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1 (ie, amyloid-B, neurofibrillary tangles, and neuritic plaques).
2 er's disease, the neurofibrillary tangle and neuritic plaque.
3 brillar core of the Alzheimer's disease (AD) neuritic plaque.
4 eta burden and the subsequent development of neuritic plaques.
5 n of beta-amyloid (Abeta) peptide containing neuritic plaques.
6  in YFP-labeled varicosities associated with neuritic plaques.
7 the neuroimmune response to Abeta42-positive neuritic plaques.
8 umulation of amyloid-beta (Abeta)-containing neuritic plaques.
9 on of the amyloid beta-peptide (A beta) into neuritic plaques.
10 ur before the deposition of Abeta-containing neuritic plaques.
11  the accumulation of beta-amyloid peptide in neuritic plaques.
12 urofibrillary tangles (NFTs) and diffuse and neuritic plaques.
13 re with tau pathology as well as amyloid and neuritic plaques.
14 a microwave king silver stain to demonstrate neuritic plaques.
15 fuse plaques, to the fibrillar form found in neuritic plaques.
16 sence of a PS-1 carboxyl-terminal epitope in neuritic plaques.
17 e to AD have now been found as components of neuritic plaques.
18 esent in some swollen dystrophic neurites of neuritic plaques.
19 resence of this epitope ultrastructurally in neuritic plaques.
20 peptide is also present in low quantities in neuritic plaques.
21 in, APLP-2 antibodies also label a subset of neuritic plaques.
22 ked staining within neurons, astrocytes, and neuritic plaques.
23 0, resulting in the formation of innumerable neuritic plaques.
24 ated within focal tau swellings and human AD neuritic plaques.
25  the underlying disease pathology, including neuritic plaques.
26 rofibrillary tangles (NFTs) and amyloid-rich neuritic plaques.
27 ffuse plaques were a stronger correlate than neuritic plaques.
28 o significant reductions in both diffuse and neuritic plaques.
29 g., neurofibriliary tangles (NFTs) vs tau in neuritic plaques].
30 association was strongest in men with sparse neuritic plaques (1-3/mm(2)) where dementia frequency mo
31     Of the 37 APOE4 noncarriers with minimal neuritic plaques, 16 individuals (43.2%) had Braak stage
32        Of the 13 APOE4 carriers with minimal neuritic plaques, 6 individuals (46.2%) had Braak stages
33 lar samples showed frequent diffuse Abeta or neuritic plaques; 8 samples showed frequent vascular Abe
34 se results establish that in addition to the neuritic plaque, a second determinant is required to dri
35                                              Neuritic plaques, a pathological hallmark in Alzheimer's
36 llum (in areas where diffuse plaques but not neuritic plaques accumulate) to examine the relationship
37 s the burden of tau neurofibrillary tangles, neuritic plaques, alpha-synuclein inclusions, and other
38 g Abeta immunoreactive lesions, which unlike neuritic plaque amyloid are Congo red-negative and large
39 ), the astrocytic ADPRS affected diffuse and neuritic plaques (amyloid-beta), while microglial ADPRS
40 ved between the abundance of these UFAs with neuritic plaque and neurofibrillary tangle burden as wel
41 ly to have LBD, whereas women showed greater neuritic plaque and neurofibrillary tangle burdens.
42 severity or neuropathologically as increased neuritic plaque and neurofibrillary tangle density.
43    Follow-up for candidate variants included neuritic plaque and neurofibrillary tangle pathology; lo
44 y), large peptides that comprise the bulk of neuritic plaques and are potential biomarkers for Alzhei
45 ariants 40 and 42 residues long are found in neuritic plaques and are secreted constitutively by cult
46 ilarly, of the 7 APOE4 carriers with minimal neuritic plaques and Braak stages 0 to II, 4 participant
47 whereas APOEepsilon4 is associated with more neuritic plaques and CAA, but has no independent effect
48  (Abeta) peptide in the brain in the form of neuritic plaques and cerebral amyloid angiopathy (CAA) i
49 he deposition of the beta amyloid peptide in neuritic plaques and cerebral blood vessels is a hallmar
50  Deposits of amyloid beta-protein (Abeta) in neuritic plaques and cerebral vessels are a pathological
51 ncreased approximately sevenfold, leading to neuritic plaques and cerebrovascular accumulation of amy
52  receptor (alpha7nAChR), are both present in neuritic plaques and co-localize in individual cortical
53 ed for by a higher proportion of neocortical neuritic plaques and diffuse plaques (frequent in 79 [53
54  of extracellular beta-amyloid deposition as neuritic plaques and intracellular accumulation of hyper
55  Extracellular deposition of amyloid-beta as neuritic plaques and intracellular accumulation of hyper
56 preamyloid and compared it to amyloid in the neuritic plaques and leptomeninges in the same patients.
