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1 al filaments/fibrils (the main component of "tangles").
2 venting and reducing both brain "plaques and tangles".
3 to cognitive deficits even in the absence of tangles.
4 at the expense of increasing neurofibrillary tangles.
5 sease before the accumulation of plaques and tangles.
6 amyloid angiopathy (CAA) and neurofibrillary tangles.
7  of amyloid beta (Abeta) and neurofibrillary tangles.
8 s: amyloid abeta1-42 and Tau neurofibrillary tangles.
9 loid (Abeta) plaques and tau neurofibrillary tangles.
10 arkers of senile plaques and neurofibrillary tangles.
11 ) peptides and intracellular neurofibrillary tangles.
12  threads and neurofibrillary tangles and pre-tangles.
13 nal transport independently from plaques and tangles.
14 th increased risk for AD and neurofibrillary tangles.
15 opposite to the female excess of plaques and tangles.
16 t knit together to form a mesh of disordered tangles.
17 aques and tau-immunoreactive neurofibrillary tangles.
18 ia, AD, neuritic plaques, or neurofibrillary tangles.
19 lly by neuronal vacuoles and neurofibrillary tangles.
20  leading to the formation of neurofibrillary tangles.
21 e intracellular formation of neurofibrillary tangles.
22 au aggregates in the form of neurofibrillary tangles.
23 e identified 542 proteins in neurofibrillary tangles.
24  and subsequent formation of neurofibrillary tangles.
25 dysfunction and formation of neurofibrillary tangles.
26 t tau fragments ending at 368 are present in tangles.
27 amyloid-beta plaques and tau neurofibrillary tangles.
28 ggregated tau in the form of neurofibrillary tangles, (18)F-flortaucipir has been reported to bind to
29 e model of AD that develops both plaques and tangles (3xTg).
30  we first assessed the patterns of brain tau tangle accumulation (measured with the positron emission
31                             While plaque and tangle accumulation likely contributes to neuron and syn
32 he spread of tau aggregates (neurofibrillary tangles) across the cerebral cortex parallels symptom se
33                                          Tau tangle aggregation in this region may develop concurrent
34 multaneously account for tau neurofibrillary tangles, alpha-synuclein inclusions, neuritic plaques, i
35 ex-specific association with neurofibrillary tangles among males (P = 2.5 x 10-8) but not females (P
36 co-occurrence of both LB and neurofibrillary tangles, among other protein inclusions.
37 ase (AD) is characterized by neurofibrillary tangles, amyloid plaques, and neurodegeneration.
38 er) and pathologic burden of neurofibrillary tangles, amyloid plaques, vascular lesions, and Lewy bod
39  co-localized with phosphorylated tau in pre-tangle and tangle-bearing neurons.
40 g, flexible physical filaments are naturally tangled and knotted, from macroscopic string down to lon
41 ven without Abeta.SIGNIFICANCE STATEMENT Tau tangles and beta-amyloid (Abeta) plaques are key lesions
42 n precedes the appearance of neurofibrillary tangles and contributes to neuronal loss.
43 otein (APP), and presence of neurofibrillary tangles and dystrophic neurites containing hyperphosphor
44  brains (eg, intraneuronal and extraneuronal tangles and dystrophic neurites), but does not seem to b
45 eactivity is associated with neurofibrillary tangles and is involved in tau degradation.
46  phenotype which includes Abeta plaques, tau tangles and memory impairments remain unknown.
47  beta (Abeta) plaques may possibly clear tau tangles and modestly slow cognitive decline in symptomat
48 a-amyloid) plaques and tau neural fibrillary tangles and neural inflammation; these pathologies lead
49 fied by a summary measure of neurofibrillary tangles and neuritic and diffuse plaques.
50 re abnormal at old age (7-9 months) when tau tangles and neurodegeneration are extensive.
51 on and exhibit age-dependent neurofibrillary tangles and neurodegeneration, overexpressed CX3CL1 in b
52 he first rise of amyloid beta through to Tau tangles and neurodegeneration.
53 f hyperphosphorylated tau in neurofibrillary tangles and neuroinflammation, together resulting in neu
54 ng) pathological inclusions, neurofibrillary tangles and neuropil threads but only in the patient who
55 h four of these animals showing tau-positive tangles and neuropil threads.
56 gs] pathological inclusions, neurofibrillary tangles and neuropil threads.
