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1 d those who subsequently died were evaluated neuropathologically.
2 multiple system atrophy, both clinically and neuropathologically.
3 grel dogs weighing 23 to 30 kg and validated neuropathologically.
4 Each sample was individually evaluated neuropathologically.
5 or without cerebrovascular disease, defined neuropathologically.
6 s have been the most commonly affected cells neuropathologically.
7 our with Parkinson's disease, both confirmed neuropathologically.
8 gnosis of multiple system atrophy, confirmed neuropathologically.
10 were highly abundant and were found only in neuropathologically affected areas of ALS patients but n
12 renia (N=26) were compared with those from a neuropathologically and neuropsychiatrically normal elde
13 ltiple system atrophy (MSA) cases, confirmed neuropathologically, and eight age-matched controls.
14 identified in the tissue, blindly described neuropathologically, and subsequently divided into ische
15 easured functionally as dementia severity or neuropathologically as increased neuritic plaque and neu
17 ases, which were confirmed biochemically and neuropathologically as variably protease-sensitive prion
22 is a primary mitochondrial disorder defined neuropathologically by a subacute necrotizing encephalom
23 and Alzheimer's diseases, are characterized neuropathologically by accumulation of misfolded protein
24 progressive myoclonus epilepsy characterized neuropathologically by aggregates of abnormally structur
26 Both human and murine NPC are characterized neuropathologically by ballooned neurons distended with
27 order characterized clinically by ataxia and neuropathologically by cerebellar atrophy and granule ce
30 features, as well as cerebellar ataxia, and neuropathologically by neuronal loss, gliosis, and iron
31 ) was associated with dementia characterized neuropathologically by neuronal vacuoles and neurofibril
32 sive neurodegenerative disease characterized neuropathologically by presence of extracellular amyloid
33 sive neurodegenerative disease characterized neuropathologically by presence of extracellular amyloid
37 odegenerative disorder that is characterized neuropathologically by the presence of neuropil aggregat
38 causes and disease symptoms, and are linked neuropathologically by the RNA binding protein TDP-43 (T
39 analysis on transcriptomic data from a large neuropathologically characterised patient cohort reveale
41 more than 5,000 clinically characterized and neuropathologically characterized Alzheimer's dementia c
42 with no available disease-modifying therapy, neuropathologically characterized by intraneuronal aggre
43 n hippocampal subfields in 95 clinically and neuropathologically characterized human cases of DLB, fi
44 prefrontal cortex of antemortem-assessed and neuropathologically characterized schizophrenic and comp
45 From these studies, it is clear that MCI is neuropathologically complex and cannot be understood wit
46 eresting that, in four of four patients with neuropathologically confirmed acute hypoxic changes, we
49 cohort study included 2422 participants with neuropathologically confirmed ADP, LRP, or mixed ADP-LRP
51 ed brains of 4 individuals from Belgium with neuropathologically confirmed Alzheimer disease for the
53 e United Kingdom, of which 33 cases had been neuropathologically confirmed and 2 classified as probab
54 ositive corticobasal syndrome, including two neuropathologically confirmed cases of Alzheimer's disea
55 linical features in clinically diagnosed and neuropathologically confirmed cases of corticobasal synd
58 and spinal cord samples originating from 137 neuropathologically confirmed control individuals to stu
59 fidence interval: 1.06-1.20) and presence of neuropathologically confirmed degenerative changes (that
60 biggest driver of risk, with odds ratios for neuropathologically confirmed E44 carriers exceeding 30
61 d with a novel PRNP mutation associated with neuropathologically confirmed Gerstmann-Straussler-Schei
62 4 gene dose was significantly greater in the neuropathologically confirmed group than in more than 24
63 current study, we examined a large series of neuropathologically confirmed LBD cases (n = 980 in the
64 Center (1985-2015) and 1115 individuals with neuropathologically confirmed LOAD were included from th
65 ts (8 men, 3 women, age 64 +/- 3 years) with neuropathologically confirmed MSA and 11 control subject
67 controls with (n = 397) or without (n = 37) neuropathologically confirmed neurodegenerative disease.
