ライフサイエンスコーパス: cell-to-cell

1 that restrict the transmission of virus from cell to cell.

2 nctions that transmit mechanical stress from cell to cell.

3 n the ability of the bacteria to spread from cell to cell.

4 ytosis, since they can use it to spread from cell to cell.

5 w, and action potential (AP) generation from cell-to-cell.

6 lein that can self-propagate and spread from cell to cell(3-6).

7 fact, two major hallmarks of cancer, loss of cell-to-cell adhesion and anchorage-independent growth,

8 stasis in healthy tissues strongly relies on cell-to-cell adhesion and cell-to-extracellular matrix i

9 1 (ICAM-1), a membrane protein that mediates cell-to-cell adhesion and communication, as a mechanism

10 ain calcification, suggesting that defective cell-to-cell adhesion and dysfunction of the movement of

11 The molecular interactions that influence cell-to-cell adhesion are not fully understood.

12 following extrusion; and the enhancement of cell-to-cell adhesion in the seed coat epidermis.

13 Cell-to-cell adhesion is essential for establishment of

14 (growth factors; transcriptional regulators; cell-to-cell adhesion; extracellular matrix), suggesting

15 aggregation has been reported to spread from cell to cell and exosomes are considered as important me

16 Rhes tunnels," through which Rhes moves from cell to cell and transports Huntington disease (HD) prot

17 oscopy, FACS and investigations of bacterial cell-to-cell and bacteria-host cell interactions.

18 However, the extent and nature of cell-to-cell and cell-intrinsic variability in genome ar

19 nm nanovesicles that play important roles in cell-to-cell and/or cell-to-tissue communications and cr

20 hat ZIKV infection in NPCs spreads primarily cell-to-cell as an expanding infectious center, and NPCs

21 However, despite pronounced cell-to-cell ATP differences observed across biological

22 ion-making regulatory network, and show that cell-to-cell ATP variability changes the sets of decisio

23 e mobile genetic elements that transfer from cell to cell by conjugation (like plasmids) and integrat

24 egates are able to spread the pathology from cell-to-cell by a prion like seeding mechanism.

25 Quorum sensing is a process of bacterial cell-to-cell chemical communication that relies on the p

26 This is likely achieved through cell-to-cell communication and a biological clock.

27 Extracellular vesicles (EV) are mediators of cell-to-cell communication and contain different RNA typ

28 ar vesicles (EVs) are important mediators of cell-to-cell communication and have been implicated in s

29 on and cell wall modifications, which impair cell-to-cell communication and meristem maintenance.

30 ing miRNAs (ECmiRNAs) play a crucial role in cell-to-cell communication and serve as non-invasive bio

31 eat attention due to their essential role in cell-to-cell communication as well as their potential as

32 extracellular vesicles (EVs) as vehicles for cell-to-cell communication between a tumour and its envi

33 Cell-to-cell communication by exosomes controls normal a

34 ing oscillations in an otherwise dissipative cell-to-cell communication channel.

35 ctivity and provide new insights into remote cell-to-cell communication function of inflammasomes via

36 titative rules that govern cytokine-mediated cell-to-cell communication is still lacking.

37 highlight how redox signalling via paracrine cell-to-cell communication may act as a central mechanis

38 differential expression of genes involved in cell-to-cell communication may contribute greatly to phe

39 ive behaviors are controlled by the chemical cell-to-cell communication process called quorum sensing

40 age genetic elements, virulence factors, and cell-to-cell communication signaling compounds.

41 uch as proteins and RNAs, play a key role in cell-to-cell communication, and particularly in epigenet

42 rally and spatially organized largely due to cell-to-cell communication, which promotes synergistic i

43 rs for disease pathogenesis and mediators of cell-to-cell communication.

44 oned them as a novel and effective method of cell-to-cell communication.

45 direct pathway for metabolic and electrical cell-to-cell communication.

46 endently by individual cells rather than via cell-to-cell communication.

47 ), highlighting their key signaling roles in cell-to-cell communication.

48 Cell-to-cell communications are critical determinants of

49 ith their receptors are important players in cell-to-cell communications in plants.

50 , which will be useful to further understand cell-to-cell communications involved in the regulation o

51 ubes (TNT) are thin, membranous, tunnel-like cell-to-cell connections, but the mechanisms underlying

52 le connectivity rules, to create millions of cell-to-cell connections.

