ライフサイエンスコーパス: astrocytosis

1 neuronal atrophy, microglial activation, and astrocytosis.

2 ix (bHLH) transcription factors and promotes astrocytosis.

3 seizure-affected brains and less in reactive astrocytosis.

4 unded by comorbidities accompanying reactive astrocytosis.

5 of plaque-associated neuritic dystrophy and astrocytosis.

6 onal loss, but did not alter microgliosis or astrocytosis.

7 ecule fluorescein, concomitant with reactive astrocytosis.

8 eurons and glia, abnormal myelination and an astrocytosis.

9 Both groups had reduction in astrocytosis.

10 s, resulting in the development of prominent astrocytosis.

11 ges, serum protein extravasation, and marked astrocytosis.

12 macrophages, fibrinogen leakage, and marked astrocytosis.

13 lated neurofilament inclusions, and reactive astrocytosis.

14 n areas where there is neurodegeneration and astrocytosis.

15 ted inclusions in the brain and spinal cord, astrocytosis, a reduction in the number of hippocampal n

16 opening of the blood-brain barrier (BBB) and astrocytosis accompanied by activation of brain microgli

17 These leaks were often associated with astrocytosis and apoptotic cells.

18 as performed to investigate fibrillar Abeta, astrocytosis and cerebral glucose metabolism with the ra

19 , accompanied by enhanced neuroinflammation, astrocytosis and gliosis, and eventually neuronal loss.

20 ration is accompanied by pronounced reactive astrocytosis and is preceded by an accumulation of ultra

21 Astrocytosis and microglia/monocyte activation were dram

22 ulation of autofluorescent storage material, astrocytosis and microglial activation in the brain.

23 ta, but deficient in CD40L, showed decreased astrocytosis and microgliosis associated with diminished

24 ese results indicate that the progression of astrocytosis and microgliosis diverges from that of amyl

25 emyelination, oxidative damage, inflammatory astrocytosis and microgliosis in the brain, and eventual

26 reached a plateau early after symptom onset, astrocytosis and microgliosis increased linearly through

27 deposition of extracellular amyloid plaques, astrocytosis and neuritic dystrophy.

28 ive histopathological scoring of spongiosis, astrocytosis and prion protein deposition.

29 The patterns of astrocytosis and PrPSc formation were different between

30 Topical MSCs triggered earlier astrocytosis and reactive microglia.

31 elates temporally with the onset of reactive astrocytosis and the appearance of phosphorylated neurof

32 diffuse extracellular deposition but reduced astrocytosis and TUNEL and was not associated with intra

33 H-Tau triggered neuronal death (60% in CA3), astrocytosis, and loss of the processes in CA1.

34 INCL mice also had decreased brain atrophy, astrocytosis, and microglial activation, as well as inte

35 stimuli (ubiquitinated dystrophic neurites, astrocytosis, and microglial infiltrates) in the ventrom

36 of CD40 or CD40L alleviates amyloid burden, astrocytosis, and microgliosis in transgenic animal mode

37 g tau hyperphosphorylation, (Abeta) deposit, astrocytosis, and microgliosis, which were correlated wi

38 -amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis.

39 elopmental retardation, inflammation, death, astrocytosis, and neuron loss.

40 , in affected areas, there is neuronal loss, astrocytosis, and neuronal intracytoplasmic aggregates o

41 motor and respiratory dysfunction, reactive astrocytosis, and reduced GLT-1 transporter expression i

42 nflammatory reaction marked by microgliosis, astrocytosis, and the release of proinflammatory cytokin

43 AIDS brains where brain injury and reactive astrocytosis are common.

44 signaling, plaque density, microgliosis, and astrocytosis are not altered.

45 eract with inflammatory responses indicating astrocytosis as an early contributory driving force in A

46 functional (brain perfusion) and pathologic (astrocytosis) aspects from a single PET scan.

47 idosis, while amyloidosis may induce further astrocytosis at least in 263K-infected hamsters.

