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1 found in progressive supranuclear palsy and corticobasal degeneration.
2 some 17, progressive supranuclear palsy, and corticobasal degeneration.
3 s a neurodegenerative disease that resembles corticobasal degeneration.
4 ce of alien limb syndorme separated PSP from corticobasal degeneration.
5 supranuclear palsy, Parkinson's disease and corticobasal degeneration.
6 lopathy, progressive supranuclear palsy, and corticobasal degeneration.
7 disease, progressive supranuclear palsy and corticobasal degeneration.
8 uals were diagnosed clinically with probable corticobasal degeneration.
9 e (AGD), progressive supranuclear palsy, and corticobasal degeneration.
10 can be a clinicopathological presentation of corticobasal degeneration.
11 pathology, including Alzheimer's disease and corticobasal degeneration.
12 l tau deposition in a pattern reminiscent of corticobasal degeneration.
13 atrophy, progressive supranuclear palsy, and corticobasal degeneration.
14 , such as progressive supranuclear palsy and corticobasal degeneration.
15 ith progressive supranuclear palsy (PSP) and corticobasal degeneration.
16 disease, progressive supranuclear palsy and corticobasal degeneration; 3) alpha-synuclein inclusion
17 ents with Alzheimer's disease (10 patients), corticobasal degeneration (5 patients), and progressive
18 ated pattern provided excellent specificity (corticobasal degeneration: 92.7%; progressive supranucle
19 ns in GLT-1 expression were also observed in corticobasal degeneration, a tauopathy with prominent pa
20 alsy, 10 with Parkinson's disease, nine with corticobasal degeneration and 11 age-matched normal cont
21 cal temporal lobe atrophy and the third with corticobasal degeneration and biparietal atrophy-on test
22 k's disease, progressive supranuclear palsy, corticobasal degeneration and familial frontotemporal de
23 in brains of progressive supranuclear palsy, corticobasal degeneration and familial tauopathy due to
25 h diagnoses of multiple sclerosis, dementia, corticobasal degeneration and new variant CJD have been
26 individual patients included Pick's disease, corticobasal degeneration and other tauopathies, Lewy bo
27 ease, some cases of frontotemporal dementia, corticobasal degeneration and progressive supranuclear p
28 is report presents evidence to indicate that corticobasal degeneration and progressive supranuclear p
29 ion of this extensive white matter lesion in corticobasal degeneration and progressive supranuclear p
30 and also thioflavin-S-negative pathology in corticobasal degeneration and progressive supranuclear p
31 Clinical diagnoses of progressive apraxia, corticobasal degeneration and progressive supranuclear p
32 e, it detects only the neuronal pathology in corticobasal degeneration and progressive supranuclear p
33 123 patients with FTLD, Alzheimer's disease, corticobasal degeneration and progressive supranuclear p
35 rogressive supranuclear palsy, patients with corticobasal degeneration and Richardson syndrome had le
37 lesions in the typically affected regions in corticobasal degeneration and the pathognomonic astrocyt
38 is strongly associated with the risk of PSP, corticobasal degeneration and, to a lesser extent, AD an
39 s, including progressive supranuclear palsy, corticobasal degeneration, and argyrophilic grain diseas
40 ick disease, progressive supranuclear palsy, corticobasal degeneration, and chronic traumatic encepha
41 disease, progressive supranuclear palsy and corticobasal degeneration, and in the glial and neuronal
42 , non-amnestic as frontotemporal dementia or corticobasal degeneration, and non-specific as dementia
43 all patient groups, Parkinson's disease with corticobasal degeneration, and Parkinson's disease with
44 causes, including dementia with Lewy bodies, corticobasal degeneration, and prion disease, have also
45 ific modification in Alzheimer disease (AD), corticobasal degeneration, and progressive supranuclear
46 approximately 24%) that existed between the corticobasal degeneration- and the progressive supranucl
48 nsidering progressive supranuclear palsy and corticobasal degeneration as tauopathies, and multiple s
50 show additional similarities between PSP and corticobasal degeneration, but unlike corticobasal degen
51 obar dementias, including Pick's disease and corticobasal degeneration, by the absence of abnormally
59 neration cases and six age-matched end-stage corticobasal degeneration cases were included in this st
60 (sum of all regional tau load) of end-stage corticobasal degeneration cases were nine times greater
63 Frontotemporal dementias (FTDs), including corticobasal degeneration (CBD) and progressive supranuc
64 To highlight the fact that patients with corticobasal degeneration (CBD) and progressive supranuc
