ライフサイエンスコーパス: intraneuronal

1 n essential role of ApoE in the mechanism of intraneuronal Abeta accumulation and provide evidence th

2 To characterize ApoE involvement in the intraneuronal Abeta accumulation and to investigate whet

3 t that the early dysfunction associated with intraneuronal Abeta accumulation in AD involve the assoc

4 Furthermore, we showed significantly reduced intraneuronal Abeta accumulation in APPSW/PS1dE9/ApoE KO

5 Tg mice, the APOE genotypes had no effect on intraneuronal Abeta accumulation in EFAD mice.

6 PP processing, Abeta peptide generation, and intraneuronal Abeta accumulation in inducible p25 transg

7 Consequently, intraneuronal Abeta accumulation is thought to be a crit

8 Abeta12-28P treatment significantly reduced intraneuronal Abeta accumulation, including Abeta oligom

9 asculature, emerging evidence indicates that intraneuronal Abeta also plays a pathophysiological role

10 Our double-labeling analyses of intraneuronal Abeta and CD40 revealed that intraneuronal

11 These findings provide further support for intraneuronal Abeta as a cause of cognitive impairment,

12 g neurofibrillary tangles of phospho-Tau and intraneuronal Abeta associated with neuronal cell death.

13 ctivity to elevate secreted Abeta and reduce intraneuronal Abeta becomes impaired in AD-transgenic bu

14 king the ApoE/Abeta interaction could reduce intraneuronal Abeta buildup, we used a noncontact neuron

15 mpairments and then show that "clearance" of intraneuronal Abeta by anti-Abeta antibodies restores co

16 Compared with neurons cultured alone, intraneuronal Abeta content was significantly increased

17 impaired ability to secrete Abeta and reduce intraneuronal Abeta has important implications for the p

18 In patients with mild cognitive impairment, intraneuronal Abeta immunoreactivity was found especiall

19 etting of reduced Abeta plaques but elevated intraneuronal Abeta immunoreactivity.

20 hase kinase-3beta and enhanced expression of intraneuronal Abeta in AAV1-I(2CTF) animals.

21 y may be considered as a cause for increased intraneuronal Abeta in Alzheimer disease.

22 Using sandwich ELISA technique, we measured intraneuronal Abeta in Tg2576 mice injected with GM-CSF

23 tion and correlates with the accumulation of intraneuronal Abeta in the hippocampus and amygdala.

24 This study strongly implicates intraneuronal Abeta in the onset of cognitive dysfunctio

25 amyloid plaque formation but with extensive intraneuronal Abeta in transfected cells and transgenic

26 f intraneuronal Abeta and CD40 revealed that intraneuronal Abeta is associated with neuronal expressi

27 ts provide strong experimental evidence that intraneuronal Abeta may serve as a source for some of th

28 nal degradation of Abeta, increased level of intraneuronal Abeta oligomers, and marked down-regulatio

29 r, little is known about the consequences of intraneuronal Abeta on signaling mechanisms.

30 analysis allows for better visualization of intraneuronal Abeta pathology and provides new insights

31 Clearance of the intraneuronal Abeta pathology by immunotherapy rescues t

32 Early intraneuronal Abeta pathology was studied in AD transgen

33 though we cannot corroborate the presence of intraneuronal Abeta peptide in 3xTg-AD mice, our finding

34 nding of E22Delta explains the high level of intraneuronal Abeta seen in this pedigree.

35 s the observation that these mice accumulate intraneuronal Abeta that has been linked to synaptic dys

36 disease, Billings et al. link appearance of intraneuronal Abeta to cognitive impairments and then sh

37 studies suggest a novel pathogenic role for intraneuronal Abeta with regards to synaptic plasticity.

38 ) reversed these effects, demonstrating that intraneuronal Abeta(1-42) is a toxic peptide that lies u

39 nimal model, which is a useful tool to study intraneuronal Abeta(1-42)-induced pathology in the absen

40 and is restricted to brain regions that show intraneuronal Abeta(42) accumulation.

