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1 mor and hallucinations were more frequent in Lewy body disease.
2 stent with the limbic (transitional) form of Lewy body disease.
3 of delusions distinguished PSP from diffuse Lewy body disease.
4 rkinson disease and the neocortex of diffuse Lewy body disease.
5 were not assigned pathological diagnoses of Lewy body disease.
6 majority of cases, indicative of underlying Lewy body disease.
7 ll groups in Alzheimer's disease compared to Lewy body disease.
8 some of the clinical disparities observed in Lewy body disease.
9 mechanisms underlying Lewy body formation in Lewy body disease.
10 aspects of the underlying neuropathology in Lewy body disease.
11 ges in both prodromal and manifest phases of Lewy body disease.
12 nt to understand cholinergic degeneration in Lewy body disease.
13 m 12 controls and 6 patients with Incidental Lewy Body Disease.
14 ontribute to alpha-synuclein accumulation in Lewy body disease.
15 res were striking and reminiscent of diffuse Lewy body disease.
16 sight into the role of glucocerebrosidase in Lewy body disease.
17 ivity in a pattern characteristic of diffuse Lewy body disease.
18 has been widely used as a diagnostic aid in Lewy body disease.
19 ent probably reflects brainstem and cerebral Lewy body disease.
20 re subsequently found to have autopsy-proven Lewy body disease.
21 or and cognitive deficits similar to diffuse Lewy body disease.
22 imilar mechanisms could be at play in PD and Lewy body disease.
23 Jointly, these disorders are denominated Lewy body disease.
24 of G2019S-associated Parkinson's disease is Lewy body disease.
25 nd in brains of patients with PD and diffuse Lewy body disease.
26 in sporadic Parkinson's disease and diffuse Lewy body disease.
27 se at high risk of developing PD and related Lewy body diseases.
28 gs support a role for tau copathology in the Lewy body diseases.
29 ion of alpha-synucleinopathy in PD and other Lewy body diseases.
30 for the formation of Lewy bodies in various Lewy body diseases.
31 ogenic pathway for both genetic and sporadic Lewy body diseases.
32 athogenesis of Parkinson's disease and other Lewy body diseases.
33 er of neurodegenerative disorders, including Lewy body diseases.
34 ional diversion of ERK-signaling pathways in Lewy body diseases.
35 em tissues representing the full spectrum of Lewy body diseases.
36 ementia (progressive supranuclear palsy = 1, Lewy body disease = 1, vascular brain injury = 1, and fr
37 alternative pathological diagnoses including Lewy body disease (12.8%; n = 26), progressive supranucl
38 even with Alzheimer's disease (11%), 11 with Lewy body disease (16%) and four with frontotemporal lob
39 were common in Alzheimer's disease (58%) and Lewy body disease (37%) and were observed in all groups.
40 l amyloid angiopathy (71%, 54-88; I(2)=89%), Lewy body disease (44%, 25-62; I(2)=77%), and cerebrovas
41 athy: 86% versus 79%, Fisher exact P = 0.33; Lewy body disease: 49% versus 42%, P = 0.48, respectivel
43 heimer disease, cerebrovascular disease, and Lewy body disease accumulate in the brains of older pers
44 rains of AR-JP and idiopathic PD and diffuse Lewy body disease also exhibit increased level of p38.
45 occurred more frequently in the FTLD-TDP and Lewy body disease/Alzheimer's disease categories compare
47 gnificantly more frequently in patients with Lewy body disease/Alzheimer's disease than all other pat
48 dentification as frequently as patients with Lewy body disease/Alzheimer's disease, and were signific
53 ology: 111 with Alzheimer's disease, 59 with Lewy body disease and concomitant Alzheimer's disease, 1
56 es, including comparative conditions such as Lewy body disease and limbic-predominant age-related TDP
57 are little data on the relationship between Lewy body disease and mild cognitive impairment syndrome
58 likelihood of multiple system atrophy versus Lewy body disease and progressive supranuclear palsy if
59 ations for understanding the pathobiology of Lewy body disease and the continued use of reduced pS129
60 combination of changes seen in pure forms of Lewy body disease and those seen in Alzheimer's disease.
