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1 er's disease, the neurofibrillary tangle and neuritic plaque.
2 brillar core of the Alzheimer's disease (AD) neuritic plaque.
3 eta burden and the subsequent development of neuritic plaques.
4 n of beta-amyloid (Abeta) peptide containing neuritic plaques.
5  in YFP-labeled varicosities associated with neuritic plaques.
6 the neuroimmune response to Abeta42-positive neuritic plaques.
7 umulation of amyloid-beta (Abeta)-containing neuritic plaques.
8 on of the amyloid beta-peptide (A beta) into neuritic plaques.
9 ur before the deposition of Abeta-containing neuritic plaques.
10  the accumulation of beta-amyloid peptide in neuritic plaques.
11 urofibrillary tangles (NFTs) and diffuse and neuritic plaques.
12 re with tau pathology as well as amyloid and neuritic plaques.
13 a microwave king silver stain to demonstrate neuritic plaques.
14 fuse plaques, to the fibrillar form found in neuritic plaques.
15 sence of a PS-1 carboxyl-terminal epitope in neuritic plaques.
16 e to AD have now been found as components of neuritic plaques.
17 esent in some swollen dystrophic neurites of neuritic plaques.
18 resence of this epitope ultrastructurally in neuritic plaques.
19 peptide is also present in low quantities in neuritic plaques.
20 in, APLP-2 antibodies also label a subset of neuritic plaques.
21 ked staining within neurons, astrocytes, and neuritic plaques.
22 0, resulting in the formation of innumerable neuritic plaques.
23  the underlying disease pathology, including neuritic plaques.
24 rofibrillary tangles (NFTs) and amyloid-rich neuritic plaques.
25 ffuse plaques were a stronger correlate than neuritic plaques.
26 o significant reductions in both diffuse and neuritic plaques.
27 association was strongest in men with sparse neuritic plaques (1-3/mm(2)) where dementia frequency mo
28     Of the 37 APOE4 noncarriers with minimal neuritic plaques, 16 individuals (43.2%) had Braak stage
29        Of the 13 APOE4 carriers with minimal neuritic plaques, 6 individuals (46.2%) had Braak stages
30 lar samples showed frequent diffuse Abeta or neuritic plaques; 8 samples showed frequent vascular Abe
31 se results establish that in addition to the neuritic plaque, a second determinant is required to dri
32 llum (in areas where diffuse plaques but not neuritic plaques accumulate) to examine the relationship
33 s the burden of tau neurofibrillary tangles, neuritic plaques, alpha-synuclein inclusions, and other
34 g Abeta immunoreactive lesions, which unlike neuritic plaque amyloid are Congo red-negative and large
35 ved between the abundance of these UFAs with neuritic plaque and neurofibrillary tangle burden as wel
36 severity or neuropathologically as increased neuritic plaque and neurofibrillary tangle density.
37    Follow-up for candidate variants included neuritic plaque and neurofibrillary tangle pathology; lo
38 y), large peptides that comprise the bulk of neuritic plaques and are potential biomarkers for Alzhei
39 ariants 40 and 42 residues long are found in neuritic plaques and are secreted constitutively by cult
40 ilarly, of the 7 APOE4 carriers with minimal neuritic plaques and Braak stages 0 to II, 4 participant
41 whereas APOEepsilon4 is associated with more neuritic plaques and CAA, but has no independent effect
42  (Abeta) peptide in the brain in the form of neuritic plaques and cerebral amyloid angiopathy (CAA) i
43 he deposition of the beta amyloid peptide in neuritic plaques and cerebral blood vessels is a hallmar
44  Deposits of amyloid beta-protein (Abeta) in neuritic plaques and cerebral vessels are a pathological
45  receptor (alpha7nAChR), are both present in neuritic plaques and co-localize in individual cortical
46 preamyloid and compared it to amyloid in the neuritic plaques and leptomeninges in the same patients.
47 myloid angiopathy, in which patients develop neuritic plaques and massive vascular deposition predomi
48 icroglial activation in an animal model with neuritic plaques and memory deficits.
49                                  Neocortical neuritic plaques and neurofibrillary tangles are hallmar
50 (AD) at present is postmortem observation of neuritic plaques and neurofibrillary tangles in brain se
51 r characterized by the gradual deposition of neuritic plaques and neurofibrillary tangles in the brai
52 nclear whether atherosclerosis can cause the neuritic plaques and neurofibrillary tangles that define
53  including concurrent Alzheimer's pathology (neuritic plaques and neurofibrillary tangles) and the in
54 d, Congo red negative deposits, while mature neuritic plaques and neurofibrillary tangles, hallmark l
55 evelop antibodies that bind to Abeta in both neuritic plaques and neurofibrillary tangles, whereas an
56 cal lesions of AD, as measured by density of neuritic plaques and neurofibrillary tangles.