57 myloid angiopathy, in which patients develop neuritic plaques and massive vascular deposition predomi
58 icroglial activation in an animal model with neuritic plaques and memory deficits.
59                                  Neocortical neuritic plaques and neurofibrillary tangles are hallmar
60 europathological correlates of the disorder, neuritic plaques and neurofibrillary tangles have been p
61 (AD) at present is postmortem observation of neuritic plaques and neurofibrillary tangles in brain se
62 r characterized by the gradual deposition of neuritic plaques and neurofibrillary tangles in the brai
63 nclear whether atherosclerosis can cause the neuritic plaques and neurofibrillary tangles that define
64  including concurrent Alzheimer's pathology (neuritic plaques and neurofibrillary tangles) and the in
65 d, Congo red negative deposits, while mature neuritic plaques and neurofibrillary tangles, hallmark l
66 typical neuropathological hallmarks, such as neuritic plaques and neurofibrillary tangles, preferenti
67 evelop antibodies that bind to Abeta in both neuritic plaques and neurofibrillary tangles, whereas an
68 cal lesions of AD, as measured by density of neuritic plaques and neurofibrillary tangles.
69 yloid lesions followed by the development of neuritic plaques and neurofibrillary tangles.
70 athology is characterized by the presence of neuritic plaques and the loss of cholinergic neurons in
71   The selective expression of CYP46A1 around neuritic plaques and the potent inhibition of APP proces
72                                     Although neuritic plaques and vascular deposits have similar prot
73 ) levels of proteins associated with senile (neuritic) plaques and neurofibrillary tangles.
74 of both diffuse (an earlier manifestation of neuritic plaques) and fibrillar plaques in Alzheimer's d
75 ding severe cerebral amyloid angiopathy, non-neuritic plaques, and fibrillary tangles as in Alzheimer
76 ofibrillary tangle (NFT) stage, frequency of neuritic plaques, and LBD stage to determine whether pat
77 ng was correlated with amyloid beta plaques, neuritic plaques, and neurofibrillary tangles observed i
78 xtensively to neurofibrillary tangles (NFT), neuritic plaques, and neuropil threads in brains from in
79  of oligomeric tau conformers in pretangles, neuritic plaques, and neuropil threads in the frontal co
80  lesions, including neurofibrillary tangles, neuritic plaques, and, to a lesser extent, neuropil thre
81                                              Neuritic plaques are a defining feature of Alzheimer dis
82  and reactive glia in temporal cortex, where neuritic plaques are abundant, and cerebellum (in areas
83     The major constituents of preamyloid and neuritic plaques are amyloid beta (Abeta) peptides.
84                                              Neuritic plaques are one of the stereotypical hallmarks
85 ons of hippocampal CA1 pyramidal neurons and neuritic plaques are strongly reactive for tau protein k
86 e data therefore challenge the importance of neuritic plaques as the sole contributors for the develo
87 n is highly concentrated in both diffuse and neuritic plaques as well as neurofibrillary tangles; neu
88 though it sometimes occurs in the absence of neuritic plaques, as AD also occurs without accompanying
89 protein (APP), is a major constituent of the neuritic plaques associated with Alzheimer's disease (AD
90 as cognitively normal at 90 years and had no neuritic plaques at autopsy; the other was cognitively h
91 isease score, which describes the density of neuritic plaques based on certain key locations in the n
92 disease pathology including lower density of neuritic plaques (beta = -0.69 score units [95% CI, -1.3
93 tical/limbic-type vs none) and AD, including neuritic plaques (beta-amyloid plaques surrounded by dys
94 a registry for Alzheimer's disease score for neuritic plaques between, but Lewy bodies were less sign
95 two cohorts, and autopsy measures of amyloid neuritic plaque burden across two cohorts.
96 id angiopathy pathology and higher levels of neuritic plaque burden had greater tau burden and faster
97 onal preservation occurred despite increased neuritic plaque burden in the hippocampus of double-tran
98 B and PDD groups, in which the overall brain neuritic plaque burden was low, indicates that apoE migh
99 ociations of cerebral amyloid angiopathy and neuritic plaque burden with tau burden and longitudinal
100  a Registry for Alzheimer's Disease (CERAD) (neuritic plaque burden), and Braak (neurofibrillary path
101 vels were causally associated with increased neuritic plaque burden, although the effects were driven
102 ferentially methylated genes associated with neuritic plaque burden-significantly outperforming conve
103 itive decline among participants with higher neuritic plaque burden.
