ライフサイエンスコーパス: cerebral atrophy

1 acterized by amyloid plaques and progressive cerebral atrophy.

2 were highly correlated with Braak stage and cerebral atrophy.

3 ge, peripheral neuropathy, hearing loss, and cerebral atrophy.

4 the patient's epileptic phenotype as well as cerebral atrophy.

5 iable cerebellar atrophy and highly variable cerebral atrophy.

6 nt of overt clinical symptoms and detectable cerebral atrophy.

7 eased CSF tau and structural MRI measures of cerebral atrophy.

8 quantitative MRI indices suggesting greater cerebral atrophy.

9 tter high signal, and the notable absence of cerebral atrophy.

10 and 57% following correction for effects of cerebral atrophy.

11 individuals reveals delay in myelination and cerebral atrophy.

12 ll as early onsets of tau/MAPT pathology and cerebral atrophy.

13 haracterized by signal intensity changes and cerebral atrophy.

14 in cerebellar cortex as well as subcortical cerebral atrophy.

15 Brain MRI findings included cerebral atrophy (13/20), supported by post-mortem histo

16 y significant neuroimaging features included cerebral atrophy (75%), cerebellar atrophy (60%), callos

17 which was significantly correlated with age, cerebral atrophy and ADC stage and (b) the striatum, whi

18 the development of LE with its potential for cerebral atrophy and cognitive impairment.

19 c treatment exacerbated alpha-syn pathology, cerebral atrophy and motor behavioural deficits in mice.

20 re, MSIS-29 (psychological) and EDSS and MRI cerebral atrophy and MTR.

21 However, varying degrees of cerebral atrophy and residual cognitive impairment were

22 lectual disability, ataxia, axial hypotonia, cerebral atrophy and speech delay/apraxia/dysarthria.

23 We identified clusters of cerebral atrophy and tau PET uptake using a data-driven

24 ), suggesting a substantial heterogeneity in cerebral atrophy and tau spreading patterns.

25 thy consistently associated with progressive cerebral atrophy and variable involvement of the white m

26 oundary shift integral to determine rates of cerebral atrophy and ventricular expansion in six patien

27 Patients with PSP had a rate of cerebral atrophy and ventricular expansion of 1.3 and 7.

28 ing showed two patients had mild generalized cerebral atrophy, and both patients and unaffected famil

29 5, and included multifocal hyperintensities, cerebral atrophy, and confluent cortical and subcortical

30 ount for the remaining difference, including cerebral atrophy, and enhanced vasoconstrictor and blunt

31 ephaly, intellectual disability, progressive cerebral atrophy, and intractable seizures.

32 development of motor deficits, weight loss, cerebral atrophy, and neuronal intranuclear inclusions i

33 NS) has been shown to improve memory, reduce cerebral atrophy, and reverse neurodegeneration.

34 used severity of white matter lucencies and cerebral atrophy, and the number of lacunes to calculate

35 malities in several brain regions, including cerebral atrophy (aOR = 2.69, p = 0.027), cerebellar atr

36 However, unlike the latter, the patterns of cerebral atrophy associated with DLB have not been well

37 to quantify the severity and distribution of cerebral atrophy by using automated volumetric analysis

38 lated synaptic loss, in turn contributing to cerebral atrophy, cognitive decline, and increased risk

39 There is an age-related cerebral atrophy, demyelination of the corpus callosum,

40 indicative of a disease-specific pattern of cerebral atrophy for the HIV+ patients.

41 The extent and magnitude of the cerebral atrophy further progressed by the time the subj

42 nts had more neurodegeneration, evidenced by cerebral atrophy, hippocampal atrophy and locus coeruleu

43 multiple MRI scans to measure progression of cerebral atrophy in 12 patients with Alzheimer's disease

44 ed resolution of early lesions in 8 and mild cerebral atrophy in 2.

45 CT and MRI showed mild to moderate cerebral atrophy in 4 patients.

46 Brain MRI showed mild cerebral atrophy in a subset of patients (n = 3/6).

47 imaging findings of vascular brain injury or cerebral atrophy in adult American Indians.

48 The extent to which cerebral atrophy in Alzheimer's disease changes with tim

49 g brain imaging technologies have identified cerebral atrophy in diabetic patients, suggesting that t

50 study was to identify a signature pattern of cerebral atrophy in DLB and to compare it with the patte

51 s important information about the pattern of cerebral atrophy in Parkinson's disease and PDD.

52 needed to detect the effects of treatment on cerebral atrophy in this population of patients with adv

53 tment reduces, by as much as seven fold, the cerebral atrophy in those gray matter (GM) regions speci

54 Measures of cerebral atrophy included VAS scores, the bvFTD atrophy

55 Cerebral atrophy is a correlate of clinical progression

56 rrect for the dilution effect of age-related cerebral atrophy may confound interpretation of previous

57 D), an early-onset dementia characterized by cerebral atrophy, myelin loss and gliosis.

58 ontal cortex, we showed that neither diffuse cerebral atrophy nor neocortical thickness explained the

59 tensities, microbleeds, microinfarctions and cerebral atrophy on magnetic resonance imaging scans.

60 ntrol group, the SLE patients more often had cerebral atrophy on MRI (32% versus 0%), confirmed by an

61 tional study was to establish the pattern of cerebral atrophy on MRI in Parkinson's disease patients

62 on scanning, whereas all other scans showed cerebral atrophy only.

63 ar atrophy was universal on MRI (100%), with cerebral atrophy or dentate and pontine T2 hyperintensit

64 this study was to assess the progression of cerebral atrophy over multiple serial MRI during the per

65 ed in patients, including cerebellar damage, cerebral atrophy, peripheral nerves pathology, and photo

66 ciated pathologies segregated based on their cerebral atrophy profiles, according to the following sc

67 imilar phenotypes typified by cerebellar and cerebral atrophy, seizures, irritability, ataxia, and ex

68 Neuroimaging variably demonstrated cerebral atrophy (sometimes unilateral initially) or hig

69 e interactions between amyloid pathology and cerebral atrophy, such that whole-brain and hippocampal

70 omprehensive view on diabetic encephalopathy/cerebral atrophy, taking into account neuroimaging data,

71 type that was consistent with cerebellar and cerebral atrophy that could be rescued by wild-type, but

72 a VPS53 allele causing progressive cerebello-cerebral atrophy type 2 (PCCA2) in humans exhibits simil

73 n (GARP) complex cause progressive cerebello-cerebral atrophy type 2 (PCCA2).

74 nd corrected for partial-volume effects from cerebral atrophy using an MR-based algorithm.

75 rtunity to assess the impact of treatment on cerebral atrophy using serial MRI.

76 abnormalities, abnormal cortical formation, cerebral atrophy, ventriculomegaly, hydrocephaly, and ce

77 .001); in infants who subsequently developed cerebral atrophy versus those who did not: 7.23 (SD, 0.1

78 ion of surgical pathology, signal change and cerebral atrophy visible on structural MRI can be used t

79 scle biopsy revealed ragged red fibers; mild cerebral atrophy was evident by magnetic resonance imagi

80 us callosum or basal ganglia alterations and cerebral atrophy were common.

81 mer's disease is associated with progressive cerebral atrophy, which can be seen on MRI with high res

82 Neuroimaging features included cerebral atrophy, white matter volume loss, corpus callo

83 hanisms of post-ischemic retinal atrophy and cerebral atrophy with cognitive impairment may be simila

84 Postmortem examination confirmed cerebral atrophy with enlarged lateral ventricles.