57 au inclusions in the form of neurofibrillary tangles and Pick bodies and in some cases glial Tau path
58 he resulting sera recognized neurofibrillary tangles and plaque-associated dystrophic neurites in AD
59                                    Recently, tangles and plaque-like aggregates have been identified
60 form of neuropil threads and neurofibrillary tangles and pre-tangles.
61 es were accompanied by the resolution of tau tangles and significantly decreased neurodegenerative pa
62  the first appearance of amyloid plaques and tangles and the manifestation of dementia is now well es
63 marks of the disease such as neurofibrillary tangles and widespread neuronal losses.
64 cting incidental age-related neurofibrillary tangles) and neuromelanin-containing neurons in the subs
65 hology (neuritic plaques and neurofibrillary tangles) and the interval between time of testing and ti
66 ading to dissociation of Tau, formation of a tangle, and loss of the axon.
67 altered Tau phosphorylation, neurofibrillary tangles, and accumulation of insoluble protein plaques.
68  have shown an overlap of Abeta plaques, tau tangles, and alpha-synuclein (alpha-syn) pathologies in
69 , are found in association with neurons, tau tangles, and beta-amyloid in specimens from the brains o
70 increase in amyloid plaques, neurofibrillary tangles, and cognitive decline.
71 amyloid (Abeta) plaques, tau neurofibrillary tangles, and cognitive deficits, suggesting that it cont
72 ression, amyloid deposition, neurofibrillary tangles, and composite neuropathological scores, indepen
73 atter damage, brain atrophy, neurofibrillary tangles, and dementia.
74 -amyloid senile plaques, tau neurofibrillary tangles, and fused in sarcoma (FUS) and TAR DNA-binding
75 s and cognitive performance, neurofibrillary tangles, and neuritic plaque burden.
76 myloid-beta (Abeta) plaques, neurofibrillary tangles, and reactive gliosis.
77 a protein and tau associated neurofibrillary tangles; and (iv) four common non-Alzheimer's pathologie
78                              Neurofibrillary tangles are a pathological hallmark of Alzheimer's disea
79      Although amyloid plaques and fibrillary tangles are hallmarks of AD, research suggests that path
80                 We show that neurofibrillary tangles are neither sufficient nor required for the sile
81  alpha-synuclein (aSyn), and neurofibrillary tangles are primarily composed of tau protein.
82 opathological lesions (i.e., neurofibrillary tangles) are apparent.
83 d, nor can they easily unbundle, if they are tangled around one another.
84 n of extracellular plaques and intracellular tangles as playing a fundamental role in the course and
85 , neuronal loss and reverses neurofibrillary tangle-associated brain dysfunction.
86  associations between age and 18F-MK-6240 in tangle-associated regions, which were negligible after a
87 ed with phosphorylated tau in pre-tangle and tangle-bearing neurons.
88              Neurons, including tau-positive tangle-bearing ones, showed decreased chromogenic and im
89 , less severe and widespread neurofibrillary tangles (beta = -0.77 score units [95% CI, -1.52 to -0.0
90 rticobasal degeneration, and neurofibrillary tangle Braak stage regions of interest, and these values
91 a pair of rigid helical filaments can form a tangled bundle, and we compare these constraints with ex
92 a are too straight and too far apart to form tangled bundles based on their intrinsic, undeformed geo
93 FAs with neuritic plaque and neurofibrillary tangle burden as well as domain-specific cognitive perfo
94 ossibility that knowledge of neurofibrillary tangle burden in the presence of moderate or frequent pl
95                     Cerebral neurofibrillary tangles burden, in addition to alpha-synuclein pathology
96 athology literature, which suggests that tau tangles but not amyloid-beta plaques correlate with cogn
97 ary constituent of Alzheimer neurofibrillary tangles, can form liquid droplets and therefore has the
98 io, and hippocampal volume), neurofibrillary tangles (cerebrospinal fluid phosphorylated tau181 assay
99          Amyloid plaques and neurofibrillary tangles co-occur in Alzheimer disease, but with differen
100 ing amyloid-beta (Abeta) and neurofibrillary tangles composed of aggregated, hyperphosphorylated tau.
101 le plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated tau.
102 t of involvement (spread) by neurofibrillary tangles (composed of hyperphosphorylated tau proteins) b
103 re and a neuritic component; neurofibrillary tangles, composed predominantly of hyperphosphorylated t
104 ed with deposition of intracellular neuronal tangles consisting primarily of hyperphosphorylated micr
105 ar plaques and intracellular neurofibrillary tangles, constituted by hyperphosphorylated tau protein.
106 pment of amyloid plaques and neurofibrillary tangles contributes to neuronal loss.