61 On autopsy, six had neocortical-predominant Lewy body disease and two had limbic-predominant Lewy bo
62 sm is a significant predictor of survival in Lewy body diseases and may allow an earlier survival pre
63 rative diseases such as Alzheimer's disease, Lewy body disease, and frontotemporal lobar degeneration
64 body variant of Alzheimer's disease, diffuse Lewy body disease, and Parkinson's disease and suggests
65 body variant of Alzheimer's disease, diffuse Lewy body disease, and Parkinson's disease, NACP was fou
66 throughout the striatum in individuals with Lewy body disease, and serotonergic degeneration in huma
68 e therapeutic imperative for Alzheimer's and Lewy body diseases, and provide evidence to support the
69 id deposits, the alpha-synuclein deposits in Lewy body diseases are intracellular, and thus it is les
70 ism, sporadic Parkinson disease, and diffuse Lewy Body disease as well as the 1-methyl-4-phenyl-1,2,3
71 Alzheimer disease with or without concurrent Lewy body disease as well as three cellular models of pr
73 s disease pathology frequently coexists with Lewy body disease at autopsy in patients with probable d
74 ed the growth of asyn fibrils amplified from Lewy Body Disease brain tissue, further validating the i
77 ntribute to the pathogenesis of PD and other Lewy body diseases by promoting alterations in parkin an
78 eptides may contribute to the development of Lewy-body diseases by promoting the aggregation of alpha
81 Alzheimer's/Parkinson's disease and diffuse Lewy body disease cases had significantly higher amounts
84 ases with pathologically defined neocortical Lewy body disease confirmed the link between bradykineti
85 on into fibrils similar to those observed in Lewy body disease, confirming the prion-like capacity of
87 poral degeneration (FTD) (n = 9), or diffuse Lewy body disease (DLB) with mixed AD or FTD pathologies
89 hallmark of Parkinson's disease and diffuse Lewy body disease (DLBD) is the aggregation of alpha-syn
90 ed from postmortem human brains with diffuse Lewy body disease (DLBD) preferentially show endocytosis
92 ody variant of AD [LBVAD] and 4 pure diffuse Lewy body disease [DLBD]) who had antemortem position em
93 If this topography and temporal evolution of Lewy body disease does occur, other manifestations of th
94 mprehensive review of cholinergic changes in Lewy body disease, encompassing both central and periphe
95 in neuropathologically defined samples with Lewy body disease from the Netherlands Brain Bank (n = 2
96 urodegenerations, such as Alzheimer disease, Lewy body disease, frontotemporal lobar degeneration, an
97 28; hippocampus -21%, P = 0.002), but in the Lewy body diseases group only the amygdala was smaller i
99 trophy is challenging and many patients with Lewy body disease (i.e. Parkinson's disease or dementia
100 early stage PD cases and cases of incidental Lewy body disease (ILBD), which is thought to represent
101 tients met pathologically based criteria for Lewy body disease in relation to (1) the presence and se
102 s a predictable topography of progression of Lewy body disease in the CNS, beginning in olfactory str
103 ly to neurons in the brains of patients with Lewy body disease, in co-transduced cells alpha-synuclei
104 Cholinergic degeneration is significant in Lewy body disease, including Parkinson's disease, dement
105 us on hallmark neuropathological findings in Lewy body diseases, including abnormal alpha-synuclein a
106 were eventually shown to have autopsy-proven Lewy body disease, indicating that rapid eye movement sl
107 ve disorders such as Parkinson's disease and Lewy body disease is increased upon injury to the nervou
108 We conclude that sympathetic denervation in Lewy body diseases is associated with decreased vesicula
109 hat occur in Parkinson's disease and related Lewy body diseases is essential for development of new t
112 NAs are differentially affected in brains of Lewy body disease (LBD) and Alzheimer's disease (AD) pat
114 Alzheimer's disease (AD) and neocortical Lewy body disease (LBD) are the most common neurodegener
115 f alpha-Synuclein (alphaSyn) aggregates from Lewy body disease (LBD) brains has been widely described
118 ociations with neuropathological features in Lewy body disease (LBD) have been limited to candidate g
121 D) neuropathologic changes (NCs) but without Lewy body disease (LBD) NCs (AD group; n=244), dementia
122 s a hallmark of Parkinson's disease (PD) and Lewy body disease (LBD), a heterogeneous group of disord
123 , encoded by the SNCA gene, are hallmarks of Lewy body disease (LBD), affecting multiple brain region
124 gies, including CTE, Alzheimer disease (AD), Lewy body disease (LBD), and transactive response DNA-bi
126 without pathologic change or with pure AD or Lewy body disease (LBD), nonhuman primates (NHPs), and P
133 m of neurodegenerative diseases that include Lewy body diseases (LBD) and Multiple System Atrophy (MS
139 both classifiers) than those diagnosed with Lewy-body diseases (LBDs; majority Parkinson disease [PD
140 pha-syn has been investigated extensively in Lewy body disease, less is known about the role of this
142 gic measures representing Alzheimer disease, Lewy body disease, limbic-predominant age-related transa