53 oral windows revealed a remarkable degree of cell-to-cell conservation in RT, particularly at the ver

54 hat delivery of a CdiA-CT domain upon direct cell-to-cell contact can inhibit replication of a suscep

55 ria propagated the competence signal through cell-to-cell contact rather than the classically describ

56 Direct cell-to-cell contact was required for N1 to influence mi

57 conclude that NK cell proliferation requires cell-to-cell contact, activation of the CD137 axis, and

58 oportion of stem cell-like cancer cells in a cell-to-cell contact- or (at least) proximity-dependent

59 T6SS and plasmid conjugation both involve cell-to-cell contact.

60 embrane TNF signaling via MVs without direct cell-to-cell contact.

61 from infected to uninfected cells by direct cell-to-cell contact.

62 an be delivered to host cells independent of cell-to-cell contact.

63 Similarly organized cell-to-cell contacts also facilitate DC-mediated transf

64 Intercalated discs (ICD), specific cell-to-cell contacts that connect adjacent cardiomyocyt

65 cond case, viral transmission occurs through cell-to-cell contacts via a mechanism that is still poor

66 rticles to the surface of allogeneic DCs via cell-to-cell contacts.

67 e and high efficiency being achieved through cell-to-cell cooperation between degraders.

68 and consequently do not leverage the strong cell-to-cell correlation present in most datasets.

69 AP duration) and tissue structural (reduced cell-to-cell coupling caused by atrial fibrosis) remodel

70 ed ion channel remodelling and a decrease in cell-to-cell coupling due to fibrosis increased the hear

71 r the possibility of ephaptic coupling (i.e. cell-to-cell coupling through the extracellular potentia

72 the sodium channels and potentially provide cell-to-cell coupling when the gap junction connection i

73 K by decreasing extrinsic noise (preexisting cell-to-cell differences in kinase activity) in PI3K and

74 n-associated temporal dynamics versus stable cell-to-cell differences.

75 vels of organization ranging from individual cells to cell ensembles and whole organisms.

76 pimutation rate, with low variability in the cell-to-cell epimutation rate.

77 nto an enhancer of SARS-CoV-2 infection, and cell-to-cell fusion assays confirmed the ability of endo

78 through time-of-addition studies, transient cell-to-cell fusion assays, and chimeric vesicular stoma

79 fusion loop that were confirmed in transient cell-to-cell fusion assays.

80 ns are key players mediating early events in cell-to-cell fusion, vital for intercellular viral sprea

81 and T enable a rapid spread of infection by cell-to-cell fusion, whereas viruses harboring L or S at

82 ability of the fusion protein (F) to mediate cell-to-cell fusion.

83 characterized Env incorporation, maturation, cell-to-cell fusogenicity, and virus-to-cell fusogenicit

84 Strikingly, cell-to-cell genetic diversity was almost twice as high

85 tivity of short-term drug response assays to cell-to-cell heterogeneities and the presence of drug-to

86 gether, our data reveal a mechanism by which cell-to-cell heterogeneities that appear before the segr

87 tobacco smoking increases mutational burden, cell-to-cell heterogeneity and driver mutations, but qui

88 Thus, cell-to-cell heterogeneity can be simply uncovered via t

89 results reveal that the spatial structure of cell-to-cell heterogeneity can have important consequenc

90 particular, is thought to be a key driver of cell-to-cell heterogeneity in gene expression, even in o

91 e dynamic nature of chromatin, together with cell-to-cell heterogeneity in its structure, limits our

92 utrient-limiting conditions, we discover the cell-to-cell heterogeneity in protein and fatty-acid rec

93 on, but it remains challenging to define how cell-to-cell heterogeneity in protein-DNA binding influe

94 with slab-gel western blot, while revealing cell-to-cell heterogeneity in stress responses.

95 hat individual rDNA genes have high level of cell-to-cell heterogeneity in their expression in Drosop

96 Cell-to-cell heterogeneity is a ubiquitous feature of mu

97 Cell-to-cell heterogeneity is driven by stochasticity in

98 of interrupted and intact rDNAs and removes cell-to-cell heterogeneity leading to uniformly high exp

99 Our observations suggest that cell-to-cell heterogeneity of active contractile propert

100 n ensemble of informative plots to visualise cell-to-cell heterogeneity of alternative splicing profi

101 vides critical information to understand the cell-to-cell heterogeneity of chromatin states within a

102 he least studied chemical classes, and their cell-to-cell heterogeneity remains largely unexplored.

