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1 ary tangles and not with neuropil threads or dystrophic neurites.
2 bsence of PHF/tau-positive plaque-associated dystrophic neurites.
3 brain in diffuse deposits and in a subset of dystrophic neurites.
4 ice and selectively localized to presynaptic dystrophic neurites.
5 gnificantly ameliorates these phenotypes and dystrophic neurites.
6 ed tau-positive neurofibrillary tangles, and dystrophic neurites.
7 ed tau-positive neurofibrillary tangles, and dystrophic neurites.
8  accumulation of LC3-GFP positive puncta and dystrophic neurites.
9  plaque growth and attenuates plaque-related dystrophic neurites.
10 e deposition, and reduced tau immunoreactive dystrophic neurites.
11 d was associated with a ninefold increase of dystrophic neurites.
12 TN3, but not RTN1, is abundantly enriched in dystrophic neurites.
13 n Abeta levels, Abeta plaque deposition, and dystrophic neurites.
14  were unable to detect the majority of these dystrophic neurites.
15 -amyloid fibrils, microglia, astrocytes, and dystrophic neurites.
16 d neocortex, and a decrease in the number of dystrophic neurites.
17 ctivation, age-related amyloid deposits, and dystrophic neurites.
18 nd over time, accumulated in cell bodies and dystrophic neurites.
19 of AD, including A beta-amyloid deposits and dystrophic neurites.
20 gnificantly fewer immunoreactive plaques and dystrophic neurites.
21 ne deletion resulted in a marked increase in dystrophic neurites (2- to 3-fold higher than APP/PS1 Gf
22 of ERC lesion, numbers of APP-immunoreactive dystrophic neurites and Abeta burden were significantly
23    Plaques are associated with synapse loss, dystrophic neurites and altered neurite trajectories.
24 unimmunized AD, but lacked plaque-associated dystrophic neurites and astrocyte clusters; (iii) in som
25                                              Dystrophic neurites and astroglia showed no M-CSFR label
26 i-hAPP- and antineurofilament-immunoreactive dystrophic neurites and astroglial cells.
27 ltured rat hippocampal neurons, resulting in dystrophic neurites and axonal swelling.
28 osphorylated tau accumulating in surrounding dystrophic neurites and early tangle-like structures.
29        Amyloid deposition is associated with dystrophic neurites and extensive gliosis.
30  Alzheimer disease (AD), are associated with dystrophic neurites and glial responses, both astrocytic
31 served in small numbers of plaque-associated dystrophic neurites and in focal regions of pyramidal ne
32 ases show accumulation of alpha-synuclein in dystrophic neurites and in Lewy bodies.
33 r around Abeta plaques, leading to augmented dystrophic neurites and increased Abeta plaque load.
34 r abundance, morphology, and distribution of dystrophic neurites and neuronal cytoplasmic inclusions
35  neurofilament immunostaining revealed a few dystrophic neurites and neurons, choline acetyltransfera
36  tau aggregates in pre-NFTs and mature NFTs, dystrophic neurites and neuropil threads in the hippocam
37 ous A beta 42-reactive plaques, many bearing dystrophic neurites and reactive glia.
38  microglia, plaque formation, and numbers of dystrophic neurites and results in improved cognitive fu
39 o decreased the numbers of ubiquitin-labeled dystrophic neurites and the percentage area per plaque o
40 unded by large, swollen axons and dendrites (dystrophic neurites) and activated glia.
41  plaques (beta-amyloid plaques surrounded by dystrophic neurites) and neurofibrillary tangles.
42 as reactive astrocytes, activated microglia, dystrophic neurites, and a few NFTs.
43 ents with HD, both in the cytoplasm, forming dystrophic neurites, and in the nucleus, forming intranu
44  by senile plaques, neurofibrillary tangles, dystrophic neurites, and reactive glial cells.