65 quitin-only-immunoreactive changes (FTLD-U), corticobasal degeneration (CBD) and progressive supranuc
66 Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are neurodegenerative fo
67 Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are sporadic neurodegene
72 of progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) suggest that mitigating
73 itrated tau in the insoluble fraction of AD, corticobasal degeneration (CBD), and Pick's disease (PiD
81 rogressive supranuclear palsy (PSP-tau), and corticobasal degeneration (CBD-tau) patients into differ
82 clinical phenotype originally described for corticobasal degeneration, characterized by asymmetric r
83 43 (TDP-43), progressive supranuclear palsy, corticobasal degeneration, dementia with Lewy bodies, mu
84 H-MRSI in progressive supranuclear palsy and corticobasal degeneration, detection of specific cortica
85 both the variability of presentation of true corticobasal degeneration, for example as a dementing il
86 es for this pattern accurately discriminated corticobasal degeneration from multiple system atrophy a
87 fic network that can be used to discriminate corticobasal degeneration from other atypical parkinsoni
88 tential neuroimaging marker to differentiate corticobasal degeneration from progressive supranuclear
89 metric, predominantly extratemporal atrophy (corticobasal degeneration, fused-in-sarcoma pathology).
91 h clinical PSP and pathological diagnosis of corticobasal degeneration had severe tau pathology in PS
93 sive supranuclear palsy, Pick's disease, and corticobasal degeneration-illustrates the types of analy
94 obasal syndrome or pathological diagnosis of corticobasal degeneration in an attempt to identify the
95 ese diagnostic difficulties we conclude that corticobasal degeneration is a discrete clinicopathologi
100 neuronal lesions leads one to speculate that corticobasal degeneration may begin as an astrogliopathy
101 found in progressive supranuclear palsy and corticobasal degeneration may help in the diagnostic eva
102 SP and corticobasal degeneration, but unlike corticobasal degeneration, more abundant white matter ta
103 son disease, progressive supranuclear palsy, corticobasal degeneration, multiple system atrophy, and
104 neuropathologically, including PSP (n = 24), corticobasal degeneration (n = 11), Parkinson's disease
105 imary progressive aphasia had evolved either corticobasal degeneration (n = 5) or progressive supranu
106 nfluent aphasia, n = 8), and motor variants (corticobasal degeneration, n = 9; and motor neuron disea
107 TLD were distributed between FTLD-tau (34 10 corticobasal degeneration, nine progressive supranuclear
108 , although the values for every patient with corticobasal degeneration or progressive supranuclear pa
109 s, including progressive supranuclear palsy, corticobasal degeneration, Parksinson's disease and poss
110 osis of corticobasal syndrome, only five had corticobasal degeneration pathology, giving a positive p
113 disease, progressive supranuclear palsy, and corticobasal degeneration patient brain tissue slices us
116 of this study was to identify differences in corticobasal degeneration presenting with corticobasal s
117 nerative tauopathies exemplified by sporadic corticobasal degeneration, progressive supranuclear pals
118 non-fluent primary progressive aphasia (the corticobasal degeneration/progressive supranuclear palsy
120 ifications of progressive supranuclear palsy/corticobasal degeneration (PSP/CBD) or multiple-system a
122 the combined group to identify a significant corticobasal degeneration-related metabolic pattern that
124 mputing hemispheric asymmetry scores for the corticobasal degeneration-related pattern on a prospecti
127 chardson's syndrome, and we propose the term corticobasal degeneration-Richardson's syndrome for this
131 ars duration: idiopathic Parkinson's disease corticobasal degeneration, Steele-Richardson-Olszewski s
132 ing with either a frontotemporal dementia or corticobasal degeneration syndrome with a mean age of on
133 s included dementia with spastic paraplegia, corticobasal degeneration syndrome, and stroke disorders
134 sporadic progressive supranuclear palsy and corticobasal degeneration, tau abnormalities are linked
135 atrophy, progressive supranuclear palsy, and corticobasal degeneration was consistently shown to be h
137 ile pathologically proven Pick's disease and corticobasal degeneration were clinically heterogeneous,
139 disease, progressive supranuclear palsy and corticobasal degeneration, which are characterized by in
140 me-like condition, Christianson syndrome and corticobasal degeneration with tau deposition, with each
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