57 yloid lesions followed by the development of neuritic plaques and neurofibrillary tangles.
58 athology is characterized by the presence of neuritic plaques and the loss of cholinergic neurons in
59   The selective expression of CYP46A1 around neuritic plaques and the potent inhibition of APP proces
60 ) levels of proteins associated with senile (neuritic) plaques and neurofibrillary tangles.
61 of both diffuse (an earlier manifestation of neuritic plaques) and fibrillar plaques in Alzheimer's d
62 ofibrillary tangle (NFT) stage, frequency of neuritic plaques, and LBD stage to determine whether pat
63 ng was correlated with amyloid beta plaques, neuritic plaques, and neurofibrillary tangles observed i
64 xtensively to neurofibrillary tangles (NFT), neuritic plaques, and neuropil threads in brains from in
65  of oligomeric tau conformers in pretangles, neuritic plaques, and neuropil threads in the frontal co
66  lesions, including neurofibrillary tangles, neuritic plaques, and, to a lesser extent, neuropil thre
67                                              Neuritic plaques are a defining feature of Alzheimer dis
68  and reactive glia in temporal cortex, where neuritic plaques are abundant, and cerebellum (in areas
69     The major constituents of preamyloid and neuritic plaques are amyloid beta (Abeta) peptides.
70                                              Neuritic plaques are one of the stereotypical hallmarks
71 ons of hippocampal CA1 pyramidal neurons and neuritic plaques are strongly reactive for tau protein k
72 e data therefore challenge the importance of neuritic plaques as the sole contributors for the develo
73 n is highly concentrated in both diffuse and neuritic plaques as well as neurofibrillary tangles; neu
74 protein (APP), is a major constituent of the neuritic plaques associated with Alzheimer's disease (AD
75 disease pathology including lower density of neuritic plaques (beta = -0.69 score units [95% CI, -1.3
76 onal preservation occurred despite increased neuritic plaque burden in the hippocampus of double-tran
77 B and PDD groups, in which the overall brain neuritic plaque burden was low, indicates that apoE migh
78 ) AD susceptibility loci are associated with neuritic plaque burden.
79 for targeting the deposition of amyloid into neuritic plaques, but attention has also turned to abnor
80 llary tangle (NFT) stages and possibly fewer neuritic plaques, but has no direct effect on cerebral a
81  inversely proportional to NFT formation and neuritic plaques, but was not related significantly to d
82 ice resulted in fibrillar Abeta deposits and neuritic plaques by 15 months of age and substantially (
83 peptide 1-42 (Abeta), a major constituent of neuritic plaques, can itself induce glial activation.
84 zheimer disease (AD) include the presence of neuritic plaques composed of amyloid beta-protein (Abeta
85 heimer's disease is to decrease or eliminate neuritic plaques composed of fibrillar beta-amyloid (Abe
86 e function and the presence of extracellular neuritic plaques composed of the beta-amyloid peptide (A
87  neurofibrillary tangles composed of tau and neuritic plaques comprising amyloid-beta peptides (Abeta
88 ive limbic and neocortical NFT formation and neuritic plaques consistent with a Braak stage of VI.
89                              The presence of neuritic plaques containing abundant Abeta-derived amylo
90                              The presence of neuritic plaques containing aggregated amyloid-beta (Abe
91 and old mice (> 14 months old) form abundant neuritic plaques containing amyloid-beta.
92 At a voxel resolution of 5.9 x 10(-5) mm(3), neuritic plaques could be detected by T2*.
93 ement with histopathologic classification of neuritic plaque density and a strong concordance with vi
94 ated with Braak neuropathological stages and neuritic plaque density counts.
95                       Using postmortem brain neuritic plaque density data as a truth standard to deri
96 Establish a Registry for Alzheimer's Disease neuritic plaque density score, diffuse plaque density sc
97 whereas, Braak neuropathological staging and neuritic plaque density were used as an index of the neu
98 dementia frequency increased with increasing neuritic plaque density, and increased further in the pr
99     We show that this tau fragment seeds the neuritic plaque-dependent pathological conversion of wil
100 gimen prevents Abeta peptides generation and neuritic plaque deposition in the brain of a mouse model
101                                              Neuritic plaques did not display consistent asymmetry.
102                                The number of neuritic plaques, diffuse plaques, and neurofibrillary t
103  the influence of Abeta pathology, including neuritic plaques, diffuse plaques, and vascular deposits
104  independent of Braak NFT stage or extent of neuritic plaque disease.
