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1 f tau oligomers at the expense of increasing neurofibrillary tangles.
2 did not demonstrate amyloid-beta plaques or neurofibrillary tangles.
3 d around the blood vessels, and formation of neurofibrillary tangles.
4 are inversely proportional to the number of neurofibrillary tangles.
5 turb cellular interactions and accumulate in neurofibrillary tangles.
6 aques, cerebral amyloid angiopathy (CAA) and neurofibrillary tangles.
7 n the complete absence of amyloid plaques or neurofibrillary tangles.
8 rized by the formation of senile plaques and neurofibrillary tangles.
9 horylated and aggregates into characteristic neurofibrillary tangles.
10 d yeast prion proteins, and Tau, which forms neurofibrillary tangles.
11 ation of hyperphosphorylated tau proteins in neurofibrillary tangles.
12 erphosphorylation that leads to formation of neurofibrillary tangles.
13 e in the formation of Alzheimer's-associated neurofibrillary tangles.
14 es, loss of neurons, and the accumulation of neurofibrillary tangles.
15 undant neuronal tau inclusions that resemble neurofibrillary tangles.
16 o those formed by tau protein in Alzheimer's neurofibrillary tangles.
17 by accumulation of amyloid beta (Abeta) and neurofibrillary tangles.
18 erphosphorylated tau, the major component of neurofibrillary tangles.
19 f beta-amyloid (Abeta) plaques and tau-laden neurofibrillary tangles.
20 cular pathologies: amyloid abeta1-42 and Tau neurofibrillary tangles.
21 ulation of beta-amyloid (Abeta) peptides and neurofibrillary tangles.
22 associated pathology of amyloid plaques and neurofibrillary tangles.
23 rotubule binding protein tau, a component of neurofibrillary tangles.
24 gical features including amyloid plaques and neurofibrillary tangles.
25 ized by beta-amyloid (Abeta) plaques and tau neurofibrillary tangles.
26 s, where it correlated with the abundance of neurofibrillary tangles.
27 ic neuronal somatic accumulations resembling neurofibrillary tangles.
28 tau) forms intracellular inclusions known as neurofibrillary tangles.
29 active inclusions were usually distinct from neurofibrillary tangles.
30 y pathological features: amyloid plaques and neurofibrillary tangles.
31 cerebral patterns of amyloid plaques and tau neurofibrillary tangles.
32 europathologic markers of senile plaques and neurofibrillary tangles.
33 be associated with increased risk for AD and neurofibrillary tangles.
34 amyloid-beta plaques and tau-immunoreactive neurofibrillary tangles.
35 , but not dementia, AD, neuritic plaques, or neurofibrillary tangles.
36 ion of tau, thus leading to the formation of neurofibrillary tangles.
37 ) peptide and the intracellular formation of neurofibrillary tangles.
38 ological hallmarks: amyloid-beta plaques and neurofibrillary tangles.
39 phorylation of Tau leads to the formation of neurofibrillary tangles, a hallmark of Alzheimer disease
40 ation of paired helical filaments (PHFs) and neurofibrillary tangles, a key neuropathological feature
41 egates of hyperphosphorylated tau protein in neurofibrillary tangles, a process that occurs late in t
44 Alzheimer's disease (AD) is characterized by neurofibrillary tangles, amyloid plaques, and neurodegen
45 ium (never vs ever) and pathologic burden of neurofibrillary tangles, amyloid plaques, vascular lesio
46 euritic plaque, paired helical filaments tau neurofibrillary tangle and cerebral amyloid angiopathy r
47 y associated with age, presence of infarcts, neurofibrillary tangle and neuritic plaque scores, APOE
48 Alzheimer's disease (AD) is characterized by neurofibrillary tangle and neuropil thread deposition, w
49 es, which are proposed to contribute to both neurofibrillary tangles and amyloid plaque formation.
