ライフサイエンスコーパス: neuropathogenesis

1 egeneration is likely a critical step in the neuropathogenesis.

2 ighting a pivotal role for astrocytes in HIV neuropathogenesis.

3 -induced BBB damage and is relevant to viral neuropathogenesis.

4 mportant pathogenic factor in HIV-associated neuropathogenesis.

5 ient mice provide a model for evaluating VZV neuropathogenesis.

6 f p35, p25, and hence cdk5 activation in NPC neuropathogenesis.

7 play central roles in Alzheimer disease (AD) neuropathogenesis.

8 ory cytokines in the CNS are associated with neuropathogenesis.

9 ht function as key players influencing viral neuropathogenesis.

10 (APP) plays a key role in Alzheimer disease neuropathogenesis.

11 on with hMR plays an important role in HIV-1 neuropathogenesis.

12 port a critical role of Tat protein in HIV-1 neuropathogenesis.

13 chemokines might be involved in induction of neuropathogenesis.

14 ype BHV-1 and -5 based on their differential neuropathogenesis.

15 -1 disease may play an important role in HAD neuropathogenesis.

16 d microglia is a critical component of viral neuropathogenesis.

17 strains indicates that it may play a role in neuropathogenesis.

18 cytokines is important in delineating HIV-1 neuropathogenesis.

19 gain insight into key events underlying the neuropathogenesis.

20 at may be of importance in understanding HIV neuropathogenesis.

21 o the central nervous system to cause severe neuropathogenesis.

22 esponse, which are the major hallmark of HIV neuropathogenesis.

23 mechanisms underlying neuroinflammation and neuropathogenesis.

24 nvasion might not be a prerequisite for this neuropathogenesis.

25 ay contribute to immune cell recruitment and neuropathogenesis.

26 M-F50S, when added to other mutations, drove neuropathogenesis.

27 ontributing to control of flavivirus-induced neuropathogenesis.

28 al sclerosis and frontotemporal degeneration neuropathogenesis.

29 nd subsequent efficacy of EVG, including HIV neuropathogenesis.

30 g individuals, rather than a single unifying neuropathogenesis.

31 lial activation and the development of prion neuropathogenesis.

32 s-frame (TF) protein, which is important for neuropathogenesis.

33 erated disease progression as well as severe neuropathogenesis.

34 on of OL maturation alone cannot account for neuropathogenesis.

35 a better understanding of SARS-CoV-2 related neuropathogenesis.

36 ional framework for further investigating DS neuropathogenesis.

37 l neurodegenerative disease-related genes to neuropathogenesis.

38 ficiency virus (HIV) intrahost evolution and neuropathogenesis.

39 he relevance of astrocytes to HIV-associated neuropathogenesis.

40 e few studies that examine its impact on HIV neuropathogenesis.

41 differentiation is critical to understanding neuropathogenesis.

42 odeficiency viruses that could contribute to neuropathogenesis.

43 or understanding host-virus interactions and neuropathogenesis.

44 g therapeutic targeting of this aspect of AD neuropathogenesis.

45 n the brain parenchyma important for altered neuropathogenesis.

46 astrocyte dysregulation contributing to HIV neuropathogenesis.

47 have elucidated the role of diabetes in WNV neuropathogenesis.

48 function of carbohydrate binding in reovirus neuropathogenesis.

49 lls play a critical role in the induction of neuropathogenesis.

50 des of parasite-host interactions leading to neuropathogenesis.

51 ersistent WNV or its products contributed to neuropathogenesis.

52 n, the hallmark feature of Alzheimer disease neuropathogenesis.

53 s not appear to be the basis of LCMV-induced neuropathogenesis.

54 s system, play a central role in HIV-induced neuropathogenesis.

55 sted to contribute to Alzheimer disease (AD) neuropathogenesis.

56 vide novel insights into how mhtt may elicit neuropathogenesis.

57 mine the role of the BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 deletion recombinant was

58 duced neuroinflammation in tauopathy-related neuropathogenesis, age-matched TTBK1/JNPL3, JNPL3, TTBK1

59 f this study provide new insights into HIV-1 neuropathogenesis aimed at the development of future HIV

60 vant animal model for investigating COVID-19 neuropathogenesis among human subjects.