103 ifications and gene expression attributed to cell-to-cell heterogeneity.

104 state is dynamically switching, resulting in cell-to-cell heterogeneity.

105 ces sampling variability without sacrificing cell-to-cell heterogeneity.

106 RNA-seq that can facilitate investigation of cell-to-cell heterogeneity.

107 on variability alone may lead to non-genetic cell-to-cell heterogeneity.

108 nuclein aggregates, which may propagate from cell-to-cell in a prion-like manner.

109 We show that ZIKV spreads cell-to-cell in NPCs as an infectious center and that NP

110 ed survival and lacked the ability to spread cell to cell, indicating ppiB is essential for B. pseudo

111 ng that MT-4 cells are highly susceptible to cell-to-cell infection.

112 cellular vesicles (EVs) that are involved in cell-to-cell inflammatory and trophic signaling can enha

113 racellular vesicles (MSC-EVs), which mediate cell-to-cell inflammatory and trophic signaling, are tho

114 tic Elucidation and Assessment of Regulatory Cell-to-cell Interaction Networks (SEARCHIN) to identify

115 ), through deregulation of the expression of cell-to-cell interaction proteins and protein secretion.

116 bind avidly to C. albicans hyphae via direct cell-to-cell interaction, while the cariogenic pathogen

117 hat influence survival, cell morphology, and cell-to-cell interaction.

118 ass of biological systems exhibiting typical cell to cell interactions.

119 ecies that colonize human host via extensive cell-to-cell interactions and biofilm formation.

120 This might influence directly cell-to-cell interactions and the community effects with

121 chanisms of inter-leukemic communication and cell-to-cell interactions are proposed to be important f

122 Microenvironment cues and cell-to-cell interactions balance stem cell quiescence w

123 ed a computational method to infer potential cell-to-cell interactions based on transcriptome data of

124 Furthermore, analyses of cell-to-cell interactions highlight different networks o

125 ine how alterations in cellular function and cell-to-cell interactions of pulmonary resident cells an

126 gth and whether pilus length is critical for cell-to-cell interactions remain unknown.

127 al lipid nanodisc system, mimicking a native cell-to-cell junction.

128 n must be transported throughout plants in a cell-to-cell manner to affect its various physiological

129 be highly specialized to either cell-free or cell-to-cell mechanisms, and this was not strictly linke

130 Cell-to-cell mobility of fluorescent molecules and PD di

131 llular mechanisms of Gram-negative bacterial cell-to-cell movement in plant phloem.

132 e found that the replication of TuMV and the cell-to-cell movement of its replication vesicles are im

133 Our data show that cell-to-cell movement of plant rhabdoviruses is highly s

134 PDLP5, which functions to restrict the cell-to-cell movement of signals via plasmodesmata, is i

135 ed by five distinct rhabdoviruses to support cell-to-cell movement of two positive-stranded RNA virus

136 In marked contrast, cell-to-cell movement of two recombinant plant rhabdovir

137 lular mechanisms that take place during CLas cell-to-cell movement.

138 as being necessary and sufficient for SRBP1 cell-to-cell movement.

139 proteins that evolved specifically to induce cell-to-cell, not virus-cell, membrane fusion.

140 ed by antibiotics or previously unrecognized cell-to-cell phenotypic heterogeneity among pathogenic b

141 t side of the plasma membrane; the resulting cell-to-cell, polar transport of auxin would coordinate

142 erm layer specification is robust to altered cell-to-cell positioning, we separated embryonic cells f

143 e proposed to include impaired autophagy and cell-to-cell propagation of alpha-synuclein pathology.

144 enable noninvasive monitoring of changes in cell-to-cell proximity, transcription, translation, prot

145 e.g., length instead of area), combined with cell-to-cell radius variability.

146 The cell-to-cell release and uptake of alphasyn are consider

147 conditions crosstalk between organelles and cell to cell response is imperative.

148 e known to travel as a silencing signal from cell to cell, root to shoot, and even between host and p

149 somal origin, emerge as master regulators of cell-to-cell signaling in physiology and disease.