41 uble-labeling immunofluorescence analysis of intraneuronal Abeta, Abeta deposits and pro-inflammatory

42 ally inhibiting synapses, but also decreases intraneuronal Abeta, protecting synapses.

43 the APOE genotype affects plaque morphology, intraneuronal Abeta, soluble Abeta42, and oligomeric Abe

44 analyses confirmed that at least some of the intraneuronal Abeta-like immunoreactivity (iAbeta-LIR) r

45 ion is caused by multiple factors, including intraneuronal Abeta-oligomers, chronic oxidative stress,

46 plaques was preceded by the accumulation of intraneuronal Abeta.

47 ologically abnormal neuron soma that contain intraneuronal Abeta.

48 lasticity correlate with the accumulation of intraneuronal Abeta.

49 Intraneuronal Abeta42 accumulates in 5XFAD brain startin

50 ective effects of neuronal NEP expression on intraneuronal Abeta42 accumulation and neurodegeneration

51 Intraneuronal Abeta42 accumulation is also associated wi

52 in neuronal dysfunction and that preventing intraneuronal Abeta42 aggregation may be an important th

53 NEP efficiently suppressed the formation of intraneuronal Abeta42 deposits and Abeta42-induced neuro

54 Induction of intraneuronal Abeta42 expression leads to a sequential d

55 gamma-cleaved Abeta42 and suggest that this intraneuronal Abeta42 immunoreactivity appears to preced

56 stochemical methods, we observed significant intraneuronal Abeta42 in the hippocampus and frontal cor

57 In addition to the extracellular Abeta, intraneuronal Abeta42 may contribute to AD pathogenesis.

58 myloid pathology and may be useful models of intraneuronal Abeta42-induced neurodegeneration and amyl

59 acking apolipoprotein E (apoE) had much less intraneuronal Abeta42.

60 for E22Delta but not Abeta40 with subsequent intraneuronal accumulation in lysosomes.

61 Experimental evidence has shown intraneuronal accumulation of Abeta peptides and interfe

62 Moreover, the intraneuronal accumulation of Abeta(1-42) was shown to b

63 e HIV coat protein gp120 that facilitate the intraneuronal accumulation of Abeta.

64 enic mice and in human AD brain, progressive intraneuronal accumulation of Abeta42 occurs especially

65 of alpha-synuclein in a cell-free system and intraneuronal accumulation of alpha-synuclein in cell cu

66 Our results show intraneuronal accumulation of amyloid-beta peptide (Abet

67 single transgenic and bigenic mice developed intraneuronal accumulation of APP/Abeta, although only A

68 in the 3xTg-AD mouse model of AD reduced the intraneuronal accumulation of both amyloid-beta (Abeta)

69 rophy are characterized by the formation and intraneuronal accumulation of fibrillar aggregates of al

70 are both characterized by the formation and intraneuronal accumulation of fibrillar aggregates of al

71 lzheimer's disease is defined in part by the intraneuronal accumulation of filaments comprised of the

72 lzheimer's disease is defined in part by the intraneuronal accumulation of filaments comprised of the

73 lzheimer's disease is defined in part by the intraneuronal accumulation of filaments comprised of the

74 ciated fraction of HEXB KO mouse brains, and intraneuronal accumulation of ganglioside-bound Abeta (G

75 Recent data suggest that intraneuronal accumulation of metabolites of the amyloid

76 These findings suggest a role for the intraneuronal accumulation of oAbeta and APP-CTFs and re

77 f gangliosides, autophagic vacuoles, and the intraneuronal accumulation of proteins associated with A

78 disorders of aging are characterized by the intraneuronal accumulation of ubiquitin conjugates into

79 The mechanism for intraneuronal accumulation, however, is not well underst

80 Intraneuronal acidosis activates the Na(+)/H(+) exchange

81 y by selectively inhibiting the formation of intraneuronal aggregates and increasing the degradation

82 e condition associated with the formation of intraneuronal aggregates by mutant huntingtin.