104 ) AD susceptibility loci are associated with neuritic plaque burden.
105 ve performance, neurofibrillary tangles, and neuritic plaque burden.
106 for targeting the deposition of amyloid into neuritic plaques, but attention has also turned to abnor
107 llary tangle (NFT) stages and possibly fewer neuritic plaques, but has no direct effect on cerebral a
108  inversely proportional to NFT formation and neuritic plaques, but was not related significantly to d
109 ice resulted in fibrillar Abeta deposits and neuritic plaques by 15 months of age and substantially (
110 peptide 1-42 (Abeta), a major constituent of neuritic plaques, can itself induce glial activation.
111 zheimer disease (AD) include the presence of neuritic plaques composed of amyloid beta-protein (Abeta
112 heimer's disease is to decrease or eliminate neuritic plaques composed of fibrillar beta-amyloid (Abe
113 e function and the presence of extracellular neuritic plaques composed of the beta-amyloid peptide (A
114  neurofibrillary tangles composed of tau and neuritic plaques comprising amyloid-beta peptides (Abeta
115 ive limbic and neocortical NFT formation and neuritic plaques consistent with a Braak stage of VI.
116                              The presence of neuritic plaques containing abundant Abeta-derived amylo
117                              The presence of neuritic plaques containing aggregated amyloid-beta (Abe
118 and old mice (> 14 months old) form abundant neuritic plaques containing amyloid-beta.
119 At a voxel resolution of 5.9 x 10(-5) mm(3), neuritic plaques could be detected by T2*.
120 platform, we applied this program to analyze neuritic plaque count data from the ROSMAP cohort.
121 ement with histopathologic classification of neuritic plaque density and a strong concordance with vi
122  and PTM profiles were associated with Abeta neuritic plaque density and differentiated ADNC from PAR
123 ated with Braak neuropathological stages and neuritic plaque density counts.
124                       Using postmortem brain neuritic plaque density data as a truth standard to deri
125 Establish a Registry for Alzheimer's Disease neuritic plaque density score, diffuse plaque density sc
126 whereas, Braak neuropathological staging and neuritic plaque density were used as an index of the neu
127 dementia frequency increased with increasing neuritic plaque density, and increased further in the pr
128     We show that this tau fragment seeds the neuritic plaque-dependent pathological conversion of wil
129 gimen prevents Abeta peptides generation and neuritic plaque deposition in the brain of a mouse model
130                                              Neuritic plaques did not display consistent asymmetry.
131 s reason, we asked whether the AB fibrils in neuritic plaques differed structurally from those in cer
132                                The number of neuritic plaques, diffuse plaques, and neurofibrillary t
133  the influence of Abeta pathology, including neuritic plaques, diffuse plaques, and vascular deposits
134  independent of Braak NFT stage or extent of neuritic plaque disease.
135                                          The neuritic plaques emerged as black, spherical elements on
136  whether individuals with sparse neocortical neuritic plaques experience increased odds of crossing t
137 peat domain and show that in these mice, the neuritic plaque facilitates the pathological conversion
138 oid formation and trigger the development of neuritic plaques followed by neuronal damage in AD.
139 udy shows that PDAPP tg mice develop massive neuritic plaque formation and neuronal degeneration simi
140 itical and isoform-specific role for apoE in neuritic plaque formation, a pathological hallmark of AD
141 naling markedly reduced Abeta deposition and neuritic plaque formation, and rescued memory deficits i
142 Abeta) deposition, amyloid accumulation, and neuritic plaque formation.
143 -acid peptide that is the major component of neuritic plaques found in Alzheimer's disease (AD).
144  marked excess of dementia in cases with low neuritic plaque frequency.
145 teraction terms for neurofibrillary tangles, neuritic plaques, gross infarcts, microinfarcts, amyloid
146 eamyloid deposits in the cerebellum, without neuritic plaques; hence, DS cerebellums are a source of
147 e-related tauopathy) or moderate to frequent neuritic plaques (i.e. Alzheimer neuropathological chang
148 gnitive impairment at baseline and either no neuritic plaques (i.e. primary age-related tauopathy) or
149     In the same year, Oskar Fischer reported neuritic plaques in 12 cases of senile dementia.
150 eta (A beta) peptide, a major constituent of neuritic plaques in AD, has been implicated as a primary
151 beta peptide that accumulates in diffuse and neuritic plaques in AD.
152  peptide is the major protein constituent of neuritic plaques in Alzheimer disease and appears to pla
153  protein (Abeta) comprise the characteristic neuritic plaques in Alzheimer's disease (AD).