150 rd patterning in an optogenetic setup, where cell-to-cell signaling is emulated with light inputs cal

151 Their primary roles are in cell-to-cell signaling, as biogenic amines are not norma

152 uced by Gram-negative bacteria have roles in cell-to-cell signaling, biofilm formation, and stress re

153 enotype markers in a network associated with cell-to-cell signaling, hematological system development

154 ir, gene expression, organismal development, cell-to-cell signaling/interaction, cellular development

155 tosis, chemotaxis, antigen presentation, and cell-to-cell signalling are enriched among the over-expr

156 olves drop-out information to accounting for cell-to-cell similarity estimation, which is crucial in

157 identification are inferred via a structured cell-to-cell similarity matrix.

158 alteration in the viral cycle, which reduces cell-to cell spread of HSV-1.

159 V-1) is a critical mediator of virus-induced cell-to-cell spread and cell-cell fusion.

160 Extracellular virions are required for cell-to-cell spread and pathogenesis.

161 the trans-Golgi network and are required for cell-to-cell spread and pathogenesis.

162 1 or RL13 loci.IMPORTANCE Both cell-free and cell-to-cell spread are likely important for the natural

163 gies for their ability to limit cell-free or cell-to-cell spread as independent processes.

164 y can have dramatic impacts on cell-free and cell-to-cell spread as well as on antibody neutralizatio

165 e to type I IFN and leads to 1) promotion of cell-to-cell spread by L. monocytogenes, 2) defective le

166 is and cholesterol trafficking to facilitate cell-to-cell spread in a LAMP-1-dependent mechanism.IMPO

167 e MeV fusion complex that promote fusion and cell-to-cell spread in the absence of known MeV receptor

168 , our results indicate that L. monocytogenes cell-to-cell spread is heterogeneous, and that rare pion

169 nt at cell-to-cell spread, whereas TB and TR cell-to-cell spread is poor.

170 cell junctions, but the mechanism of direct cell-to-cell spread is poorly understood.

171 A better understanding of the mechanism of cell-to-cell spread may enable the development of drugs

172 t infectivity, suggesting that the efficient cell-to-cell spread mechanism of ME depends on features

173 This cell-to-cell spread mechanism requires the viral fusion

174 only modestly reduced, further supporting a cell-to-cell spread mechanism.

175 or are indicative of particularly efficient cell-to-cell spread mechanisms.

176 ession comparably reduced both cell-free and cell-to-cell spread of all three strains, suggesting tha

177 ation of Listeria protrusions and subsequent cell-to-cell spread of bacteria.

178 The participation of MAL in the cell-to-cell spread of HSV-1 may shed light on the invol

179 al migration efficiency, leading to impaired cell-to-cell spread of infection.

180 question about the mechanism involved in the cell-to-cell spread of MDV.

181 n UL128-131 was transcriptionally repressed, cell-to-cell spread of ME was still more efficient than

182 e integrity of HA protein trimers, inhibited cell-to-cell spread of virus in culture, and protected m

183 odeling to demonstrate that L. monocytogenes cell-to-cell spread proceeds anisotropically in an epith

184 issues than RSV, suggesting HMPV may promote cell-to-cell spread via these extensions.

185 The reduced cell-to-cell spread was due to ICP27 since plaque sizes

186 MPORTANCE The HSV-1 gI is required for viral cell-to-cell spread within the host, but the molecular m

187 distinct roles for gH/gL/gO in cell-free and cell-to-cell spread, (ii) gO isoforms can differentially

188 ghly specialized for either for cell-free or cell-to-cell spread, and these phenotypes are determined

189 determined that MDV CHPK is not required for cell-to-cell spread, for disease induction, and for onco

190 of individual accessory proteins will block cell-to-cell spread, forcing the virus to transmit in a

191 free spread but is particularly efficient at cell-to-cell spread, whereas TB and TR cell-to-cell spre

192 s results in increased viral replication and cell-to-cell spread.

193 f BST2 demonstrated that BST2 restricts HCMV cell-to-cell spread.

194 through host tissues using a process called cell-to-cell spread.

195 to neutralize HCMV and also to prevent virus cell-to-cell spread.

196 ation of HCMV infection, and attenuate viral cell-to-cell spread.

197 tiation of infection, viral replication, and cell-to-cell spread.

198 ors or gene silencing reduced MDV titers and cell-to-cell spread.