83 Here we report the accumulation of intraneuronal aggregates containing the macroautophagy a

84 oluntary motor system and ubiquitin-positive intraneuronal aggregates in anterior horn cells.

85 Intraneuronal aggregates of alpha-synuclein occur in Lew

86 nclusions are morphologically similar to the intraneuronal aggregates that have been identified in th

87 t of proteins with polyglutamine tracts into intraneuronal aggregates.

88 These results indicate that intraneuronal aggregation of cytoskeletal proteins can b

89 ion of extracellular amyloid plaques and the intraneuronal aggregation of hyperphosphorylated tau int

90 lzheimer's disease is defined in part by the intraneuronal aggregation of tau protein into filamentou

91 ted by the ionophore and that an increase of intraneuronal Al concentration potentiated Fe-induced ox

92 Intraneuronal Al concentration was ascertained by laser

93 thies are characterized by the deposition of intraneuronal alpha-synuclein (alphaSyn) inclusions.

94 However, mechanisms that promote intraneuronal alpha-synuclein assembly remain poorly und

95 In addition, intraneuronal alpha-synuclein deposits formed in a mouse

96 l neurodegenerative diseases are typified by intraneuronal alpha-synuclein deposits, synaptic dysfunc

97 data reveal an unexpected role for soluble, intraneuronal alphaSyn in AD pathophysiology.

98 etic reduction of Becn1 expression increased intraneuronal amyloid beta (Abeta) accumulation, extrace

99 D-like amyloid pathology we found that early intraneuronal amyloid beta build-up is sufficient to unl

100 with bexarotene resulted in the clearance of intraneuronal amyloid deposits.

101 As intraneuronal amyloid protein is detected before markers

102 Intraneuronal amyloid-beta (Abeta) may contribute to ext

103 Selective intraneuronal amyloid-beta accumulation in adult life an

104 Our results demonstrate that intraneuronal amyloid-beta accumulation is a relatively

105 y explored the extent and characteristics of intraneuronal amyloid-beta accumulation, particularly of

106 s within autolysosomes/lysosomes and reduced intraneuronal amyloid-beta peptide.

107 Here, we identified and characterized marked intraneuronal amyloid-beta peptide/amyloid and lysosomal

108 ) senile plaques (SPs) and the production of intraneuronal amyloid-beta peptides (Abeta) prompted ana

109 might be associated with the accumulation of intraneuronal and extracellular proteins commonly observ

110 beta oligomer-induced toxicities within both intraneuronal and extracellular sites.

111 d helical filaments in Alzheimer brains (eg, intraneuronal and extraneuronal tangles and dystrophic n

112 Alzheimer's disease (AD) have ubiquitinated intraneuronal and neuritic accumulations of alpha-synucl

113 , we determined the localization of Drp1 and intraneuronal and oligomeric Abeta in the AD brains and

114 pil of hippocampus or cerebellum, and one to intraneuronal antigens.

115 e presence of free GSH, ascorbic acid, other intraneuronal antioxidants/reductants, and molecular oxy

116 In the absence of Abeta production, robust intraneuronal APP immunostaining was detected in the 3xT

117 anti-ganglioside mAb was used for selective intraneuronal/axonal delivery of fluorescent agents to v

118 Intraneuronal beta-amyloid (Abeta(i)) accumulates early

119 Increasing evidence links intraneuronal beta-amyloid (Abeta42) accumulation with t

120 n transgenic mice and human Alzheimer brain, intraneuronal beta-amyloid 42 increased with aging and b

121 We show that synaptic activity reduces intraneuronal beta-amyloid and protects against beta-amy

122 cent evidence supports an important role for intraneuronal beta-amyloid in the pathogenesis of Alzhei

123 tease neprilysin is involved in reduction of intraneuronal beta-amyloid with synaptic activity.