52 ligomer formation precedes the appearance of neurofibrillary tangles and contributes to neuronal loss
53 oid precursor protein (APP), and presence of neurofibrillary tangles and dystrophic neurites containi
54 AD, p62 immunoreactivity is associated with neurofibrillary tangles and is involved in tau degradati
55 nantly associated with thioflavin-S-positive neurofibrillary tangles and less reactive in neuropil th
56 In Alzheimer disease (AD), deposition of neurofibrillary tangles and loss of synapses in the neoc
58 ody), an early precursor to the formation of neurofibrillary tangles and neurodegeneration of the kin
59 uorescent staining) pathological inclusions, neurofibrillary tangles and neuropil threads but only in
62 l pathological Tau inclusions in the form of neurofibrillary tangles and Pick bodies and in some case
64 esis of the two canonical Alzheimer lesions--neurofibrillary tangles and senile plaques--are present
65 red helical filaments in Alzheimer's disease neurofibrillary tangles and through mutations linking it
66 ce of other hallmarks of the disease such as neurofibrillary tangles and widespread neuronal losses.
67 al cortex (reflecting incidental age-related neurofibrillary tangles) and neuromelanin-containing neu
68 Alzheimer's pathology (neuritic plaques and neurofibrillary tangles) and the interval between time o
69 isease, such as altered Tau phosphorylation, neurofibrillary tangles, and accumulation of insoluble p
70 d estimates of the densities of Lewy bodies, neurofibrillary tangles, and aminergic neurons in the lo
72 including beta-amyloid (Abeta) plaques, tau neurofibrillary tangles, and cognitive deficits, suggest
74 mulation of phosphorylated tau, formation of neurofibrillary tangles, and eventual neurodegeneration.
75 , including beta-amyloid senile plaques, tau neurofibrillary tangles, and fused in sarcoma (FUS) and
76 normalities, brain accumulation of Abeta and neurofibrillary tangles, and influence of apolipoprotein
77 ells and patient brains accumulate less tau, neurofibrillary tangles, and neuritic plaques, respectiv
80 of amyloid-beta (Abeta)-containing plaques, neurofibrillary tangles, and neuronal loss in the brain.
84 sease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neurona
86 Neuritic dystrophy with amyloid burden and neurofibrillary tangles are pathological hallmarks of Al
87 res of TDP-43 pathology, density of neuronal neurofibrillary tangles, area occupied by amyloid-beta p
88 en shown to produce hyperphosphorylated tau, neurofibrillary tangles as well as aberrant amyloid prec
89 nt-insoluble tau, neuronal loss and reverses neurofibrillary tangle-associated brain dysfunction.
91 -1.34 to -0.04]), less severe and widespread neurofibrillary tangles (beta = -0.77 score units [95% C
92 racellular amyloid plaques and intraneuronal neurofibrillary tangles, both of which comprise highly i
94 dance of these UFAs with neuritic plaque and neurofibrillary tangle burden as well as domain-specific
95 t to model the possibility that knowledge of neurofibrillary tangle burden in the presence of moderat
97 e model that co-develops amyloid plaques and neurofibrillary tangles but also because it enabled us t
98 rotein, the primary constituent of Alzheimer neurofibrillary tangles, can form liquid droplets and th
99 brain volume ratio, and hippocampal volume), neurofibrillary tangles (cerebrospinal fluid phosphoryla
101 loidosis, familial Danish dementia, in which neurofibrillary tangles coexist with extensive pre-amylo
102 Alzheimer disease (AD) include intraneuronal neurofibrillary tangles composed of abnormally hyperphos
103 ccumulation of amyloid-beta peptide leads to neurofibrillary tangles composed of aggregated hyperphos
104 nset Alzheimer-like dementia associated with neurofibrillary tangles composed of hyperphosphorylated
105 d beta peptide (Abeta) in brain is linked to neurofibrillary tangles composed of hyperphosphorylated
106 ining the amyloid-beta (Abeta) peptides, and neurofibrillary tangles composed of hyperphosphorylated
107 amyloid-beta (Abeta)-containing plaques and neurofibrillary tangles composed of hyperphosphorylated
108 Alzheimer's disease (AD) is the formation of neurofibrillary tangles composed of hyperphosphorylated
112 yloid (Abeta) core and a neuritic component; neurofibrillary tangles, composed predominantly of hyper
113 zed by the intracellular accumulation of the neurofibrillary tangles comprised mainly of the microtub
114 the post-traumatic brain frequently exhibits neurofibrillary tangles comprised of aggregates of the p
115 many frontotemporal dementias (FTDs) contain neurofibrillary tangles comprised of hyperphosphorylated
116 n of insoluble protein aggregates, including neurofibrillary tangles comprised of tau in Alzheimer's
117 thologically by abundant amyloid plaques and neurofibrillary tangles concurrent with synaptic and neu
118 ic vesicles, hyperphosphorylated tau (pTau), neurofibrillary tangle conformational-epitope (cNFT), am
120 ther, the development of amyloid plaques and neurofibrillary tangles contributes to neuronal loss.