61 an enhance an understanding of virus-induced neuropathogenesis and aid in development of therapeutics

62 2, ORF3a expression in brain cells may drive neuropathogenesis and be an important mediator of both s

63 echanisms by which NF-kappaB regulates viral neuropathogenesis and contributes to viral encephalitis

64 We explored the source of neuropathogenesis and HIV-1 RNA in the CSF during NSE by

65 evious studies reported associations between neuropathogenesis and human immunodeficiency virus (HIV)

66 and assess their utility in inhibiting HIV-1 neuropathogenesis and neuroinvasion.

67 humans may allow better understanding of HIV neuropathogenesis and provide a dynamic biomarker for th

68 oroid plexus may play a critical role in NPC neuropathogenesis and serve as a novel biomarker for mon

69 autonomic networks in CWD neuroinvasion and neuropathogenesis and suggest that enteroglial cells may

70 se results implicate HPA dysregulation in AD neuropathogenesis and suggest that prolonged stress may

71 as a TBEV receptor has implications for TBEV neuropathogenesis and the development of antiviral count

72 oxidative stress on events involved in AIDS neuropathogenesis and the HIV-1 proteins responsible for

73 congenital infection, the mechanism of HCMV neuropathogenesis and the roles of individual viral gene

74 quirements for HIV adaptation to the CNS for neuropathogenesis and the value of CSF virus as a surrog

75 ging is a promising biomarker for studies of neuropathogenesis and therapeutic interventions in HIV.

76 t isoflurane may promote Alzheimer's disease neuropathogenesis and, as such, have implications for us

77 closely resembles HIV-1 immunopathogenesis, neuropathogenesis, and disease progression in humans.

78 ated NCI, considering recent evidence of HIV neuropathogenesis, and the pivotal role of cART.

79 of diagnosis and staging of CNS disease, its neuropathogenesis, and the possibility of new therapies

80 The tempo and intensity of retroviral neuropathogenesis are dependent on the capacity of the v

81 omplexities, accelerating discoveries in HIV neuropathogenesis are yielding potentially druggable tar

82 These results provide insight into the neuropathogenesis associated with attenuated flaviviruse

83 arrier (BBB) tissue chips that recapitulates neuropathogenesis associated with infection by SARS-CoV-

84 Recent advances in the understanding of neuropathogenesis associated with Zika virus (ZIKV) infe

85 ested to be important in HIV persistence and neuropathogenesis but has not been definitively demonstr

86 are documented as tools to study aspects of neuropathogenesis, but few have focused on modeling infe

87 s (HIV) infection is crucial to knowledge of neuropathogenesis, but these have not previously been de

88 at such studies help identify key players in neuropathogenesis by HIV-1.

89 We investigated WNV neuropathogenesis by using human neuroblastoma cells and

90 tributed to the development of prion disease neuropathogenesis by using three different scrapie strai

91 onstrate that this SCID mouse model of HIV-1 neuropathogenesis can reproduce key aspects of disease (

92 d it is responsible for protecting mice from neuropathogenesis caused by vesicular stomatitis virus.

93 onists against processes implicated in HIV-1 neuropathogenesis could block HIV-1 protein-induced neur

94 Mechanisms for neuropathogenesis could include irregular immune activat

95 cific NF-kappaB-dependent signaling to viral neuropathogenesis could inform development of new therap

96 in vivo may be associated with HCMV-mediated neuropathogenesis during congenital infection in the fet

97 r (BBB) permeability and its relationship to neuropathogenesis during primary human immunodeficiency

98 Relevant to HIV-1 neuropathogenesis, enhanced adhesion and migration of HI

99 mic inflammation is probably contributing to neuropathogenesis following SARS-CoV-2 infection, and th

100 cytokines critical to the development of HIV neuropathogenesis, gamma interferon (IFN-gamma), granulo

101 However, ZIKV neuropathogenesis has not yet been fully understood.

102 SFTS have been commonly reported, but their neuropathogenesis has rarely been studied.

103 Mechanisms of VZV neuropathogenesis have been challenging to study due to

104 Molecular determinants of neuropathogenesis have been shown to be present in the h

105 However, the effects of desflurane on AD neuropathogenesis have not been previously determined.

106 These mechanisms of VZV neuropathogenesis help to account for the often severe n

107 these mutations, matrix protein F50S, drove neuropathogenesis in an SSPE case.

108 does not play a necessary role in selective neuropathogenesis in BACHD mice.

109 olvement of cholesterol and metal ions in AD neuropathogenesis in both individual and interrelated ma

110 tein (PrP) have indicated its importance for neuropathogenesis in certain contexts, and have analysed

111 s in astrocytes may contribute to the severe neuropathogenesis in clade B infection.