124 t cultured neurons from cell death caused by intraneuronal beta-amyloid.

125 ant-expressing mice, consistent with initial intraneuronal C1q induction, followed by global activati

126 es also attenuated NMDA-induced increases in intraneuronal Ca(2+).

127 NAAG reduced neuronal survival and increased intraneuronal Ca(2+); these effects were only marginally

128 ion of the glutamate-stimulated increases in intraneuronal Ca2+ ([Ca]i) that occur with epileptic act

129 The loss of a putative intraneuronal Ca2+ buffer, the Ca2+-binding protein calb

130 for reducing glutamate-induced elevations in intraneuronal Ca2+.

131 DA receptor calcium channels which increases intraneuronal calcium levels.

132 mediated excitotoxicity entails elevation of intraneuronal calcium levels.

133 transduction involves stimulation of PLC and intraneuronal calcium mobilization and is independent of

134 calcium in the brain, together with impaired intraneuronal calcium regulation in the aging brain and

135 attenuated a rapid ADDL-induced increase in intraneuronal calcium, which was essential for stimulate

136 Our results indicate that elevations of intraneuronal cAMP concentration have differential effec

137 identify EP activation as the earliest known intraneuronal change to occur in sporadic AD, the most c

138 KCC2 regulates intraneuronal chloride and extracellular potassium level

139 ter, underlies a rapid perinatal decrease in intraneuronal chloride concentration (chloride shift), w

140 ptor-mediated transmission by regulating the intraneuronal chloride concentration [Cl(-)]i.

141 GABAergic activity can become excitatory if intraneuronal chloride rises.

142 reased KCC2 protein expression and decreased intraneuronal chloride.

143 Intraneuronal Cl(-) concentration ([Cl(-)]i) regulation

144 H(2)O(2), a membrane permeant ROS, to alter intraneuronal Cl(-), an important regulator of neuronal

145 K-Cl cotransporter KCC2 establishes the low intraneuronal Cl- levels required for the hyperpolarizin

146 fluorescence for Abeta42 and pT231 revealed intraneuronal co-localization.

147 ology compared to normal controls but little intraneuronal colocalization.

148 iated effects to not only modulate immediate intraneuronal communication, but also to control longer-

149 Our findings further shed light on which intraneuronal compartments exhibit increased or decrease

150 1beta-HSD-1 knockout mice, implicating lower intraneuronal corticosterone levels through lack of 11-D

151 eit indirectly, to a greater contribution of intraneuronal DA redistribution rather than extraneurona

152 ultured with astrocytes also showed impaired intraneuronal degradation of Abeta, increased level of i

153 , the reduction in KLC1 was prevented by the intraneuronal delivery of Alz50 antibodies.

154 genic gp120/APP/PS1 mouse that recapitulates intraneuronal deposition of Abeta in a manner reminiscen

155 Intraneuronal deposition of alpha-synuclein as fibrils a

156 the formation of alpha-synuclein-containing intraneuronal deposits and the degeneration of nigrostri

157 The intraneuronal deposits are formed by neurofibrillary tan

158 The presence of intraneuronal deposits mainly formed by amyloid fibrils

159 aight and paired helical filaments that form intraneuronal deposits of neurofibrillary tangles (NFTs)

160 n is developmentally regulated, and that the intraneuronal distribution of huntingtin increases in pa

161 munogold localization demonstrated a similar intraneuronal distribution, but in addition showed that

162 These data indicate that intraneuronal dopamine levels can be a major modulator o

163 g from non-receptor mediated displacement of intraneuronal dopamine.