121 predominant, and typical AD--on the basis of neurofibrillary tangle counts in hippocampus and cortex
124 enuated the effect of the epsilon4 allele on neurofibrillary tangle density (interaction estimate, -0
126 In addition to amyloid-beta plaque and tau neurofibrillary tangle deposition, neuroinflammation is
127 's disease via its presence in intraneuronal neurofibrillary tangle deposits, where it takes the form
128 otective mechanisms, such as the presence of neurofibrillary tangles, disconnection, as well as compe
130 (18)F]RO6958948)) with high affinity for tau neurofibrillary tangles, excellent selectivity against A
131 ampal insoluble pathological tau species and neurofibrillary tangles following a single dose of AAV-v
132 f Alzheimer's Disease (AD) in regard to both neurofibrillary tangle formation and neuronal network hy
133 rtantly, oligomer injections induced AD-type neurofibrillary tangle formation in the macaque brain.
134 cellular deposition of amyloid-beta (Abeta), neurofibrillary tangle formation, and a microglial-drive
136 in the neocortex precedes the spread of tau neurofibrillary tangles from the limbic areas to the cor
137 se is characterized by amyloid-beta plaques, neurofibrillary tangles, gliosis, and neuronal loss.
138 k neuropathology of Alzheimer's disease (AD; neurofibrillary tangles) had its first foothold in speci
139 Prion-like seeding of amyloid fibrils and neurofibrillary tangles has been invoked to explain the
140 sitron emission tomography tracers targeting neurofibrillary tangles has enabled the distribution of
144 associated protein Tau, a major component of neurofibrillary tangles in Alzheimer disease and other t
145 merly (18) F-AV1451 or (18) F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue
146 pathology including dystrophic neuritis and neurofibrillary tangles in Alzheimer's disease (AD) brai
147 ncluding Lewy bodies in Parkinson's disease, neurofibrillary tangles in Alzheimer's disease, polyQ in
148 PINK1 was absent in cortical Lewy bodies, in neurofibrillary tangles in Alzheimer's disease, progress
150 ites has been implicated in the formation of neurofibrillary tangles in Alzheimer's disease; however,
151 to reduce the risk of AD and development of neurofibrillary tangles in APOE epsilon4+ individuals.
152 beta-amyloid (Abeta) protein deposits and/or neurofibrillary tangles in association with progressive
153 well as plaques (diffuse and neuritic), and neurofibrillary tangles in autopsy specimens from age-ma
155 nd forms insoluble inclusion bodies known as neurofibrillary tangles in the brain tissue of patients
156 position of amyloid-beta (Abeta) plaques and neurofibrillary tangles in the brain, accompanied by syn
161 typical AD, hippocampal-sparing AD has more neurofibrillary tangles in the cortex and fewer in the h
162 verity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to seve
163 reamyloid deposits, severe CAA, and abundant neurofibrillary tangles in the presence of remarkably fe
164 assessed the density and the distribution of neurofibrillary tangles in three cortical regions and tw
165 ptide (amyloid plaques) and the tau protein (neurofibrillary tangles) in the brains of affected indiv
166 and (or) association with senile plaques and neurofibrillary tangles is a major feature of several ne
169 logical hallmark of Alzheimer's disease; the neurofibrillary tangle load correlates strongly with cli
170 ar plaques of amyloid-beta and intraneuronal neurofibrillary tangles made from tau are the histopatho
171 eptide forming extracellular senile plaques, neurofibrillary tangles made of hyperphosphorylated tau
172 stmortem studies have long demonstrated that neurofibrillary tangles made of hyperphosphorylated tau
173 ved from amyloid precursor protein (APP) and neurofibrillary tangles made of hyperphosphorylated Tau.
