120 1991 to 2010 incident-cohort study of alpha-synucleinopathies.
121 a potential therapeutic target in the alpha-synucleinopathies.
122 ion of Parkinson's disease and related alpha-synucleinopathies.
123 urodegenerative disorders referred to as the synucleinopathies.
124 progression of Parkinson's disease and other synucleinopathies.
125 ity, could be the critical dyshomeostasis in synucleinopathies.
126 llmark of Parkinson's disease and many other synucleinopathies.
127 a hallmark of Parkinson's disease and other synucleinopathies.
128 odegenerative disorders, collectively termed synucleinopathies.
129 nhibitory GCase modulators in PD and related synucleinopathies.
130 resents an important therapeutic strategy in synucleinopathies.
131 these features of clinical heterogeneity in synucleinopathies.
134 0, 461 individuals received a diagnosis of a synucleinopathy (309 [67%] of Parkinson disease, 81 [17.
140 low-up, 68.6% (n = 316) of the patients with synucleinopathies and 48.7% (n = 220) of the referent pa
141 patients with incident, clinically diagnosed synucleinopathies and age- and sex-matched referent part
142 alpha-Syn oligomers are a toxic species in synucleinopathies and are suspected to cause neuritic pa
143 difying therapeutic strategy for GBA-related synucleinopathies and conceivably for certain forms of s
144 heimer's disease neuropathology is common in synucleinopathies and confers a worse prognosis for each
145 guish alpha-synucleinopathies from non-alpha-synucleinopathies and controls was 84% (sensitivity = 75
146 between OH and cognitive impairment in alpha-synucleinopathies and discuss possible mechanisms and im
147 O-GlcNAcylation may slow the progression of synucleinopathies and further support a general function
148 ydrolase trafficking may prove beneficial in synucleinopathies and indicates that human midbrain dise
149 tial to be utilized towards immunotherapy in synucleinopathies and may also have applications in ante
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 ir clinical implications for tauopathies and synucleinopathies and propose a working hypothesis for f
154 y prevented the gut-to-brain spread of alpha-synucleinopathy and associated neurodegeneration and beh
155 ular screen allows probing the mechanisms of synucleinopathy and refining drug candidates, including
156 between OH and cognitive impairment in alpha-synucleinopathies, and 'indirect-evidence studies' based
157 ein accumulation as occurs in PD and related synucleinopathies, and accumulation of lipofuscin deposi
158 aggregates that are implicated in different synucleinopathies, and may also enable the development o
159 rodegenerative diseases like prion diseases, synucleinopathies, and tauopathies that are collectively
160 for Gaucher disease for the treatment of the synucleinopathies, and the role of lysosomal pathways in
161 imary outcome is phenoconversion to an overt synucleinopathy, and stratification features should be u
162 pting to tackle the pathological features of synucleinopathies, antibody-based immunotherapy holds mu
170 a novel drug target that can be explored in synucleinopathies as well as in other neurodegenerative
171 body disorders with autopsy-confirmed alpha synucleinopathy (as of Oct 1, 2015) who were previously
172 sleep behavior disorder (RBD) is a prodromal synucleinopathy, as >80% will eventually convert to over
175 we describe a new Drosophila model of alpha-synucleinopathy based on widespread expression of wild-t
177 oup of other disorders collectively known as synucleinopathies, but the precise molecular mechanisms
178 iver of neurodegenerative diseases known as "synucleinopathies," but the mechanisms underlying this t
179 candidate to achieve disease modification in synucleinopathies by limiting alpha-syn accumulation.
181 survival and causes of death of persons with synucleinopathies compared with the general population h
182 The prevalence of idiopathic RBD at alpha-synucleinopathy diagnosis was 3.4%, increasing to 23.8%
185 in dementia with Lewy bodies and other alpha-synucleinopathies, direct evidence for the precise synap
186 lysosomal enzyme glucocerebrosidase, and the synucleinopathies directly resulted from the clinical re
188 e kinase 2 (PLK2), an enzyme up-regulated in synucleinopathy-diseased brains, interacts with, phospho
189 asyn misfolding and neurotoxicity in various synucleinopathy disorders and provides an overview of cu
190 ase pathogenesis, available animal models of synucleinopathy do not replicate the full range of cellu
191 opulations differ in when they exhibit alpha-synucleinopathies during PD pathogenesis, they could als
192 ing that DMV neurons display extensive alpha-synucleinopathies earlier than SN dopamine neurons while
194 ently, the exact reasons why different alpha-synucleinopathies exhibit variable pathologies and pheno
195 cognitive impairment in patients with alpha-synucleinopathies exists, but the underlying mechanisms
196 cocerebrosidase activity in murine models of synucleinopathy (expressing wild type Gba1) affected alp
197 a localized fashion in human tauopathies and synucleinopathies, followed by seed-dependent propagatio
199 Diagnostic accuracy to distinguish alpha-synucleinopathies from non-alpha-synucleinopathies and c
200 tool to help clinicians differentiate alpha-synucleinopathies from other forms of parkinsonism when
202 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
207 Aggregates of alpha-synuclein in distinct synucleinopathies have been proposed to represent differ
209 ng protein 43 immunoreactive deposits, alpha-synucleinopathies, hippocampal sclerosis and prion disea
210 o functional and structural brain imaging of synucleinopathies in humans have provided a rich new und
212 s translational importance for understanding synucleinopathies in humans.SIGNIFICANCE STATEMENT alpha
214 of this signature predicted conversion to a synucleinopathy in iRBD (p = 0.036, odds ratio [OR] = 2.