164 mic conditions led to the robust, widespread intraneuronal expression of beta-APP immunoreactivity in

165 hyperglycemic conditions leads to the early intraneuronal expression of beta-APP within neuronal pop

166 eletion augments conditioning lesion-induced intraneuronal expression of SPRR1A, a regeneration-assoc

167 ough regulation of neurotransmitter receptor intraneuronal fate, we hypothesized that the ubiquitine-

168 derstanding mechanisms underlying halpha-Syn intraneuronal fibrillization and its contribution to PD

169 ers are characterized by the accumulation of intraneuronal fibrils comprised of the protein Tau.

170 Intraneuronal filamentous tau inclusions such as neurofi

171 Thus, intraneuronal formation of 1 and HO. as a consequence of

172 Importantly, intraneuronal GAbeta immunoreactivity, a proposed prefib

173 tors provide a novel approach for modulating intraneuronal GAP-43 expression in the adult brain.

174 Immunohistochemistry demonstrated intraneuronal glucocerebrosidase.

175 Neurons in double-deficient mice lacked intraneuronal GM2 accumulation as expected, but remarkab

176 tic model of PD, PLK2 overexpression reduces intraneuronal human alpha-synuclein accumulation, suppre

177 lular deposition of beta-amyloid (Abeta) and intraneuronal hyperphosphorylation of microtubule-associ

178 ibrillary tangles (NFTs) are the most common intraneuronal inclusion in the brains of patients with n

179 e substantia nigra, formation of filamentous intraneuronal inclusions (Lewy bodies) and an extrapyram

180 rmal protein is an abundant component of the intraneuronal inclusions (Lewy bodies) characteristic of

181 ted tau proteins in swollen (Pick) cells and intraneuronal inclusions (Pick bodies).

182 n alpha-synuclein develop motor impairments, intraneuronal inclusions and loss of dopaminergic termin

183 is a 140-residue protein that aggregates in intraneuronal inclusions called Lewy bodies in Parkinson

184 ease (PD) is characterized pathologically by intraneuronal inclusions called Lewy bodies, largely com

185 thological hallmark of PD is the presence of intraneuronal inclusions composed of fibrillized alpha-s

186 in the substantia nigra and the presence of intraneuronal inclusions consisting of aggregated and po

187 Lewy bodies (LBs) are intraneuronal inclusions consisting primarily of fibrill

188 et loss of dopaminergic neurons, filamentous intraneuronal inclusions containing alpha-synuclein and

189 le, hyperphosphorylated tau and argyrophilic intraneuronal inclusions formed by tau-immunoreactive fi

190 urin (OPTN) proteins were identified to form intraneuronal inclusions in ALS patients.

191 Our previous work has shown that the intraneuronal inclusions in FENIB result from the sequen

192 a-synuclein (alphaSyn), which constitute the intraneuronal inclusions in PD patients known as Lewy bo

193 polymers, similar to those isolated from the intraneuronal inclusions in the brains of individuals wi

194 (alpha-Syn), the principal component of the intraneuronal inclusions known as Lewy bodies (LBs), and

195 athologically by distinct tau-immunoreactive intraneuronal inclusions known as Pick bodies and by ins

196 neurodegenerative diseases characterized by intraneuronal inclusions of hyperphosphorylated tau prot

197 l dominant dementia that is characterized by intraneuronal inclusions of mutant neuroserpin.

198 cause the protein aggregates in the hallmark intraneuronal inclusions of the disorder, Lewy bodies.

199 nson disease, alpha-synuclein accumulates in intraneuronal inclusions often containing ubiquitin chai

200 erpin polymerization in the formation of the intraneuronal inclusions that are characteristic of FENI

201 Lewy bodies (LBs) are filamentous intraneuronal inclusions that are hallmark lesions of Pa

202 component of Lewy bodies and Lewy neurites, intraneuronal inclusions that are neuropathological hall

203 re axonal spheroids, but Lewy body (LB)-like intraneuronal inclusions, glial inclusions, and rare neu

204 clein accumulates in dopaminergic neurons as intraneuronal inclusions, Lewy bodies, which are charact

205 Thus, A53T mutant mice develop intraneuronal inclusions, mitochondrial DNA damage and d

206 gregation-prone polyQ proteins accumulate in intraneuronal inclusions.