45     These data suggest that PHF/tau-positive dystrophic neurites are a common component of all subtyp
46 ed helical filament (PHF)/tau immunoreactive dystrophic neurites are a common pathological feature in
47 dy, we investigated whether PHF/tau-positive dystrophic neurites are located in all subtypes of plaqu
48 en reported that phosphorylated tau-positive dystrophic neurites are observed in transgenic mice over
49  this system suggest that amyloid-associated dystrophic neurites are relatively stable structures in
50                                              Dystrophic neurites are swollen dendrites or axons recog
51                                              Dystrophic neurites are thought to disrupt neuronal func
52 or CD40 deficiency reduces the mean ratio of dystrophic neurite area to congophilic plaque area and t
53  less cortical amyloid-beta (Abeta) and less dystrophic neurites around amyloid plaques compared with
54 0 days after immunotherapy, there were fewer dystrophic neurites around each plaque, a recovery of sy
55 ved cells, which showed signs of AB plaques, dystrophic neurites around plaques, synapse loss, dendri
56                   Notably, plaque-associated dystrophic neurites associated with disruption of axonal
57  a variety of noxious stimuli (ubiquitinated dystrophic neurites, astrocytosis, and microglial infilt
58 parenchymal plaque burden, astrogliosis, and dystrophic neurites at doses 10- to 50-fold lower than u
59  enhances amyloid plaque compaction, reduces dystrophic neurites, attenuates plaque-associated synapt
60  intraneuronal and extraneuronal tangles and dystrophic neurites), but does not seem to bind to a sig
61 hore methoxy-X04, and individual YFP-labeled dystrophic neurites by their inherent fluorescence.
62                     alpha-Syn immunoreactive dystrophic neurites contained numerous electrodense lami
63  and presence of neurofibrillary tangles and dystrophic neurites containing hyperphosphorylated tau.
64 ulation not only in Lewy bodies, but also in dystrophic neurites decorating Abeta plaques.
65 produce a virtual phenocopy of Abeta-induced dystrophic neurites, dendritic simplification, and dendr
66                                              Dystrophic neurites displayed intense immunoreactivity d
67 by the presence of neuritic plaques in which dystrophic neurites (DNs) are typical constituents.
68 brains include mitochondrial dysfunction and dystrophic neurites (DNs) in areas surrounding amyloid p
69  neuronal intranuclear inclusions (NIIs) and dystrophic neurites (DNs) in the HD cortex and striatum,
70 ely in degenerated neurons, and localizes to dystrophic neurites during Alzheimer's progression.
71 gions emerging as particularly vulnerable to dystrophic neurites (e.g. amygdala, caudate and putamen)
72 es, impairs Abeta clearance, and exacerbates dystrophic neurite formation.
73  plaque-centered quantification of SMI312(+) dystrophic neurites, GFAP(+) reactive astrocytes, and IB
74  co-localization of PS1 with NFTs and plaque dystrophic neurites implicates a role for PS1 in the div
75 any alpha-synuclein-positive Lewy bodies and dystrophic neurites in 50% of amygdala samples from Down
76                        PHFtau was evident in dystrophic neurites in 55% of cases with AD, 34% with no
77               alpha-Synuclein was present in dystrophic neurites in 7 cases, 6 of which also had cere
78 s Abeta levels, amyloid plaque deposits, and dystrophic neurites in a mouse transgenic AD model.
79 s and, along with C5b-9 IR, was localized to dystrophic neurites in a subset of neuritic plaques, neu
80              In addition, in AD brain, large dystrophic neurites in a subset of senile plaques are co
81 eurofibrillary tangles and plaque-associated dystrophic neurites in AD brain sections.
82 synaptophysin that may resemble formation of dystrophic neurites in AD.
83 or of synapse density because it is found in dystrophic neurites in Alzheimer's disease-affected brai
84 Fs produced by eta-secretase are enriched in dystrophic neurites in an AD mouse model and in human AD
85 ng frequent neuronal cytoplasmic inclusions, dystrophic neurites in both grey and white matter and al
86 loss of dendritic spines and the presence of dystrophic neurites in both the hippocampi of transgenic
87                       The immunophenotype of dystrophic neurites in conjunction with the results of h
88                We found abundant clusters of dystrophic neurites in layers 2 to 3 of the neocortex, t
89                                              Dystrophic neurites in plaques of PDAPP tg mouse and AD
90    Importantly, we show that the presence of dystrophic neurites in Tg-RTN3 mice causes impairments i
91 ral amyloid burden and BACE1 accumulation in dystrophic neurites in the absence of BACE1 S-palmitoyla
92 tment strongly resembled AVs that collect in dystrophic neurites in the AD brain and in an AD mouse m
93 urofibrillary tangles, neuropil threads, and dystrophic neurites in the AD brain.
94 (Abeta)-containing plaques are surrounded by dystrophic neurites in the Alzheimer's disease (AD) brai
95 hanced amyloid plaque compaction and reduced dystrophic neurites in the APP/PS1 and 5xFAD mouse model
96 DP-A and TDP-B, are not associated with long dystrophic neurites in the cerebral cortex, and do not s
97 showed the occurrence of RTN3-immunoreactive dystrophic neurites in the cortex.