174 gyrus in THY-Tau22 mice, the development of neurofibrillary tangles made of mutant human tau was not
175 ques and markers to assess the burden of tau neurofibrillary tangles, neuritic plaques, alpha-synucle
176 hippocampal) and time interaction terms for neurofibrillary tangles, neuritic plaques, gross infarct
179 ascade of events leading to the formation of neurofibrillary tangles, neurodegeneration, and the symp
180 tween the numbers of neuropil threads and of neurofibrillary tangles: neurofibrillary tangles were sp
181 dementia, characterized by amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal
182 aque burden, stereologically-based counts of neurofibrillary tangles, neurons and reactive glia, and
184 ressed human tau protein, the development of neurofibrillary tangles, neuropil threads and ghost tang
186 Aberrant tau protein accumulation drives neurofibrillary tangle (NFT) formation in several neurod
187 an trigger increased tau phosphorylation and neurofibrillary tangle (NFT) formation in vivo, the mole
188 and facilitates amyloid plaque deposits and neurofibrillary tangle (NFT) formation, resulting in cog
189 gnaling and its relation to Abeta plaque and neurofibrillary tangle (NFT) pathology during disease on
190 inical diagnoses, apolipoprotein E genotype, neurofibrillary tangle (NFT) pathology, and vascular les
192 is independently associated with lower Braak neurofibrillary tangle (NFT) stages and possibly fewer n
193 hallmarks: neurotoxic amyloid-beta (Abeta), neurofibrillary tangles (NFT), and extensive cell death.
194 Abeta-containing plaques and tau-containing neurofibrillary tangles (NFT), has not been thoroughly i
196 k amyloid-beta (Abeta) plaques or tau-filled neurofibrillary tangles (NFT), is considered the most pr
197 e location of fibrillar tau deposits, called neurofibrillary tangles (NFT), matches closely with regi
200 osis is based on density and distribution of neurofibrillary tangles (NFTs) and amyloid-rich neuritic
201 cterized by brain pathology of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid
202 by the production of amyloidogenic peptides, neurofibrillary tangles (NFTs) and neurodegeneration.
203 surrounding Abeta plaques (NP tau), AD-like neurofibrillary tangles (NFTs) and neuropil threads (NTs
208 lzheimer's disease (AD) is very distinctive: neurofibrillary tangles (NFTs) composed of hyperphosphor
209 neurodegenerative diseases characterized by neurofibrillary tangles (NFTs) comprising filamentous ta
210 mer's disease (AD), cortical neurons develop neurofibrillary tangles (NFTs) consisting of hyperphosph
211 plaques containing beta-amyloid (Abeta) and neurofibrillary tangles (NFTs) consisting of modified ta
212 n (CBF) nucleus basalis (NB) neurons display neurofibrillary tangles (NFTs) during Alzheimer's diseas
213 formed by beta-amyloid peptides (Abeta) and neurofibrillary tangles (NFTs) formed by hyperphosphoryl
214 dicated the nApoE4CF Ab specifically labeled neurofibrillary tangles (NFTs) in AD frontal cortex sect
217 a microtubule-associated protein that forms neurofibrillary tangles (NFTs) in the selective vulnerab
218 e accumulation of hyperphosphorylated tau in neurofibrillary tangles (NFTs) is a neuropathological ha
221 ion of the density and neocortical spread of neurofibrillary tangles (NFTs) with clinical AD disease
223 uggest that tau oligomers, which form before neurofibrillary tangles (NFTs), are the true neurotoxic
224 er's disease (AD), senile plaques (SPs), and neurofibrillary tangles (NFTs), but the specific contrib
227 he hallmark pathology of amyloid plaques and neurofibrillary tangles (NFTs), it has been reported tha
228 functional brain protein that accumulates in neurofibrillary tangles (NFTs), most commonly in Alzheim
230 Aggregated tau is the major component of neurofibrillary tangles (NFTs), structures present in th
231 Aggregated tau is the major component of neurofibrillary tangles (NFTs), structures present in th
232 neurodegenerative diseases characterized by neurofibrillary tangles (NFTs), the predominant tau path
233 n tissue over co-existing tau aggregates and neurofibrillary tangles (NFTs), which are associated in
234 cal hallmarks of Alzheimer's disease (AD) is neurofibrillary tangles (NFTs), which are composed of ab
235 eimer's disease pathology is the presence of neurofibrillary tangles (NFTs), which are intracellular
238 her brain weight (BW) and Alzheimer lesions (neurofibrillary tangles [NFTs] or neuritic plaques [NPs]
239 bodies associated with Parkinson disease and neurofibrillary tangles observed in Alzheimer disease.