207 and has the propensity to aggregate and form intraneuronal inclusions.

208 emistry, electrophysiological recording, and intraneuronal injection of the neuronal tracer biocytin

209 encoding the tau protein that accumulates in intraneuronal lesions in a number of neurodegenerative d

210 striking differences and is associated with intraneuronal lesions, including neurofibrillary tangles

211 U18666A treatment resulted in increased intraneuronal levels of C99 and insoluble Abeta42, which

212 y was to determine if TDI inhalation affects intraneuronal levels of SP and preprotachykinin (PPT) me

213 Intraneuronal levels of this protein appear critical in

214 aracterized by the progressive appearance of intraneuronal Lewy aggregates, which are primarily compo

215 aS which accumulate as the main component in intraneuronal Lewy bodies.

216 in an aggregated amyloid fibril form in the intraneuronal Lewy body deposits that are a defining cha

217 lysis of whole striatal tissue confirmed the intraneuronal localization of fluorodopamine most likely

218 rboring the APP(E693Q) (Dutch) mutation have intraneuronal lysosomal accumulation of APP carboxylterm

219 s not completely degraded and accumulates in intraneuronal lysosomes.

220 Hippocampal pyramidal neurons express an intraneuronal map of spectral tuning mediated by hyperpo

221 elucidate the identity of the immunoreactive intraneuronal material in 3xTg-AD mice, we conducted imm

222 We found that the intraneuronal material shared epitopes with full-length

223 To demonstrate unequivocally that this intraneuronal material was not free Abeta peptide, we ge

224 e data demonstrate a relationship between an intraneuronal measure of dorsolateral prefrontal cortex

225 PHEN were encountered, consistent with high intraneuronal metabolic activity, high catecholamine tur

226 ne (PHEN), a tracer of vesicular leakage and intraneuronal metabolic degradation with initial uptake

227 Recent evidence suggests that intraneuronal metabolism of ethanol by catalase/H2O2 and

228 Notably, intraneuronal molecular mechanisms recruited by delayed

229 ndicate that phenylephrine is metabolized by intraneuronal monoamine oxidase (MAO).

230 regated into paired helical filaments in the intraneuronal neurofibrillary tangle deposits of victims

231 d to Alzheimer's disease via its presence in intraneuronal neurofibrillary tangle deposits, where it

232 pathologic examination demonstrated abundant intraneuronal neurofibrillary tangles (NFTs) involving t

233 id plaques and co-localizes with a subset of intraneuronal neurofibrillary tangles (NFTs).

234 hallmarks of Alzheimer disease (AD) include intraneuronal neurofibrillary tangles composed of abnorm

235 iously proposed stages in the progression of intraneuronal neurofibrillary tangles in human hippocamp

236 Extracellular plaques of amyloid-beta and intraneuronal neurofibrillary tangles made from tau are

237 tructures, extracellular amyloid plaques and intraneuronal neurofibrillary tangles, both of which com

238 Family D had prominent and diffuse circular, intraneuronal, neurofibrillary tangles not seen in Famil

239 ot only causes SP release but also increased intraneuronal neuropeptide levels.

240 Intraneuronal nuclear protein aggregates of mutant hunti

241 gical alterations of tau are associated with intraneuronal oligomeric Abeta accumulation.

242 sgenic mice showed a significant decrease in intraneuronal oligomeric Abeta and hyperphosphorylated t

243 ditional age points; i.e., brain Abeta load, intraneuronal oligomeric Abeta distribution and plaque l

244 Our results revealed an accumulation of intraneuronal oligomeric Abeta, leading to mitochondrial

245 of young 3xTg-AD mice with ibuprofen reduces intraneuronal oligomeric Abeta, reduces cognitive defici

246 CA1 hippocampus of AD transgenic mice showed intraneuronal onset of Abeta42 accumulation and fibrilli

247 ite can persist within its mammalian host as intraneuronal or intramuscular cysts.