107 Flortaucipir correlated with neurofibrillary tangle counts in entorhinal cortex, but entorhinal and m
108                              Neurofibrillary tangle counts were performed using thioflavin-S microsco
109 ak staging, Abeta plaque and neurofibrillary tangle counts, and semiquantitative tau lesion scores we
110 dependently associated with an increased tau tangle density (p = 4.9 x 10(-4) ), an increased burden
111  (p value = 5.42 x 10(-13)), neurofibrillary tangle density (p value = 1.89 x 10(-6)), and global mea
112 was more pronounced in persons with more tau tangle density and with neocortical Lewy body pathologie
113 g AD pathology (Braak score, Abeta load, and tangle density) and directly with performance in episodi
114 related with both the amyloid burden and tau tangle density, and no other associations of brain insul
115 xamination assessed beta-amyloid burden, tau tangle density, neocortical Lewy bodies, hippocampal scl
116 gy, particularly beta-amyloid burden and tau tangle density.
117 d among persons with AD dementia, and PHFtau tangle density.
118 , Abeta load and paired helical filament tau tangle density.
119 e that in ageing and Alzheimer's disease tau tangles deposit early in the transentorhinal cortex, a r
120  amyloid-beta plaque and tau neurofibrillary tangle deposition, neuroinflammation is considered a key
121  disease, demonstrating that neurofibrillary tangles develop downstream of amyloid-beta-induced micro
122 images and W-score maps, and neurofibrillary tangle distribution in patients with primary Alzheimer's
123 2) is critically important for resolving DNA tangles during cell division, and as such, it is a broad
124            Our data suggest that tau368 is a tangle-enriched fragment and that the CSF ratio tau368/t
125                                          The Tangle-Entropy (TS) plots show the strong preservation o
126 em amyloid load and neuronal neurofibrillary tangles, even after accounting for APOE, validating our
127 tions among these elements and highlight the tangled evolutionary relationships within the phageome.
128 ) with high affinity for tau neurofibrillary tangles, excellent selectivity against Abeta plaques, an
129 o occurs in quantum wavefunctions, where the tangled filaments are vortices (nodal lines/phase singul
130 beta fibrils (1-42 and 1-40) and tau protein tangles/filaments.
131 pathological tau species and neurofibrillary tangles following a single dose of AAV-vectored PHF1 com
132 d-beta deposition, neuroinflammation and tau tangle formation all play a significant role in Alzheime
133  abnormal tau aggregation, which may promote tangle formation and accelerate the development of AD pa
134  Remarkably, cell death was dissociated from tangle formation in this natural 3D model of AD.
135                          Amyloid deposition, tangle formation, neuroinflammation and neuronal dysfunc
136 e may precede insoluble Abeta plaque and tau tangle formation.
137 milial neurodegeneration and neurofibrillary tangle formation.
138 ition of amyloid plaques and neurofibrillary tangles, formed by amyloid beta (Abeta) peptides and pho
139                              Neurofibrillary tangles, formed of misfolded, hyperphosphorylated tau pr
140  genomes of protists are subject to the most tangled forms of gene expression yet identified.
141 x precedes the spread of tau neurofibrillary tangles from the limbic areas to the cortex.
142  its strand-passaging activity that resolves tangled genomic DNA during mitosis.
143  that the knotting probability of the vortex tangle grows with the vortex length, as for macromolecul
144 obes for amyloid plaques and neurofibrillary tangles, hallmarks of Alzheimer disease (AD), enables mo
145 tomography tracers targeting neurofibrillary tangles has enabled the distribution of tau pathology to
146 ecently, PET tracers for tau neurofibrillary tangles have become available and have shown utility in
147  from in vivo imaging of neurofibrillary tau tangles have not yet been explored.
148 o, but subsequently, Alzheimer's plaques and tangles have received more attention.
149  Lewy bodies (LB) in PD, and neurofibrillary tangles in AD.
150 451 or (18) F-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue studies assessi
151 such as beta-amyloid (Abeta) fibrils and Tau tangles in Alzheimer's disease are accessible only via i
152 s markedly reduces tau-laden neurofibrillary tangles in FTLD mice in vivo.
153 antly in the EC that the formation of mature tangles in old mice was associated with excitatory cell
154   Plasma P-tau217 levels correlated with tau tangles in participants with (Spearman rho = 0.64; P < .
155 tive biomarker for detecting neurofibrillary tangles in preclinical Alzheimer's disease.