240 amyloid beta plaques, neuritic plaques, and neurofibrillary tangles observed in cortical biopsies ob
241 helical filaments (PHFs) that constitute the neurofibrillary tangles observed in neuronal cell bodies
242 th protein misfolding and aggregation as the neurofibrillary tangles of Alzheimer's disease, whereas
243 ase (AD) is characterized by the presence of neurofibrillary tangles of hyperphosphorylated, aggregat
244 ques and intracellular inclusions containing neurofibrillary tangles of phospho-Tau and intraneuronal
250 (p = 4.9 x 10(-4) ), an increased burden of neurofibrillary tangles (p = 9.1 x 10(-3) ), and an incr
251 with neuropathology (NIA ADC, Braak stage of neurofibrillary tangles, p = 3.9 x 10-6, and Consortium
253 s12570088 were significantly associated with neurofibrillary tangle pathology (P = .01352 and .03151,
254 lysis can reliably track the distribution of neurofibrillary tangle pathology and can predict patholo
255 dentate gyrus of patients with AD and severe neurofibrillary tangle pathology and were accompanied by
257 Calignon et al. recreated an early stage of neurofibrillary tangle pathology to show that tau aggreg
258 te widespread and established Ass plaque and neurofibrillary tangle pathology, hippocampal neural ste
259 ammatory signaling may promote or accelerate neurofibrillary tangle pathology, we explored the effect
263 didate variants included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer
265 characterize the disease-senile plaques and neurofibrillary tangles-ramify systematically through th
266 with AD, including measures of amyloid load, neurofibrillary tangles, reactive astrocytes, and activa
267 ults in tau phosphorylation and formation of neurofibrillary tangles, requires the recruitment of the
268 , which aggregate to form senile plaques and neurofibrillary tangles, respectively, are induced to mi
269 e tau pathway-leading to amyloid plaques and neurofibrillary tangles, respectively, which are histopa
270 Disease neuritic plaque score and the Braak neurofibrillary tangle score, remained significant predi
271 endent negative associations of cerebral tau neurofibrillary tangles score with the interval between
272 re Sarkosyl-insoluble and associate with Tau neurofibrillary tangles selectively in Alzheimer disease
273 nd semiquantitative scores for the burden of neurofibrillary tangles, senile plaques, Lewy bodies (LB
276 ectroscopy metabolite measurements and Braak neurofibrillary tangle stage (Braak stage), neuritic pla
278 te likelihood of having Alzheimer's disease (neurofibrillary tangle stage B2; n=56), those with hippo
279 gh likelihood of having Alzheimer's disease (neurofibrillary tangle stage B3; n=205), those with hipp
282 psy data to evaluate the effect of different neurofibrillary tangle stages on the rates of progressio
283 by accumulation of amyloid-beta plaques and neurofibrillary tangles, synaptic and neuronal loss, and
284 sclerosis can cause the neuritic plaques and neurofibrillary tangles that define Alzheimer neuropatho
285 and tauopathies, tau protein aggregates into neurofibrillary tangles that progressively spread to syn
286 re the main components of senile plaques and neurofibrillary tangles, the two histopathological hallm
287 r disease (AD) and abnormally accumulates as neurofibrillary tangles; therefore, the pathways by whic
290 relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheime
292 defined on the basis of the distribution of neurofibrillary tangles: typical AD, hippocampal-sparing
293 visualized on coronal slabs, and plaques and neurofibrillary tangles were counted and standardized to
294 pants who died, and beta-amyloid (Abeta) and neurofibrillary tangles were identified by immunohistoch
295 opil threads and of neurofibrillary tangles: neurofibrillary tangles were sparse in brains that had n
296 in vivo imaging of beta-amyloid plaques and neurofibrillary tangles, were obtained from 12 AD patien
297 t bind to Abeta in both neuritic plaques and neurofibrillary tangles, whereas antibodies to material
298 eimer's disease are amyloid-beta plaques and neurofibrillary tangles, which are primarily composed of
299 ) is associated with the accumulation of tau neurofibrillary tangles, which may spread throughout the
300 in brains of Alzheimer's disease and diffuse neurofibrillary tangles with calcification, characterize
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