105                                          The neuritic plaques emerged as black, spherical elements on
106  whether individuals with sparse neocortical neuritic plaques experience increased odds of crossing t
107 peat domain and show that in these mice, the neuritic plaque facilitates the pathological conversion
108 oid formation and trigger the development of neuritic plaques followed by neuronal damage in AD.
109 udy shows that PDAPP tg mice develop massive neuritic plaque formation and neuronal degeneration simi
110 itical and isoform-specific role for apoE in neuritic plaque formation, a pathological hallmark of AD
111 naling markedly reduced Abeta deposition and neuritic plaque formation, and rescued memory deficits i
112 Abeta) deposition, amyloid accumulation, and neuritic plaque formation.
113 -acid peptide that is the major component of neuritic plaques found in Alzheimer's disease (AD).
114  marked excess of dementia in cases with low neuritic plaque frequency.
115 teraction terms for neurofibrillary tangles, neuritic plaques, gross infarcts, microinfarcts, amyloid
116 eamyloid deposits in the cerebellum, without neuritic plaques; hence, DS cerebellums are a source of
117     In the same year, Oskar Fischer reported neuritic plaques in 12 cases of senile dementia.
118 eta (A beta) peptide, a major constituent of neuritic plaques in AD, has been implicated as a primary
119 beta peptide that accumulates in diffuse and neuritic plaques in AD.
120  peptide is the major protein constituent of neuritic plaques in Alzheimer disease and appears to pla
121  protein (Abeta) comprise the characteristic neuritic plaques in Alzheimer's disease (AD).
122 -peptide (Abeta) is the major constituent of neuritic plaques in Alzheimer's disease and occurs as a
123  distribution of alpha7nAChR correlates with neuritic plaques in Alzheimer's disease brains, we propo
124 -peptide is the major protein constituent of neuritic plaques in Alzheimer's disease.
125                               Similar to AD, neuritic plaques in PDAPP tg mouse contained a dense amy
126 tion of amyloid beta protein (Abeta) to form neuritic plaques in the brain is the pathological hallma
127 ation of the amyloid-beta (Abeta) peptide as neuritic plaques in the brain.
128                To address this, we monitored neuritic plaques in the brains of living PDAPP;Thy-1:YFP
129           There are alpha-synuclein positive neuritic plaques in the brainstem and cerebellum, but no
130 ence of abundant neurofibrillary lesions and neuritic plaques in the cerebral cortex.
131 atients, and ADx201 and ADx210 also detected neuritic plaques in the cortex of the patient brains.
132 ptide (Abeta), which has been shown to label neuritic plaques in vitro, therefore could provide a dia
133                 Here we provide MR images of neuritic plaques in vitro.
134  provide a diagnostic tool if it also labels neuritic plaques in vivo following intravenous injection
135 alpha-1-Antichymotrypsin (ACT) is present in neuritic plaques in which it participates in the inflamm
136 n4 allele had a higher number of hippocampal neuritic plaques (IRR 3.0 [CI 1.2-7.3]) and neurofibrill
137 n in Alzheimer's Disease (AD) is whether the neuritic plaque is necessary and sufficient for the deve
138 ition of amyloid-beta peptide (Abeta) within neuritic plaques is a hallmark pathology of Alzheimer's
139 ition of the amyloid-beta (Abeta) peptide in neuritic plaques is a requirement for the diagnosis of A
140 -amyloid peptides (A beta42 and A beta40) in neuritic plaques is one of the hallmarks of Alzheimer's
141 The accumulation of beta-amyloid (A beta) in neuritic plaques is thought to be causative for the prog
142 ed during the study, were autopsied, and had neuritic plaque levels determined; 25 brains (37%) were
143 nts who died, neuropathologically determined neuritic plaque levels were used to confirm scan interpr
144        It further offers a mechanism whereby neuritic plaques may be derived.
145 sed subjects with autopsy-based amyloid beta neuritic plaque measure who underwent F 18 Florbetapir P
146 c outcomes included neurofibrillary tangles, neuritic plaques, microinfarcts, cystic infarcts, Lewy b
147                                There were no neuritic plaques, neurofibrillary tangles, or amyloid de
148 alized to dystrophic neurites in a subset of neuritic plaques, neurons, and some NFTs.