98 cortical Lewy bodies, abnormal neurites, and dystrophic neurites in the plaques.
99 nsonism without Lewy bodies but demonstrated dystrophic neurites in the substantia nigra intensely st
100 aining pattern excluded neuropil threads and dystrophic neurites indicating that tyrosine phosphoryla
101                                              Dystrophic neurites (Kendall tau = 0.34, P = 0.001), rea
102 ) is accumulated in a distinct population of dystrophic neurites named as RTN3 immunoreactive dystrop
103 o mark a distinct and abundant population of dystrophic neurites named RTN3 immunoreactive dystrophic
104 ly transported in neurons and accumulates in dystrophic neurites near cerebral amyloid deposits in AD
105 phy, and for long dystrophic neurites, short dystrophic neurites, neuronal cytoplasmic inclusions, an
106 ence of immunoreactive TDP-43 short and long dystrophic neurites, neuronal cytoplasmic inclusions, ne
107           Within neurofibrillary tangles and dystrophic neurites of Alzheimer's disease (AD), the cyt
108           In sporadic AD, PS1 appears in the dystrophic neurites of mature amyloid plaques and co-loc
109 noreactivity is also present in some swollen dystrophic neurites of neuritic plaques.
110  release and its prominent deposition in the dystrophic neurites of PD, alpha-synuclein localizes alm
111 dant in autophagic vacuoles, accumulating in dystrophic neurites of PS/APP mice similar to AD brains.
112  of astrocytosis (P = 0.6060), more embedded dystrophic neurites (P < 0.0001) and were more likely to
113 ivity and to play a role in the formation of dystrophic neurites present in Alzheimer brains.
114 ously that reticulon-3 (RTN3) immunoreactive dystrophic neurites (RIDNs) are abundantly present in th
115 es with the formation of RTN3 immunoreactive dystrophic neurites (RIDNs) in brains of Alzheimer's cas
116 ystrophic neurites named RTN3 immunoreactive dystrophic neurites (RIDNs) in patients' brains of Alzhe
117 rophic neurites named as RTN3 immunoreactive dystrophic neurites (RIDNs).
118 ons were evaluated for atrophy, and for long dystrophic neurites, short dystrophic neurites, neuronal
119 ly argentophilic because both populations of dystrophic neurites stained with silver stains.
120 tures in the alphaS- and betaS-labeled hilar dystrophic neurites suggests that synaptic dysfunction m
121 ccurs in a subset of activated microglia, in dystrophic neurites surrounding Abeta deposits, and in n
122 horylated at Tyr-297) are mainly detected in dystrophic neurites surrounding Abeta plaque cores, wher
123 -relevant tau pathologies: tau aggregates in dystrophic neurites surrounding Abeta plaques (NP tau),
124 uropil threads, neurofibrillary tangles, and dystrophic neurites surrounding and invading plaques.
125  Hyperphosphorylation of tau is found within dystrophic neurites surrounding beta-amyloid deposits in
126  is associated with neurofibrillary tangles, dystrophic neurites surrounding neuritic plaques, neurop
127 to result in the accumulation of lipofuscin, dystrophic neurites, tau- and ubiquitin-positive inclusi
128 ctivity is particularly conspicuous in large dystrophic neurites that also label with antibodies spec
129 otein (TDP)-43-positive neuropil threads and dystrophic neurites (type C), and is only rarely due to
130          Pathological signs include gliosis, dystrophic neurites, vacuolated mitochondria, and accumu
131 nificant reduction in the number and size of dystrophic neurites was seen 3 days after Abeta deposits
132                  Phosphorylated tau-positive dystrophic neurites were exclusively associated with Con
133                                  p3-reactive dystrophic neurites were found both independent in the n
134 d ghost tangles with PBB3 and AV-1451, while dystrophic neurites were more clearly detected by PBB3 i
135                             PHF/tau-positive dystrophic neurites were present in and around nearly al
136           Plaque-associated PHF/tau-positive dystrophic neurites were rare or absent in the hippocamp
137    In AD brains, BACE1 is accumulated within dystrophic neurites, which is thought to augment Abeta-i
138           Tyrosine hydroxylase (TH)-positive dystrophic neurites with rosette or grape-like cluster d
139 aque burden, and associated pathology (e.g., dystrophic neurites), with maximal effects attained with
140 ed with ubiquitin labeled neurons as well as dystrophic neurites within plaque regions.

 
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