ライフサイエンスコーパス: neuropathogenesis

1 ory cytokines in the CNS are associated with neuropathogenesis.

2 ht function as key players influencing viral neuropathogenesis.

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

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

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

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

7 chemokines might be involved in induction of neuropathogenesis.

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

9 -1 disease may play an important role in HAD neuropathogenesis.

10 d microglia is a critical component of viral neuropathogenesis.

11 erated disease progression as well as severe neuropathogenesis.

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

13 cytokines is important in delineating HIV-1 neuropathogenesis.

14 at may be of importance in understanding HIV neuropathogenesis.

15 on of OL maturation alone cannot account for neuropathogenesis.

16 ional framework for further investigating DS neuropathogenesis.

17 l neurodegenerative disease-related genes to neuropathogenesis.

18 ficiency virus (HIV) intrahost evolution and neuropathogenesis.

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

20 differentiation is critical to understanding neuropathogenesis.

21 odeficiency viruses that could contribute to neuropathogenesis.

22 or understanding host-virus interactions and neuropathogenesis.

23 gain insight into key events underlying the neuropathogenesis.

24 g therapeutic targeting of this aspect of AD neuropathogenesis.

25 astrocyte dysregulation contributing to HIV neuropathogenesis.

26 have elucidated the role of diabetes in WNV neuropathogenesis.

27 function of carbohydrate binding in reovirus neuropathogenesis.

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

29 des of parasite-host interactions leading to neuropathogenesis.

30 ersistent WNV or its products contributed to neuropathogenesis.

31 n, the hallmark feature of Alzheimer disease neuropathogenesis.

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

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

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

35 vide novel insights into how mhtt may elicit neuropathogenesis.

36 ighting a pivotal role for astrocytes in HIV neuropathogenesis.

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

38 mportant pathogenic factor in HIV-associated neuropathogenesis.

39 ient mice provide a model for evaluating VZV neuropathogenesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 We investigated WNV neuropathogenesis by using human neuroblastoma cells and

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

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

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

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

66 Mechanisms for neuropathogenesis could include irregular immune activat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 he primary biochemical disruption initiating neuropathogenesis in HD.

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

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

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

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

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

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

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

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

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

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

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

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

94 The neuropathogenesis is mostly due to inflammatory response

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

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

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

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

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

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

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

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

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

104 9 is not the determinant of the differential neuropathogenesis of BHV-1 and BHV-5.

105 The neuropathogenesis of bipolar disorder remains poorly des

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

107 The neuropathogenesis of central nervous system/viral infect

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 The neuropathogenesis of the disease has not been completely

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

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

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

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

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

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

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

145 However, its neuropathogenesis remains largely unknown, partially owi

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

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

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

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

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

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

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

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

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

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