68 in human post-mortem cerebellar tissue from neuropathologically confirmed PD cases and neurologicall
69 ently examined that consisted of 67 cases of neuropathologically confirmed sCJD (33 female, 34 male;
70 analyzed 108 CSF samples from patients with neuropathologically confirmed sCJD or from control patie
71 sues obtained at necropsy from patients with neuropathologically confirmed variant CJD, but not from
72 tissues at necropsy from four patients with neuropathologically confirmed vCJD and from individuals
73 cribe a family (DUK1684) with clinically and neuropathologically confirmed, autosomal dominant, non-A
74 ortex and putamen tissues from 4 post-mortem neuropathologically-confirmed control human brains, we d
75 GWAS) of PSP which includes 2779 cases (2595 neuropathologically-confirmed) and 5584 controls and ide
76 on markers from a unique cohort of over 1600 neuropathologically defined AD cases and controls (1019
77 1, antemortem plasma P-tau217 differentiated neuropathologically defined AD from non-AD (area under t
78 e units [95% CI, -1.52 to -0.02]), and lower neuropathologically defined Alzheimer disease (beta = -0
79 obulin gene is a risk factor associated with neuropathologically defined Alzheimer's disease in our p
81 enerative diseases termed synucleinopathies, neuropathologically defined by inclusions containing agg
83 lpha2-macroglobulin gene was associated with neuropathologically defined diagnosis of Alzheimer's dis
85 genes commonly and uniquely dysregulated in neuropathologically defined LBD and AD cases, shedding l
90 opsied individuals in the FLAME cohort, 1361 neuropathologically diagnosed AD cases were evaluated.
91 uantified in temporalis muscles and brain of neuropathologically diagnosed Alzheimer disease (AD) and
92 [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87%; media
93 ychotropic medication prescription data from neuropathologically diagnosed pure ADNC (n = 78), pure L
94 rtex, and sensory cortex from clinically and neuropathologically diagnosed sporadic ALS cases and age
95 f cognitive deficits occur in AD and several neuropathologically distinct age-associated neurodegener
96 f FTD pathology, suggesting that bvFTD-SP is neuropathologically distinct from other forms of FTD.
97 Tauopathies are a group of clinically and neuropathologically diverse neurodegenerative disorders
103 cytoarchitecture of the human hippocampus in neuropathologically healthy and Alzheimer's disease (AD)
104 ofile of 788 brain samples obtained from 101 neuropathologically healthy individuals (10 distinct bra
105 RNA expression profile of brain samples from neuropathologically healthy individuals, showed that KCT
106 Frontotemporal dementia is clinically and neuropathologically heterogeneous, but neuroinflammation
107 f frontotemporal dementia are clinically and neuropathologically heterogeneous, but processes such as
109 ty, suggesting ischaemic demyelination, seen neuropathologically in SVD, may be an important predicto
110 istory of parkinsonism or dementia confirmed neuropathologically, including PSP (n = 24), corticobasa
114 received immunisation and who were examined neuropathologically, mean Abeta load was lower than in a
116 n applied to an array-based dataset from 150 neuropathologically normal adult human brains, our metho
117 uding most of the older individuals who were neuropathologically normal and individuals who carried t
119 g and expression analysis on a series of 193 neuropathologically normal human brain samples using the
120 ifferent proteinopathies (n = 64) as well as neuropathologically normal individuals (n = 10) and corr
123 one comprised of four brain regions from 150 neuropathologically normal samples and another comprised
124 ther comprised of ten brain regions from 134 neuropathologically normal samples, and show that by usi
127 under-reported lesions subsequently analysed neuropathologically, particularly those arising within t
131 included a chronic spinocerebellar syndrome, neuropathologically proven Leigh syndrome, and sudden de
132 scle tissues and is particularly abundant in neuropathologically relevant sites, such as the motor ne
133 observed increased vCSF-cfmtDNA in the more neuropathologically severe NDD cases, but no association
140 lly confirmed group than in more than 24,000 neuropathologically unconfirmed cases and controls.
141 cle events, we investigated the brains of 12 neuropathologically verified cases of Alzheimer's diseas
144 from neuropathologically verified discovery, neuropathologically verified replication, and clinically
148 ranscriptional profiles of 67 clinically and neuropathologically well-characterized controls and AD b