112 te the molecular mechanism of HIV associated neuropathogenesis in cocaine abuse and how it accelerate

113 cate myelin-related systems involved in NBIA neuropathogenesis in early responses to iron loading.

114 he primary biochemical disruption initiating neuropathogenesis in HD.

115 BBB-associated neuropathogenesis in HIV-infected patients may initiate

116 HIV-1 Tat protein contributes to HIV-neuropathogenesis in several ways including its ability

117 rotein, which could help us understand viral neuropathogenesis in SFTS patients.

118 gesting that indirect mechanisms account for neuropathogenesis in the CNS, perhaps including changes

119 as previously been shown to be important for neuropathogenesis in the related Sindbis virus.

120 is a critical factor for yellow fever virus neuropathogenesis in the SCID mouse model and that the n

121 n important aspect of both SV40 and JC virus neuropathogenesis in their respective hosts.

122 shed and emerging mechanisms of RNA-mediated neuropathogenesis in this rapidly evolving field.

123 ngs lend support to a hypothetical scheme of neuropathogenesis in which HTLV-I tax gene expression pr

124 lties in understanding the mechanisms of HIV neuropathogenesis include the inability to study dynamic

125 at host cytokine responses may influence SIV neuropathogenesis independent of disease progression.

126 These results suggest a mechanism for the neuropathogenesis induced by HCMV infection that include

127 Therefore, we investigated neuropathogenesis induced by HIV-1 clades using the seve

128 Therefore, much of our knowledge of VZV neuropathogenesis is gained from studies of VZV-infected

129 In this model, virus-induced neuropathogenesis is indirect, as the virus predominantl

130 The neuropathogenesis is mostly due to inflammatory response

131 ing acquired immunity to viral pathogens and neuropathogenesis is not entirely clear.

132 Although our understanding of SARS-CoV-2 neuropathogenesis is still incomplete and our knowledge

133 JCV neuropathogenesis is understudied, and no pro-viral host

134 mechanistic dissection of the basis of LCMV neuropathogenesis may be informative for the development

135 In a mouse neuropathogenesis model, mortality was <15% in animals i

136 and protein synthesis to rebound, triggering neuropathogenesis months after acute viral control.

137 taining major cell types important for HIV-1 neuropathogenesis; neurons and astrocytes along with inc

138 hemokines are believed to play a role in the neuropathogenesis of AIDS through their recruitment of n

139 ation of the brain is a pivotal event in the neuropathogenesis of AIDS-associated dementia.

140 IV) infection and a major contributor to the neuropathogenesis of AIDS.

141 es the involvement of stress pathways in the neuropathogenesis of AIDS.

142 This, in turn, might contribute to the neuropathogenesis of BDV.

143 determine the role of gE in the differential neuropathogenesis of BHV-1 and BHV-5, we have constructe

144 9 is not the determinant of the differential neuropathogenesis of BHV-1 and BHV-5.

145 The neuropathogenesis of bipolar disorder remains poorly des

146 ronal cells is critical to understanding the neuropathogenesis of birth defects resulting from congen

147 The neuropathogenesis of central nervous system/viral infect

148 cal to increasing basic understanding of the neuropathogenesis of congenital ZIKV disease and of the

149 urovirulence of the virus and control of the neuropathogenesis of flavivirus infection.

150 ests a role for miR-21 downregulation in the neuropathogenesis of HCMV infection of the developing CN

151 ndard laboratory system for the study of the neuropathogenesis of herpes simplex virus type 1 (HSV-1)

152 mary human astrocytes may play a role in the neuropathogenesis of HHV-6.

153 t that ET-1 may be critical in mediating the neuropathogenesis of HIV dementia and that statins may h

154 dicator of the role of viral products in the neuropathogenesis of HIV dementia.

155 on of astrocyte function could influence the neuropathogenesis of HIV infection.

156 (HIV)-Tat protein has been implicated in the neuropathogenesis of HIV infection.

157 mechanism(s) by which opioids exacerbate the neuropathogenesis of HIV-1 are not entirely known, it is

158 in chronic inflammation, contributing to the neuropathogenesis of HIV-1 associated neurologic disease

159 proteins by NHA that may play a role in the neuropathogenesis of HIV-1 disease.

160 their receptors have been implicated in the neuropathogenesis of HIV-1 infections.