156 e disease characterized by deposition of tau tangles in the brain are highly susceptible to developin
157 le inclusion bodies known as neurofibrillary tangles in the brain tissue of patients with a variety o
158 oid-beta (Abeta) plaques and neurofibrillary tangles in the brain, accompanied by synaptic dysfunctio
159 beta (Abeta) plaques and tau neurofibrillary tangles in the brain.
160 oid beta (Abeta) plaques and neurofibrillary tangles in the brain.
161 intracellular tau-containing neurofibrillary tangles in the brain.
162 ation of amyloid plaques and neurofibrillary tangles in the brain.
163 tin components causes accumulation of desmin tangles in the cytoplasm.
164 are characterized by the formation of mature tangles in the entorhinal cortex and disorientation and
165     Neuropathological data indicate that tau tangles in the medial temporal lobe (MTL) underlie episo
166 beta (Abeta) plaques and tau neurofibrillary tangles in the neocortex is linked to neural system fail
167 nd sequence of tau pathology as humans, with tangles in the oldest animals.
168 s of AD (amyloid plaques and neurofibrillary tangles) in aged chimpanzee brains provided an opportuni
169 laques) and the tau protein (neurofibrillary tangles) in the brains of affected individuals.
170 e relative mechanical stability of knots and tangles, in agreement with simulations and experiments f
171  or cat's claw) as both a potent "plaque and tangle" inhibitor and disaggregator is postulated to rep
172 ponsible for both the observed "plaque" and "tangle" inhibitory and reducing activity.
173  that 75 proteins present in neurofibrillary tangles interacted with PHF1-immunoreactive phosphorylat
174 ta-amyloid and tau proteins into plaques and tangles is a central feature of Alzheimer disease (AD).
175 tion of the tau protein into neurofibrillary tangles is believed to correlate with cognitive decline
176                                      The tau tangle ligand (18)F-AV-1451 ((18)F-T807) binds to neurom
177 yperphosphorylated tau deposition and neural tangle-like pathology occurred in cortical and hippocamp
178                 All three antibodies stained tangle-like structures in different brain sections of TH
179                              Neurofibrillary tangles likely cause neurodegeneration in Alzheimer's di
180  have long demonstrated that neurofibrillary tangles made of hyperphosphorylated tau proteins are clo
181 u22 mice, the development of neurofibrillary tangles made of mutant human tau was not accelerated in
182  proteomics was performed on neurofibrillary tangles microdissected from patients with advanced Alzhe
183  In addition to amyloid-beta plaques and tau tangles, mitochondrial dysfunction is implicated in the
184  to assess the burden of tau neurofibrillary tangles, neuritic plaques, alpha-synuclein inclusions, a
185 pathologic outcomes included neurofibrillary tangles, neuritic plaques, microinfarcts, cystic infarct
186 age point these mice exhibit neurofibrillary tangles, neurodegeneration and cognitive deficits.
187 llular aggregation of tau as neurofibrillary tangles, neuronal and synaptic loss, and eventual cognit
188 tain non-amyloid-plaque, non-neurofibrillary-tangle neuropathologies.
189  protein accumulation drives neurofibrillary tangle (NFT) formation in several neurodegenerative dise
190 ased tau phosphorylation and neurofibrillary tangle (NFT) formation in vivo, the molecular link assoc
191  amyloid plaque deposits and neurofibrillary tangle (NFT) formation, resulting in cognitive impairmen
192 relation to Abeta plaque and neurofibrillary tangle (NFT) pathology during disease onset is unknown.
193 s amyloid and tau-containing neurofibrillary tangle (NFT) pathology during the onset of Alzheimer's d
194         The study used Braak neurofibrillary tangle (NFT) stage, frequency of neuritic plaques, and L
195  associated with lower Braak neurofibrillary tangle (NFT) stages and possibly fewer neuritic plaques,
196 beta) peptide in propagating neurofibrillary tangles (NFTs) and eventual cognitive impairment in AD.
197 ta plaques (NP tau), AD-like neurofibrillary tangles (NFTs) and neuropil threads (NTs).
198                              Neurofibrillary tangles (NFTs) are the pathological hallmark of neurodeg
199                              Neurofibrillary tangles (NFTs) composed of hyperphosphorylated and misfo
200 bsequent aggregation to form neurofibrillary tangles (NFTs) is closely related to progression of neur
201  decline and the presence of neurofibrillary tangles (NFTs) of the protein tau in patients' brains.