144 Conclusions and Relevance: Patients with Lewy body disease manifest a spectrum of tau pathology.
145 entional Lewy pathology suggests that AD and Lewy body disease may be more closely related than previ
149 ased the odds of a pathological diagnosis of Lewy body disease (odds ratios = 1.98-2.73), but its pos
150 ry catheters [multiple system atrophy versus Lewy body disease: odds ratio (OR): 2.0, 95% confidence
151 for 51 cases (27 Alzheimer's disease and 24 Lewy body disease) of whom 17 had post-mortem confirmed
152 body disease and two had limbic-predominant Lewy body disease; only one had coexisting high-likeliho
154 ant cerebellar signs was also higher than in Lewy body disease (OR: 7.0, 95% CI: 2.5-19.5, P < 0.01)
155 mber of red flag features than patients with Lewy body disease (OR: 8.8, 95% CI: 3.2-24.2, P < 0.01)
156 ied with MCI were without "high"-level ADNC, Lewy body disease, or hippocampal sclerosis pathologies;
157 ry, in several conditions including cortical Lewy body disease, Parkinson's disease dementia, traumat
158 e neurodegenerative disorder associated with Lewy body disease pathology in central and peripheral ne
159 Although psychosis is a defining feature of Lewy body disease, psychotic symptoms occur in a subset
160 idor, dysphagia and falls than patients with Lewy body disease; resting tremor, pill-rolling tremor a
161 tional connectivity in 108 people across the Lewy body disease spectrum (46 Parkinson's with normal c
162 ry, but generally the dominant genes cause a Lewy body disease spectrum whereas recessive genes cause
163 Rab27b levels in human postmortem incidental Lewy body disease subjects relative to healthy controls.
164 was observed in degenerating human Parkinson/Lewy body disease substantia nigra neurons but not in ag
165 zyme glucocerebrosidase, are associated with Lewy body diseases such as Parkinson's disease and Lewy
167 129-alpha-syn) is substantially increased in Lewy body disease, such as Parkinson's disease (PD) and
168 significantly more likely than those with no Lewy body disease to have visual hallucinations of mispe
169 uclear palsy patients, whereas patients with Lewy body disease took longer to reach multiple mileston
170 Alzheimer's/Parkinson's disease, and diffuse Lewy body disease) using in situ end labeling to detect
171 lele in AD subjects with concomitant diffuse Lewy body disease was intermediate between controls and
172 respectively), although amygdala-predominant Lewy body disease was more common in early than late ons
173 ase has pathological similarities to that in Lewy body disease, we performed an observational post-mo
174 aline atherosclerosis, siderocalcinosis, and Lewy body disease were independently associated with cog
175 Patients with Braak Parkinson stage 5-6 Lewy body disease were significantly more likely than th
177 ittle is known about hospice use patterns in Lewy body disease, which includes both Parkinson disease
178 el mechanism for epigenetic dysregulation in Lewy body diseases, which might underlie the decrease in
179 inding was observed in 4 of 17 patients with Lewy body disease with low cortical [11C]PiB retention.
180 in brain donors with Alzheimer's disease or Lewy body diseases with and without co-occurring LATE-NC
181 ulnerability to specific neuropathologies in Lewy body disease, with potential relevance for the furt
183 patients with pure autonomic failure (PAF, a Lewy body disease without parkinsonism); in patients wit
184 d with disease risk and phenotypic traits in Lewy body disease, yet little is known about the genetic