199 signaling, activation, and cell death during cell-to-cell spread.

200 by two main routes: by cell-free virus or by cell-to-cell spread.

201 ns that produce Syn variants dysregulate the cell-to-cell-spread machinery in unique ways and provide

202 hyphae of the giv2 mutant were defective in cell-to-cell spreading and mainly grew intercellularly i

203 by Listeria at membrane protrusions used for cell-to-cell spreading.

204 disequilibrium and incomplete annotation of cell-to-cell state variation represent substantial chall

205 er from oversmoothing and removal of natural cell-to-cell stochasticity in gene expression.

206 a valuable tool for studying organogenesis, cell-to-cell stromal communication and disease.

207 DNA accessibility varies from cell to cell, such that essentially no sites are accessi

208 with neurodegenerative diseases spread from cell to cell through the brain in a manner akin to infec

209 The timing of cell-to-cell transfer (11.17 min) closely approximated t

210 t capable of a unique and intriguing form of cell-to-cell transfer between macrophage cells.

211 receptors resulted in a major diminution of cell-to-cell transfer events.

212 The mechanism for cell-to-cell transfer is not understood.

213 Given that a prion-like, cell-to-cell transfer of misfolded alphaSyn has been rec

214 We found that Mn induced cell-to-cell transfer of the inflammasome adaptor protei

215 ins for direct presentation are captured for cell-to-cell transfer remains enigmatic.

216 We propose that macrophage cell-to-cell transfer represents a nonlytic exocytosis e

217 ses TNT length, diminishes HIV-1 capture and cell-to-cell transfer, and abrogates the exacerbation of

218 nsposition into mobile plasmids facilitating cell-to-cell transfer.

219 expression, and increased susceptibility to cell-to-cell transmission compared to nonpermissive cell

220 pendent trafficking in Env incorporation and cell-to-cell transmission in physiologically relevant ce

221 lar proteostasis network may regulate alphaS cell-to-cell transmission not only by reducing the popul

222 nalysis revealed that Mn(2+) accelerated the cell-to-cell transmission of alphaSyn, resulting in dopa

223 Our findings suggest that cell-to-cell transmission of cGAMP via LRRC8/VRAC channe

224 ed EphA7 in BJAB B cells is critical for the cell-to-cell transmission of KSHV from producer iSLK cel

225 Cell-to-cell transmission of misfolding-prone alpha-synu

226 ecently, mouse models have recapitulated the cell-to-cell transmission of pathogenic proteins and neu

227 is to summarize our current knowledge of the cell-to-cell transmission of pathological proteins and t

228 the former can be attributed to consecutive cell-to-cell transmission of pathological proteins betwe

229 parallels models that have been proposed for cell-to-cell transmission of small amyloids in neurodege

230 Cell-to-cell transmission of toxic forms of alpha-Synucl

231 ability of brain areas to tau pathology, its cell-to-cell transmission, and characteristics of the di

232 ropagates within and between individuals via cell-to-cell transmission, and primary infection typical

233 the Env mutants to mediate highly efficient cell-to-cell transmission, resulting in an increase in t

234 iosynthesis has been largely elucidated, and cell-to-cell transport has been long postulated, benzyli

235 nopores that serve as channels for molecular cell-to-cell transport.

236 However, the origins of cell-to-cell variability are complex and the individual

237 ic elongation can either enhance or suppress cell-to-cell variability at the RNAP level.

238 ssess the function of an individual cell and cell-to-cell variability at the single cell level in an

239 us feature of multicellular communities, but cell-to-cell variability can cause propagation to be hig

240 Cell-to-cell variability generates subpopulations of dru

241 ingle-cell Hi-C (scHi-C) allows the study of cell-to-cell variability in chromatin structure and dyna

242 at genes that form stable E-P hubs have less cell-to-cell variability in gene expression.

243 ndscape at single cell level, thus revealing cell-to-cell variability in gene regulation.

244 mutated mtDNA molecules (heteroplasmy), and cell-to-cell variability in heteroplasmy (heteroplasmy v

245 Our ability to quantify cell-to-cell variability in numerous biological contexts

246 iability is consistent with extrinsic noise (cell-to-cell variability in protein levels), a short-ter

247 rm Levy flight; rather, there is substantial cell-to-cell variability in speed, which persists over t

248 Additionally, we observed significant cell-to-cell variability in the average diffusivity of G

249 le consensus structure, thereby ignoring any cell-to-cell variability in the model itself.