202 ty and neocortical spread of neurofibrillary tangles (NFTs) with clinical AD disease progression offe
203  burden of neuritic plaques, neurofibrillary tangles (NFTs), and vascular brain injury (VBI).
204                              Neurofibrillary tangles (NFTs), hippocampal sclerosis, lacunar infarcts,
205  protein that accumulates in neurofibrillary tangles (NFTs), most commonly in Alzheimer's disease (AD
206             The formation of neurofibrillary tangles (NFTs), oxidative stress and neuroinflammation h
207 ve diseases characterized by neurofibrillary tangles (NFTs), the predominant tau pathology in Alzheim
208 -existing tau aggregates and neurofibrillary tangles (NFTs), which are associated in AD and tauopathi
209 inity PET tracer for imaging neurofibrillary tangles (NFTs).
210  by a pathological hallmark: neurofibrillary tangles (NFTs).
211 hyperphosphorylated tau into neurofibrillary tangles (NFTs).
212 myloid-beta (Abeta) and Tau (neurofibrillary tangles, NFTs) deposition in the brain.
213  a critical role in inducing neurofibrillary tangles (NTFs) in human neurons.
214  tau-null background, these mice had similar tangle numbers but were protected against neurotoxicity.
215 s (PHFs) that constitute the neurofibrillary tangles observed in neuronal cell bodies in individuals
216  By numerically simulating the dynamics of a tangle of quantum vortex lines, we find that this quantu
217                 In contrast, neurofibrillary tangles of CTE contain both 3R and 4R tau, with post-tra
218 pathologically characterized by perivascular tangles of hyperphosphorylated tau at the depth of sulci
219 ular interactions are initiated by insoluble tangles of phosphorylated tau protein and plaques of amy
220                                              Tangles of string typically become knotted, from macrosc
221 as plaques and intracellular neurofibrillary tangles of tau protein.
222  of amyloid beta (Abeta) and neurofibrillary tangles of tau.
223 eriovenous malformations (AVMs) are abnormal tangles of vessels where arteries and veins directly con
224              They include Alzheimer disease, tangle-only dementia, Pick disease, argyrophilic grain d
225 bstantially different from those in a vortex tangle or on distances of the order of the vortex diamet
226 ifference in Braak stage for neurofibrillary tangles or consortium to establish a registry for Alzhei
227 kage, shunts, abnormal vessel branching, and tangles) or the posterior pole (hyperfluorescent lesions
228                 However, besides plaques and tangles, other biochemical and morphological features ar
229  frequency of Alzheimer-type neurofibrillary tangles (p < 0.05).
230 4) ), an increased burden of neurofibrillary tangles (p = 9.1 x 10(-3) ), and an increased rate of co
231 ogy (NIA ADC, Braak stage of neurofibrillary tangles, p = 3.9 x 10-6, and Consortium to Establish a R
232 t bundles, i.e. bundles which do not contain tangled pairs of filaments, may appear surprising given
233             TDP-43 and Braak neurofibrillary tangle pathological staging schemes were constructed, an
234 ive decline was greater in persons with more tangle pathology (estimate for interaction = -0.007, SE
235 ignificantly associated with neurofibrillary tangle pathology (P = .01352 and .03151, respectively);
236  Abeta40, Abeta38, sAPPalpha, and sAPPbeta), tangle pathology (P-tau), blood-brain-barrier function (
237 ing P301Ltau-overexpressing mice with severe tangle pathology and neurodegeneration.
238  patients with AD and severe neurofibrillary tangle pathology and were accompanied by changes in the
239  combination with P301L, produces an AD-type tangle pathology, focal neuroinflammation and memory imp
240 s in robust tau hyperphosphorylation without tangle pathology, gradually developing age-progressive m
241 ng may promote or accelerate neurofibrillary tangle pathology, we explored the effect of recombinant
242 detect early Braak stages of neurofibrillary tangle pathology.
243 his is insufficient in accelerating neuritic tangle pathology.
244 ignificantly reduced phospho-tau species and tangle pathology.
245 and that the CSF ratio tau368/t-tau reflects tangle pathology.
246 included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer's Disease Asses
247 oid plaques (Pearson r = -0.48; P < .01) and tangles (Pearson r = -0.55; P = .01) in the brain.
248 ease interneuronal plaques and intraneuronal tangles, presently observed aberrations in hyperinsuline
249 nergy stored in the silk threads to actively tangle prey from afar.
250 aria tomentosa that possess both "plaque and tangle" reducing and inhibitory activity.