161 Neuropathogenesis of HIV-1 is exacerbated by drugs of ab

162 ever very little information is available on neuropathogenesis of HIV-1 subtype C (clade C) that exis

163 ned the role of the autophagy pathway in the neuropathogenesis of HIV-1 using primary human microglia

164 likely contributes to the neuroinvasion and neuropathogenesis of HIV-1, through its effects on selec

165 uman macrophages that may be involved in the neuropathogenesis of HIV-associated dementia.

166 Monocytes/macrophages contribute to the neuropathogenesis of HIV-related cognitive impairment (C

167 Here, we provide an overview of the neuropathogenesis of HPAI H5Nx virus infection in mammal

168 uss the contribution of viral factors to the neuropathogenesis of HPAI H5Nx virus infections and the

169 development that is likely to impact on the neuropathogenesis of HSA21-related disorders including D

170 of the brain, play an important role in the neuropathogenesis of human immunodeficiency virus type 1

171 icular CXCR4 and CCR5 play a key role in the neuropathogenesis of Human Immunodeficiency Virus-1 (HIV

172 ) infection are critical for elucidating the neuropathogenesis of infection and disease.

173 We are investigating the neuropathogenesis of Lyme disease caused by Borrelia bur

174 ovirulence has also hindered analysis of the neuropathogenesis of mumps virus infection and the ident

175 To explore the neuropathogenesis of neonatal HIV infection, we infected

176 h, which could contribute to the progressive neuropathogenesis of Parkinson disease.

177 dent host factors have a major impact on the neuropathogenesis of pediatric AIDS.

178 Determination of biomarker and neuropathogenesis of postoperative cognitive change (POC

179 animal models has accelerated studies of the neuropathogenesis of RVFV.

180 potential for neurotropism and mechanisms of neuropathogenesis of SARS-CoV-2 as they relate to the ac

181 ill advance our current understanding of the neuropathogenesis of SARS-CoV-2 infection and demonstrat

182 ral replicase plays an important role in the neuropathogenesis of SFV.

183 The neuropathogenesis of the disease has not been completely

184 syndrome; however, little is known about the neuropathogenesis of the disease.

185 us to relate genes and sets of genes to the neuropathogenesis of this syndrome, and to better unders

186 ept that microglia play an important role in neuropathogenesis of tuberculosis and that dexamethasone

187 is not known whether sigma1s contributes to neuropathogenesis of type 3 reoviruses, which disseminat

188 l facilitate studies of the neurotropism and neuropathogenesis of VA1.IMPORTANCE Astroviruses are an

189 ed by glial cells has been implicated in the neuropathogenesis of various diseases.

190 r licensed human vaccines, understanding the neuropathogenesis of WNV is critical for rational therap

191 However, the mechanisms underlying the neuropathogenesis of ZIKV infection are not yet fully un

192 Here, we investigate the neuropathogenesis of ZIKV infection in type I interferon

193 However, the molecular events underlying HIV neuropathogenesis remain elusive, mainly due to lack of

194 However, its neuropathogenesis remains largely unknown, partially owi

195 r, the specific role each cell type plays in neuropathogenesis remains to be established.

196 hanism by which drugs of abuse intensify HIV neuropathogenesis through direct effects of the neurotra

197 tivation and apoptosis, which are part of AD neuropathogenesis, through the mitochondria-dependent ap

198 d how K. pneumoniae pathogenesis exacerbates neuropathogenesis via the gut-blood-brain axis.

199 s is the first demonstration, ever since HIV neuropathogenesis was first recognized, that viral genet

200 tanding of the roles of Tat protein in HIV-1 neuropathogenesis, we attempted to establish a transgeni

201 glioside accumulation is a crucial factor in neuropathogenesis, we bred NP-C model mice with mice car

202 determine whether NgR1 functions in reovirus neuropathogenesis, we compared virus replication and dis

203 ptors conferring reovirus serotype-dependent neuropathogenesis, we conducted a genome-wide CRISPRa sc

204 ate the possible mechanism(s) of ts1-induced neuropathogenesis, we measured CNS expression of cytokin

205 ines and chemokine receptors may play in HIV neuropathogenesis, we sought to describe their pattern o

206 fect of morphine on SIV infection-associated neuropathogenesis were analyzed for pulmonary vascular c

207 pitranscriptomic mechanisms in prion disease neuropathogenesis, whereby RNA-editing targets in a huma

208 ur study uncovers mechanisms underlying ZIKV neuropathogenesis within a susceptible mouse model and s