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 ysfunction could lead to the accumulation of intraneuronal Abeta aggregates and their subsequent rele

10 In vivo, the accumulation of intraneuronal Abeta aggregates was accompanied by increa

11 racellular metalloprotease activity controls intraneuronal Abeta aggregation and limits secretion of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 Clearance of the intraneuronal Abeta pathology by immunotherapy rescues t

35 Early intraneuronal Abeta pathology was studied in AD transgen

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

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

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

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

40 mental role of PrP(C) to bind to and deliver intraneuronal Abeta to exosomes for secretion.

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

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

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

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

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

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

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

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

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

50 plaques was preceded by the accumulation of intraneuronal Abeta.

51 ologically abnormal neuron soma that contain intraneuronal Abeta.

52 lasticity correlate with the accumulation of intraneuronal Abeta.

53 Intraneuronal Abeta42 accumulates in 5XFAD brain startin

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

55 Intraneuronal Abeta42 accumulation is also associated wi

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

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

58 Induction of intraneuronal Abeta42 expression leads to a sequential d

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

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

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

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

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

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

65 imary proinflammatory agent, implicating the intraneuronal accumulation of Abeta as a significant imm

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 Intraneuronal aggregates of alpha-synuclein occur in Lew

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

91 t of proteins with polyglutamine tracts into intraneuronal aggregates.

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

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

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

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

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

97 s characterized by the presence of abnormal, intraneuronal alpha-synuclein aggregates, which may prop

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

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

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

101 Our data indicate that intraneuronal alphaSyn fibrils impaired the initiation o

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

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

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

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

106 As intraneuronal amyloid protein is detected before markers

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

108 Selective intraneuronal amyloid-beta accumulation in adult life an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Mitochondria contribute to shape intraneuronal Ca(2+) signals.

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

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

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

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

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

136 DA receptor calcium channels which increases intraneuronal calcium levels.

137 mediated excitotoxicity entails elevation of intraneuronal calcium levels.

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

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

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

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

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

143 KCC2 regulates intraneuronal chloride and extracellular potassium level

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

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

146 GABAergic activity can become excitatory if intraneuronal chloride rises.

147 reased KCC2 protein expression and decreased intraneuronal chloride.

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

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

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

151 We explored the effect on intraneuronal Cl- using both gramicidin, perforated-patc

152 l- loading, resulting in a persistently high intraneuronal Cl-.

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

154 ology compared to normal controls but little intraneuronal colocalization.

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

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

157 1beta-HSD-1 knockout mice, implicating lower intraneuronal corticosterone levels through lack of 11-D

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

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

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

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

162 Intraneuronal deposition of alpha-synuclein as fibrils a

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

164 The intraneuronal deposits are formed by neurofibrillary tan

165 A characteristic of PD is intraneuronal deposits composed in part of alpha-synucle

166 The presence of intraneuronal deposits mainly formed by amyloid fibrils

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

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

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

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

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

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

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

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

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

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

177 Intraneuronal filamentous tau inclusions such as neurofi

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

179 Importantly, intraneuronal GAbeta immunoreactivity, a proposed prefib

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

181 Immunohistochemistry demonstrated intraneuronal glucocerebrosidase.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

203 aggregated alpha-synuclein (alpha-syn) into intraneuronal inclusions named Lewy bodies (LBs).

204 neurodegenerative diseases characterized by intraneuronal inclusions of hyperphosphorylated tau prot

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

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

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

208 fibrils injections into the putamen induced intraneuronal inclusions positive for phosphorylated alp

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

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

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

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

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

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

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

216 lpha-synuclein (alphaSyn) aggregates to form intraneuronal inclusions.

217 gregation-prone polyQ proteins accumulate in intraneuronal inclusions.

218 cological inhibition of APP processing or by intraneuronal infusion of an antibody raised against Abe

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

220 omotes ferroportin stabilization to decrease intraneuronal iron.

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

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

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

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

225 Intraneuronal levels of this protein appear critical in

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

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

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

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

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

231 s not completely degraded and accumulates in intraneuronal lysosomes.

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

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

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

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

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

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

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

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

240 Notably, intraneuronal molecular mechanisms recruited by delayed

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

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

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

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

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

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

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

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

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

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

251 Intraneuronal nuclear protein aggregates of mutant hunti

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

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

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

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

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

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

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

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

260 Intraneuronal p-tau inclusions in the hippocampus were p

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

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

263 absence of TFEB is associated with enhanced intraneuronal pathology and accelerated spreading.

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

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

266 Neuronal loss and intraneuronal protein aggregates are characteristics of

267 Intraneuronal protein aggregates of the mutated huntingt

268 These diseases are associated with intraneuronal protein aggregates.

269 Intraneuronal protein aggregation as a trigger for infla

270 Tau is predominantly an intraneuronal protein but is also secreted in physiologi

271 aracterized by progressive neuronal loss and intraneuronal proteolipid storage.

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

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

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

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

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

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

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

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

280 E gene suggest the additional possibility of intraneuronal synthesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

296 Intraneuronal TTR was seen in the brains of normal human

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

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

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

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