250 Bacteria exhibit cell-to-cell variability in their resilience to stress,

251 Although increased cell-to-cell variability in transcription or epigenetic

252 c variation explains some but not all of the cell-to-cell variability in viral gene expression and in

253 Phenotypic cell-to-cell variability is a fundamental determinant of

254 e stochastic and deterministic components of cell-to-cell variability is challenging.

255 We postulated, however, that cell-to-cell variability may constitute a strength when

256 A cited detriment of iPSC-CMs is the cell-to-cell variability observed in electrical activity

257 genotype-phenotype relationships, as well as cell-to-cell variability of cardiac electrical activity

258 ntained in multistate models, we investigate cell-to-cell variability of chromatin organization into

259 abilized, showing much more narrow ranges in cell-to-cell variability of expression compared with oth

260 pie simulations to show that measurements of cell-to-cell variability of RNAP numbers and interpolyme

261 luding histone demethylases, may control the cell-to-cell variability of transcriptomes and chromatin

262 ution, ATAC-seq provides an insight into the cell-to-cell variability that emerges from otherwise ide

263 ework for determining parameter influence on cell-to-cell variability through the inference of varian

264 We detected cell-to-cell variability using flow cytometry cell sorti

265 : high proportions of zero values, increased cell-to-cell variability, and overdispersion due to abno

266 ntricular cardiomyocytes exhibit substantial cell-to-cell variability, even when obtained from the sa

267 s of the cytoskeleton that display prominent cell-to-cell variability, triggered by heterogeneities i

268 abbit and pig myocytes, despite high overall cell-to-cell variability.

269 eterogeneous hypoxic regions and significant cell-to-cell variability.

270 he cells, its activity still shows very high cell-to-cell variability.

271 ds, and also allows for the interrogation of cell-to-cell variability.

272 to investigate the underlying mechanisms of cell-to-cell variability.

273 ally, we demonstrate that parasites have low cell-to-cell variance in cycle period, on par with a cir

274 ve very few genes with low expression and/or cell-to-cell variance.

275 gle mammalian cells in a population and thus cell-to-cell variance.

276 q) is a powerful tool for characterizing the cell-to-cell variation and cellular dynamics in populati

277 The major contributor to cell-to-cell variation in biomarker expression was gener

278 c chromosomes, generates interindividual and cell-to-cell variation in diverse meiotic phenotypes.

279 proach to dissect different contributions to cell-to-cell variation in hsp-16.2 expression in the int

280 n shape response is measured, thus unmasking cell-to-cell variation in mechanical properties.

281 Here we utilized the cell-to-cell variation in morphological features of Myco

282 First, there was substantial cell-to-cell variation in number of transcription sites

283 tially across individual cells and predicted cell-to-cell variation in proliferation, mutation outcom

284 To investigate the causes of cell-to-cell variation in proliferation, we used a high-

285 sion patterns, but also more subtle modes of cell-to-cell variation in splicing.

286 These results suggest an important role for cell-to-cell variation in the state of an organelle in s

287 r, it is unclear how resource allocation and cell-to-cell variation jointly shape the overall perform

288 In addition to genetic diversity, the cell-to-cell variation that fuels evolutionary selection

289 del of aging cells that accounts for natural cell-to-cell variations across a broad range of paramete

290 The findings of this work showed that the cell-to-cell variations can be simply and sensitively de

291 e and female rat SNc DA neurons to determine cell-to-cell variations in AIS and ABD geometry, and the

292 In the current study, we describe large cell-to-cell variations in AIS length or distance from t

293 -Broccoli fluorescence ratio to quantify the cell-to-cell variations of target concentrations.

294 measurement method is reported for screening cell-to-cell variations, in which voltage is the only in

295 the cellular populations and masks essential cell-to-cell variations.

296 ation at all length scales, reflecting large cell-to-cell variations.

297 lymphocyte protein (MAL), in the process of cell-to-cell viral spread in oligodendrocytes.

298 Enteroviruses support cell-to-cell viral transmission prior to their canonical

299 model parameters, and their variability from cell-to-cell; we use this model to suggest reasons for t

300 ansfer of pathogenic protein aggregates from cell-to-cell within affected tissues.