154 -peptide (Abeta) is the major constituent of neuritic plaques in Alzheimer's disease and occurs as a
155  distribution of alpha7nAChR correlates with neuritic plaques in Alzheimer's disease brains, we propo
156 -peptide is the major protein constituent of neuritic plaques in Alzheimer's disease.
157                               Similar to AD, neuritic plaques in PDAPP tg mouse contained a dense amy
158 xpressing microglia enveloping NA-containing neuritic plaques in postmortem brains of patients with A
159 tion of amyloid beta protein (Abeta) to form neuritic plaques in the brain is the pathological hallma
160 ation of the amyloid-beta (Abeta) peptide as neuritic plaques in the brain.
161                To address this, we monitored neuritic plaques in the brains of living PDAPP;Thy-1:YFP
162           There are alpha-synuclein positive neuritic plaques in the brainstem and cerebellum, but no
163 ence of abundant neurofibrillary lesions and neuritic plaques in the cerebral cortex.
164 atients, and ADx201 and ADx210 also detected neuritic plaques in the cortex of the patient brains.
165 ptide (Abeta), which has been shown to label neuritic plaques in vitro, therefore could provide a dia
166                 Here we provide MR images of neuritic plaques in vitro.
167  provide a diagnostic tool if it also labels neuritic plaques in vivo following intravenous injection
168 ase (AD) is characterized by the presence of neuritic plaques in which dystrophic neurites (DNs) are
169 alpha-1-Antichymotrypsin (ACT) is present in neuritic plaques in which it participates in the inflamm
170 rillary tangles, alpha-synuclein inclusions, neuritic plaques, inclusions of the transcriptional repr
171 n4 allele had a higher number of hippocampal neuritic plaques (IRR 3.0 [CI 1.2-7.3]) and neurofibrill
172 n in Alzheimer's Disease (AD) is whether the neuritic plaque is necessary and sufficient for the deve
173 ition of amyloid-beta peptide (Abeta) within neuritic plaques is a hallmark pathology of Alzheimer's
174 ition of the amyloid-beta (Abeta) peptide in neuritic plaques is a requirement for the diagnosis of A
175 -amyloid peptides (A beta42 and A beta40) in neuritic plaques is one of the hallmarks of Alzheimer's
176 The accumulation of beta-amyloid (A beta) in neuritic plaques is thought to be causative for the prog
177 ed during the study, were autopsied, and had neuritic plaque levels determined; 25 brains (37%) were
178 nts who died, neuropathologically determined neuritic plaque levels were used to confirm scan interpr
179        It further offers a mechanism whereby neuritic plaques may be derived.
180 sed subjects with autopsy-based amyloid beta neuritic plaque measure who underwent F 18 Florbetapir P
181 yloid-beta), while microglial ADPRS affected neuritic plaques, microglial activation, neurofibrillary
182 c outcomes included neurofibrillary tangles, neuritic plaques, microinfarcts, cystic infarcts, Lewy b
183 stages (III/IV) or (V/VI), moderate/frequent neuritic plaques, moderate/frequent diffuse plaques and
184 u(181) , and the neuropathological burden of neuritic plaques, neurofibrillary tangles (NFTs), and va
185 u(181) , and the neuropathological burden of neuritic plaques, neurofibrillary tangles (NFTs), and va
186 opause modified the associations of LBD with neuritic plaques, neurofibrillary tangles, and cognitive
187 eractive associations between LBD and sex on neuritic plaques, neurofibrillary tangles, and cognitive
188  decline, after adjusting for copathologies (neuritic plaques, neurofibrillary tangles, and LBD, as a
189                                There were no neuritic plaques, neurofibrillary tangles, or amyloid de
190 alized to dystrophic neurites in a subset of neuritic plaques, neurons, and some NFTs.
191                               The senile and neuritic plaque neuropathology of Alzheimer's disease (A
192 ary tangles, dystrophic neurites surrounding neuritic plaques, neuropil threads, and granulovacuolar
193 gression of AD clinical dementia and amyloid neuritic plaque (NP) neuropathology, but not neurofibril
194                             Large numbers of neuritic plaques (NP), largely composed of a fibrillar i
195 shorter bundles of 6-8 nm amyloid fibrils of neuritic plaques (NPs) and from the 24 nm paired helical
196 r lesions (neurofibrillary tangles [NFTs] or neuritic plaques [NPs]) mediate the association.
197 a peptide (Abeta), the same peptide found in neuritic plaques of AD, may play a role via its vasoacti
198 nd Abeta(1-42) are both found colocalized in neuritic plaques of human brains with AD.