149                               The senile and neuritic plaque neuropathology of Alzheimer's disease (A
150 ary tangles, dystrophic neurites surrounding neuritic plaques, neuropil threads, and granulovacuolar
151 gression of AD clinical dementia and amyloid neuritic plaque (NP) neuropathology, but not neurofibril
152                             Large numbers of neuritic plaques (NP), largely composed of a fibrillar i
153 shorter bundles of 6-8 nm amyloid fibrils of neuritic plaques (NPs) and from the 24 nm paired helical
154 r lesions (neurofibrillary tangles [NFTs] or neuritic plaques [NPs]) mediate the association.
155 a peptide (Abeta), the same peptide found in neuritic plaques of AD, may play a role via its vasoacti
156 nd Abeta(1-42) are both found colocalized in neuritic plaques of human brains with AD.
157 ano bodies, tangles, reactive astrocytes and neuritic plaques of the AD brain.
158 ition of the beta-amyloid peptide (Abeta) in neuritic plaques or in the walls of cerebral vessels.
159 th KGDHC activity than with the densities of neuritic plaques or neuritic tangles.
160 oncentrations were not related to density of neuritic plaques or neurofibrillary tangles in seven bra
161 t significantly influenced by the density of neuritic plaques or neurofibrillary tangles, or the numb
162  parkinsonism, and PD, but not dementia, AD, neuritic plaques, or neurofibrillary tangles.
163  with the density of diffuse (P < 0.001) and neuritic plaques (P < 0.01).
164 ene (APP, rs2829887) that is associated with neuritic plaques (P = 3.3 x 10-6).
165 1, is associated with an increased burden of neuritic plaques (p = 3.7 x 10(-4) ), diffuse plaques (p
166 a Registry for Alzheimer's Disease score for neuritic plaques, p = 6.8 x 10-6) and in vivo markers of
167 clerosis ratings were highly correlated with neuritic plaque, paired helical filaments tau neurofibri
168                    A quantitative measure of neuritic plaque pathologic burden, based on assessments
169 alidated susceptibility alleles to increased neuritic plaque pathology and implicate common genetic v
170 Our primary analysis was an association with neuritic plaque pathology.
171 the beta-amyloid found in the characteristic neuritic plaques present in the brains of AD patients.
172 ulate less tau, neurofibrillary tangles, and neuritic plaques, respectively, when HTRA1 is expressed
173 rval, 0.58-0.89]; P <.001]) and silver stain neuritic plaque score (Bonferroni rho, 0.71 [95% confide
174  Establish a Registry of Alzheimer's Disease neuritic plaque score and the Braak neurofibrillary tang
175 d that spine density was not associated with neuritic plaque score but did display negative correlati
176  neurofibrillary tangle stage (Braak stage), neuritic plaque score, and AD likelihood, with adjustmen
177 e associated with higher Braak stage, higher neuritic plaque score, and greater likelihood of AD.
178 stablish a Registry for Alzheimer's Disease) neuritic plaque scores at autopsy overall.
179 ence of infarcts, neurofibrillary tangle and neuritic plaque scores, APOE epsilon4 allele presence, a
180 ls that included age at death, sex, cerebral neuritic plaque scores, cerebral alpha-synuclein scores,
181  and signal-to-noise ratio needed to resolve neuritic plaques, the neuropathological hallmark of Alzh
182 using the Bielschowsky method to demonstrate neuritic plaques, we performed a neuropathologic assessm
183 = -0.19; P < .001), and frequent vs moderate neuritic plaques were associated with higher Clinical De
184 tage was five or six, amyloid angiopathy and neuritic plaques were common and more than 75% had Lewy
185                             Both diffuse and neuritic plaques were found in the cerebral cortex of 26
186                                 However, the neuritic plaques were immunonegative for Abeta, whereas
187                         However, diffuse and neuritic plaques were not more common in type 2 diabetes
188          Braak NFT stage and the presence of neuritic plaques were not significantly associated with
189 urodegeneration, neurofibrillary tangles and neuritic plaques, were prominently immunolabeled with Cd
190 -Amyloid is the primary protein component of neuritic plaques, which are degenerative foci in brains
191 ld-to-moderate probable AD have no or sparse neuritic plaques, which would expectedly yield a negativ
192 n of the 18-kd carboxy fragment of PS-1 with neuritic plaques with a start at residue 300.
193       From 12 to 23 months, diffuse plaques, neuritic plaques with amyloid cores, and biochemically e
194 s reported to have high densities of senile (neuritic) plaques with activated microglia.
195 iohigh 62.5%) for CERAD moderate-to-frequent neuritic plaques, with similar specificity (distribution
196 se nuclei are affected with a high number of neuritic plaques without ever developing neurofibrillary

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