251 f hyperphosphorylated tau as neurofibrillary tangles remains the primary neuropathologic criteria for
252 ading to amyloid plaques and neurofibrillary tangles, respectively, which are histopathological hallm
253 ly correlated with tau hyperphosphorylation, tangles score and Braak stage in human brain.
254 associations of cerebral tau neurofibrillary tangles score with the interval between onset of motor a
255  aberrant mitotic spindle with disorganized, tangle-shaped microtubules and reduced aster formation,
256 dividual was also assigned a neurofibrillary tangle stage (B1-B3), relating to the likelihood of havi
257 orrespondence of Thal amyloid phase to Braak tangle stage and ante-mortem clinical characteristics in
258 DG- and Abeta-ADCRP were compared with Braak tangle stage and Thal amyloid phase, respectively.
259  having Alzheimer's disease (neurofibrillary tangle stage B1; n=37).
260  having Alzheimer's disease (neurofibrillary tangle stage B2; n=56), those with hippocampal TDP-43 ha
261  having Alzheimer's disease (neurofibrillary tangle stage B3; n=205), those with hippocampal TDP-43 h
262  contrast, Thal amyloid phase, but not Braak tangle stage or cerebral amyloid angiopathy predicted (1
263 -Pittsburgh compound B values, but not Braak tangle stage or cerebral amyloid angiopathy.
264 nd all assigned Thal amyloid phase and Braak tangle stage using thioflavin-S fluorescent microscopy.
265 hases were older at death, had a lower Braak tangle stage, and were less frequently APOE-epsilon4 pos
266 Alzheimer's disease cases, showed that Braak tangle stage, but not Thal amyloid phase predicted age a
267   We found that knowledge of neurofibrillary tangle stage, modeled as the sort of information that co
268 n association with the Braak neurofibrillary tangle stage.
269 e-mortem clinical status was driven by Braak tangle stage.
270 amyloid angiopathy, and determined the Braak tangle stage.
271 s associated with high Braak neurofibrillary tangle stage.
272 xtent of tau pathology, as assessed by Braak tangle stage.
273 egions associated with Braak neurofibrillary tangle stages I-VI.
274 uate the effect of different neurofibrillary tangle stages on the rates of progression on several sta
275 teins known to be present in neurofibrillary tangles such as tau, ubiquitin, neurofilament proteins a
276  of amyloid-beta plaques and neurofibrillary tangles, synaptic and neuronal loss, and cognitive decli
277 ngly, we saw a higher ratio of pretangles to tangles than that in human AD, and none of the cases sho
278  tau protein aggregates into neurofibrillary tangles that progressively spread to synaptically connec
279 aining "plaques" and tau protein containing "tangles" that contribute to accelerated memory loss and
280  phenotype of a mouse model with plaques and tangles, the triple-transgenic mice.
281 onents of senile plaques and neurofibrillary tangles, the two histopathological hallmarks of Alzheime
282 d outline the principles of knot, braid, and tangle theory appropriate to chemistry and molecular str
283      Despite the increase in neurofibrillary tangles, TIA1 reduction increased neuronal survival and
284 ution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is cri
285 -mortem Braak staging of neurofibrillary tau tangle topographical distribution is one of the core neu
286                                    The p-tau tangle unit is a posttranslational modification of norma
287 sured by ELISA and the presence of tau368 in tangles was evaluated using immunohistochemistry.
288 ing plaques, but the overall distribution of tangles was extensive (Braak V/VI).
289                                            A tangled web of vicious circles, driven by cultural issue
290 eyes, leakage was noted in 1 eye, shunts and tangles were noted in 3 eyes, and macular abnormalities
291 ultimately gives way to the formation of tau tangles which track with cognitive decline in humans.
292 sociate amyloid-beta (Abeta) plaques and tau tangles, which are key pathological hallmarks of Alzheim
293 with the accumulation of tau neurofibrillary tangles, which may spread throughout the cortex by inter
294  Abeta rats that do not form neurofibrillary tangles, which support these findings as an independent
295 cells and thus their evolution is inexorably tangled with host biology.
296 paleoclimates and life history traits likely tangled with the effects of human-mediated dispersal.
297 heimer's disease and diffuse neurofibrillary tangles with calcification, characterized by accumulatio
298 ted intense labelling of non-ghost and ghost tangles with PBB3 and AV-1451, while dystrophic neurites
299 ith amyloid beta (Abeta) and neurofibrillary tangles with tau accumulation.
300 d tau aggregation, including neurofibrillary tangles, with age, making them a promising physiologic m

 
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