199 ano bodies, tangles, reactive astrocytes and neuritic plaques of the AD brain.
200 at in human AD, and none of the cases showed neuritic plaques on any of the stains used.
201 ition of the beta-amyloid peptide (Abeta) in neuritic plaques or in the walls of cerebral vessels.
202 th KGDHC activity than with the densities of neuritic plaques or neuritic tangles.
203 oncentrations were not related to density of neuritic plaques or neurofibrillary tangles in seven bra
204 t significantly influenced by the density of neuritic plaques or neurofibrillary tangles, or the numb
205  parkinsonism, and PD, but not dementia, AD, neuritic plaques, or neurofibrillary tangles.
206  with the density of diffuse (P < 0.001) and neuritic plaques (P < 0.01).
207 ene (APP, rs2829887) that is associated with neuritic plaques (P = 3.3 x 10-6).
208 1, is associated with an increased burden of neuritic plaques (p = 3.7 x 10(-4) ), diffuse plaques (p
209 a Registry for Alzheimer's Disease score for neuritic plaques, p = 6.8 x 10-6) and in vivo markers of
210 clerosis ratings were highly correlated with neuritic plaque, paired helical filaments tau neurofibri
211                    A quantitative measure of neuritic plaque pathologic burden, based on assessments
212 alidated susceptibility alleles to increased neuritic plaque pathology and implicate common genetic v
213 Our primary analysis was an association with neuritic plaque pathology.
214 the beta-amyloid found in the characteristic neuritic plaques present in the brains of AD patients.
215 ulate less tau, neurofibrillary tangles, and neuritic plaques, respectively, when HTRA1 is expressed
216 rval, 0.58-0.89]; P <.001]) and silver stain neuritic plaque score (Bonferroni rho, 0.71 [95% confide
217  Establish a Registry of Alzheimer's Disease neuritic plaque score and the Braak neurofibrillary tang
218 d that spine density was not associated with neuritic plaque score but did display negative correlati
219  neurofibrillary tangle stage (Braak stage), neuritic plaque score, and AD likelihood, with adjustmen
220 e associated with higher Braak stage, higher neuritic plaque score, and greater likelihood of AD.
221 stablish a Registry for Alzheimer's Disease) neuritic plaque scores at autopsy overall.
222 ence of infarcts, neurofibrillary tangle and neuritic plaque scores, APOE epsilon4 allele presence, a
223 ls that included age at death, sex, cerebral neuritic plaque scores, cerebral alpha-synuclein scores,
224 and facilitates the seeding and spreading of neuritic plaque tau aggregates.
225 ted tau seeding and spreading in the form of neuritic plaque-tau (NP-tau) pathology in response to ch
226      Alzheimer's disease is characterized by neuritic plaques, the main protein components of which a
227  and signal-to-noise ratio needed to resolve neuritic plaques, the neuropathological hallmark of Alzh
228  Cerebral amyloid angiopathy interacted with neuritic plaques to accelerate tau burden and cognitive
229 using the Bielschowsky method to demonstrate neuritic plaques, we performed a neuropathologic assessm
230 = -0.19; P < .001), and frequent vs moderate neuritic plaques were associated with higher Clinical De
231 tage was five or six, amyloid angiopathy and neuritic plaques were common and more than 75% had Lewy
232                             Both diffuse and neuritic plaques were found in the cerebral cortex of 26
233                                 However, the neuritic plaques were immunonegative for Abeta, whereas
234 R, 1.70; 95% CI, 1.23-2.34; P = .001), while neuritic plaques were more frequent in White compared wi
235                         However, diffuse and neuritic plaques were not more common in type 2 diabetes
236          Braak NFT stage and the presence of neuritic plaques were not significantly associated with
237 urodegeneration, neurofibrillary tangles and neuritic plaques, were prominently immunolabeled with Cd
238 of LBD with neurofibrillary tangles (but not neuritic plaques), whereby LBD was more strongly associa
239 -Amyloid is the primary protein component of neuritic plaques, which are degenerative foci in brains
240 ld-to-moderate probable AD have no or sparse neuritic plaques, which would expectedly yield a negativ
241 n of the 18-kd carboxy fragment of PS-1 with neuritic plaques with a start at residue 300.
242       From 12 to 23 months, diffuse plaques, neuritic plaques with amyloid cores, and biochemically e
243 s reported to have high densities of senile (neuritic) plaques with activated microglia.
244 iohigh 62.5%) for CERAD moderate-to-frequent neuritic plaques, with similar specificity (distribution
245 se nuclei are affected with a high number of neuritic plaques without ever developing neurofibrillary

 
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