48 tive deficits were associated with increased astrocytosis but not tau phosphorylation or amyloid beta

49 s of HIV/neuroAIDS is reactive astrocytes or astrocytosis, characterized by increased cytoplasmic acc

50 lated positively with tangle burden, whereas astrocytosis correlated negatively with cortical thickne

51 Thus, reactive astrocytosis could generate local synaptic perturbations

52 kdown of cerebellum and cortex, brain edema, astrocytosis, degeneration of neuronal dendrites, neuron

53 Reactive astrocytosis develops in many neurologic diseases, inclu

54 gest a common cascade through which aberrant astrocytosis/GFAP up-regulation potentiates neurotoxicit

55 l investigations reveal damage to myelin and astrocytosis in both white and grey matter.

56 Excessive astrocytosis in cortical tubers in tuberous sclerosis co

57 suggestive of progressive axonal damage and astrocytosis in RTT, respectively, whereas increased glu

58 Astrocytosis in spinal cord was associated with a marked

59 rillary acidic protein (GFAP) shows reactive astrocytosis in the area adjacent to the Fluoro-Jade B-p

60 revealed a significant decrease in reactive astrocytosis in the ipsilateral dorsal thalamus (P < 0.0

61 cle weakness/atrophy, motor neuron loss, and astrocytosis in the spinal cord.

62 e-associated neuritic dystrophy and reactive astrocytosis in transgenic mice expressing familial AD-m

63 However, the CCR5KO does not abrogate astrocytosis, indicating it can occur independently from

64 were markedly upregulated following reactive astrocytosis induced by focal mechanical trauma.

65 We examined the consequences of selective astrocytosis induction on synaptic transmission in mouse

66 Reactive astrocytosis is a well known phenomenon that occurs in t

67 11)C-PIB+ patients potentially suggests that astrocytosis is an early phenomenon in AD development.

68 tal cortex, glial activation (microgliosis > astrocytosis) is prominent throughout the brain and pers

69 mice, which display a prominent perivascular astrocytosis, levels of the basement membrane proteins p

70 ting the notion that astrocyte activation or astrocytosis may directly contribute to HIV-associated n

71 Astrocytosis-mediated deficits in inhibition triggered g

72 ects of disease (virus-infected macrophages, astrocytosis, microglial activation, and neuronal damage

73 eak in SOD1(G93A) mice significantly reduces astrocytosis, microgliosis and ameliorates skeletal musc

74 ndent cortical neuronal loss, accompanied by astrocytosis, microgliosis, and hyperphosphorylation of

75 axons, microglial proliferation and reactive astrocytosis, microinfacrts and diffuse ischaemic change

76 ndings suggest a 'snowball effect', that is: astrocytosis might play an important role in amyloidosis

77 neuronal loss, rhodanine-positive deposits, astrocytosis, myelin loss, and spongiosis.

78 sions of brain injury, namely, inflammation (astrocytosis), neurodegeneration, and cell death, were m

79 spongiform encephalopathies include gliosis, astrocytosis, neuronal degeneration, and spongiform chan

80 n early event in LP-BM5 infection, preceding astrocytosis, neurotransmitter loss, and development of

81 gest that Abeta plays a role in the reactive astrocytosis of AD and that the inflammatory response in

82 , cytomegaly and extensive vacuolization and astrocytosis of white matter.

83 inducing microglial activation and enhancing astrocytosis or cerebral amyloid angiopathy.

84 ing after immunization had similar degree of astrocytosis (P = 0.6060), more embedded dystrophic neur

85 Microglia activation, astrocytosis, proinflammatory cytokines, and iNOS expres

86 Myelin status, lesion activity, astrocytosis, serum protein distribution, axonal area, a

87 , SC1 may play an important role in reactive astrocytosis subsequent to a wide variety of neural trau

88 olves neuronal damage and prominent reactive astrocytosis, the latter characterized by strong upregul

89 vated in AD and the consequences of reactive astrocytosis to disease progression are not known.

90 Astrocytosis was present and white matter was atrophied

91 innervation is a factor in the regulation of astrocytosis, we measured glial fibrillary acidic protei

92 Signs of reactive astrocytosis were found in the striatum of Tat 1-72 inje

93 via adeno-associated virus induced reactive astrocytosis without altering the intrinsic properties o