215 t alpha-synuclein preformed fibrils induce a synucleinopathy in non-human primates with authentic Lew
216 l analysis showed increased risk of incident synucleinopathy in patients with abnormal DAT-SPECT than
217 d have prospect in the amelioration of alpha-synucleinopathy in PD and other Lewy body diseases.
219 e, we test this postulate by assessing alpha-synucleinopathy in the brain in a novel gut-to-brain alp
222 us translational potential for PD and other "synucleinopathies." In this work, using a variety of bio
224 n leading to motor and cognitive deficits in synucleinopathies including Parkinson's disease (PD) and
225 ermed Lewy bodies that pathologically define synucleinopathies including Parkinson's disease (PD) and
227 unds, which might yield clinical benefit for synucleinopathies including Parkinson's disease, Lewy bo
228 3) alpha-synuclein inclusion ratings in four synucleinopathies including Parkinson's disease, Parkins
230 ein is a key molecule in the pathogenesis of synucleinopathy including dementia with Lewy bodies, Par
232 nical and pathophysiological overlap seen in synucleinopathies, including Parkinson's disease, dement
238 vidence that disease heterogeneity among the synucleinopathies is caused by distinct alpha-synuclein
242 sting that targeting synaptic dysfunction in synucleinopathies may provide a promising therapeutic di
243 Similar changes are present in a mouse alpha-synucleinopathy model and in postmortem brain tissue fro
244 models of synucleinopathy (a Gaucher-related synucleinopathy model, Gba(D409V/D409V) and a A53T-alpha
245 triggering neuroprotective Treg responses in synucleinopathy models, and the combined vaccine is more
246 ne of many neurodegenerative diseases termed synucleinopathies, neuropathologically defined by inclus
248 ng of the clinical heterogeneity among alpha-synucleinopathies, offers an opportunity for a specific
250 ctors, imaging changes associated with alpha-synucleinopathy, or physical findings of parkinsonism.
251 ommon genetic risk factor for developing the synucleinopathies Parkinson disease (PD) and dementia wi
252 sorder (RBD) in patients who developed alpha-synucleinopathies (Parkinson disease, dementia with Lewy
253 28.7%) subjects developed clinically defined synucleinopathy (Parkinson's disease in 11, dementia wit
254 These findings implicate MARKs early in synucleinopathy pathogenesis and as potential therapeuti
255 time incidence was 53 times greater in alpha-synucleinopathy patients than in controls (odds ratio [O
256 53 times greater lifetime incidence in alpha-synucleinopathy patients than in controls, RBD was more
257 ed human midbrain dopamine (DA) neurons from synucleinopathy patients with different PD-linked mutati
258 In Parkinson's disease (PD) and other alpha-synucleinopathies, prefibrillar alpha-synuclein (alphaS)
260 ined negative effects on disability in alpha-synucleinopathies, reflecting a 'malignant' phenotype of
263 eveloping Parkinson's disease (PD) and other synucleinopathies, resulting in a lower age of onset and
264 rs for Alzheimer's disease neuropathology in synucleinopathies should help to identify the most appro
265 Alzheimer's disease and patients with alpha-synucleinopathy showed relatively lower burdens of their
266 of active immunotherapy for the treatment of synucleinopathies.SIGNIFICANCE STATEMENT We show that a
267 for testing disease-modifying treatments for synucleinopathies, since RBD represents an early prodrom
269 ry urgency and frequency are common in alpha-synucleinopathies such as Parkinson disease, Lewy body d
270 sociated with an enhanced risk of developing synucleinopathies such as Parkinson's disease (PD) and d
271 linical and pathological differences between synucleinopathies such as Parkinson's disease and multip
275 hies, such as frontotemporal dementia; alpha-synucleinopathies, such as Parkinson's disease or dement
276 tional vaccine approach for the treatment of synucleinopathies, such as Parkinson's disease, dementia
278 g evidence argues that prions feature in the synucleinopathies that include Parkinson's disease, Lewy
279 isease (PD), and its accumulation results in synucleinopathies that include PD, dementia with Lewy bo
280 enesis of Parkinson's disease (PD) and other synucleinopathies that leads to disruption in neuronal f
282 Multiple system atrophy is a sporadic alpha-synucleinopathy that typically affects patients in their
284 in phenotypes in both cell and fly models of synucleinopathy, the effects correlating with the extent
285 sex-adjusted risk of death for each type of synucleinopathy, the median time from diagnosis to death
286 apacity in human midbrain dopamine models of synucleinopathies through disrupting hydrolase trafficki
290 ed in the spreading of alphaSyn pathology in synucleinopathies, we investigated the biological mechan
291 y body disorder with autopsy-confirmed alpha synucleinopathy, we identified 49 (23%) patients with no
292 nsgenic (A53TalphaS Tg) mouse model of alpha-synucleinopathy, we show that disease onset in the alpha
293 aggregates in Parkinson disease and related synucleinopathies, were selectively elevated in neurons
294 e RBD represents an early prodromal stage of synucleinopathy when neuropathology may be more responsi
295 s, including Parkinson's disease and related synucleinopathies, which are characterized by the accumu
297 ementia due to Alzheimer's disease and alpha-synucleinopathies, which suggests that these disorders s
298 defects in neuronal autophagy prior to alpha-synucleinopathy, which was associated with accumulation
299 ile, synchronized rapid-onset model of alpha-synucleinopathy will be highly valuable in testing disea
300 tissue, and neurophysiological biomarkers of synucleinopathies, will enable more efficient clinical t