248 ysis revealed that the hyperglycemia-induced intraneuronal overexpression of beta-APP was not associa

249 Intraneuronal p-tau inclusions in the hippocampus were p

250 au protein through the repeat domain to form intraneuronal paired helical filaments (PHFs).

251 u seeds into T40PL-GFP mice induced abundant intraneuronal pathological inclusions of hyperphosphoryl

252 e distributed in a punctate perineuronal and intraneuronal pattern similar to that seen after their r

253 Finally, pair-wise correlations between intraneuronal percentage changes (after blocking KA chan

254 Neuronal loss and intraneuronal protein aggregates are characteristics of

255 Intraneuronal protein aggregates of the mutated huntingt

256 These diseases are associated with intraneuronal protein aggregates.

257 Intraneuronal protein aggregation as a trigger for infla

258 tility by chick collapsin is mediated by the intraneuronal protein CRMP-62.

259 aracterized by progressive neuronal loss and intraneuronal proteolipid storage.

260 that inhibit phospholipase C (PLC) or block intraneuronal receptors for inositol triphosphate.

261 tes that also redox cycle in the presence of intraneuronal reductants and molecular oxygen forming H2

262 ity to modulate NMDA receptor function by an intraneuronal signal transduction mechanism.

263 rimary striatal culture demonstrate that the intraneuronal signal transduction pathway activated by h

264 s are recognized by neurons and the types of intraneuronal signaling generated by matrix binding.

265 mitogen-activated protein kinase cascade, an intraneuronal signaling mechanism associated with neuron

266 However, the intraneuronal spatial dynamics of these events or the ro

267 e that calcium-induced calcium released from intraneuronal stores plays an important role in action p

268 ected finding was the enrichment of 3OMFD in intraneuronal striatal space which is perhaps a factor i

269 E gene suggest the additional possibility of intraneuronal synthesis.

270 mprising mostly the amyloid beta peptide and intraneuronal tangles of hyperphosphorylated microtubule

271 o-tau may increase interneuronal plaques and intraneuronal tangles, presently observed aberrations in

272 d thus promote the latter's aggregation into intraneuronal tangles.

273 f Alzheimer's disease (AD) and co-occur with intraneuronal tangles.

274 culminating in the formation of filamentous intraneuronal tau aggregates similar to that observed in

275 tracellular amyloid-beta protein (Abeta) and intraneuronal tau aggregates.

276 y well with colocalization of the probe with intraneuronal tau aggregates.

277 (AD) is characterized by the accumulation of intraneuronal tau and extracellular amyloid-beta (Abeta)

278 The present study explores the formation of intraneuronal tau and neurofilament protein aggregates u

279 This K(m) value is within the range of intraneuronal tau concentration in human brain, suggesti

280 racellular beta-amyloid (Abeta) fibrils plus intraneuronal tau filaments.

281 Extracellular deposits of Abeta and intraneuronal tau inclusions define Alzheimer's disease,

282 pathological chaperones in the formation of intraneuronal tau inclusions, we crossbred previously de

283 In dendrites, increasing intraneuronal thioflavin S correlated with decreases in

284 To characterize pathways for the uptake and intraneuronal trafficking of infectious, protease-resist

285 Intraneuronal TTR was seen in the brains of normal human

286 -/-) mice developed age-associated, abnormal intraneuronal ubiquitin-positive autofluorescent lipofus

287 d, we evaluated the contribution of NaChs to intraneuronal variability in glutamate release probabili

288 Here, we report that elevated intraneuronal zinc impairs mitochondrial trafficking.

289 We have reported that oxidant-induced intraneuronal Zn(2+) liberation triggers a syntaxin-depe