ライフサイエンスコーパス: cerebellar white matter

1 h increased complex I and IV activity in MSA cerebellar white matter.

2 with numerous lesions in the hippocampus and cerebellar white matter.

3 , including cells in the corpus callosum and cerebellar white matter.

4 s and basal ganglia, and to a lesser extent, cerebellar white matter.

5 nje cells and spongiform degeneration of the cerebellar white matter.

6 the corpus callosum and fimbria/fornix, and cerebellar white matter.

7 in mice was spatially indistinguishable from cerebellar white matter.

8 ted that placental ALLO insufficiency led to cerebellar white matter abnormalities that correlated wi

9 ntified extensive nanoparticle signal in the cerebellar white matter and circumscribed cortical gray

10 on of proliferative clusters of cells in the cerebellar white matter and dorsal brainstem of postnata

11 Brain T2 lesion load, cerebellar white matter and gray matter volumes, and tra

12 Men had higher fractional anisotropy (FA) in cerebellar white matter and in the left superior longitu

13 g normal development of cortical neurons and cerebellar white matter and may also contribute to the p

14 ]ACI-12589 demonstrates clear binding in the cerebellar white matter and middle cerebellar peduncles

15 Patients with MSA showed increased cerebellar white matter and pons atrophy (M6 = -5.9 to -

16 Cerebellar white matter and subregional gray matter volu

17 lower volume in the basilar (ventral) pons, cerebellar white matter and visual cortex.

18 ial activation was particularly prominent in cerebellar white matter and within the deep cerebellar n

19 sis pontis, middle cerebellar peduncles, and cerebellar white matter, and elevated succinate on magne

20 ence regions used, subcortical white matter, cerebellar white matter, and the pons, alone or in combi

21 t to induce axonal injury, and that axons in cerebellar white matter are particularly vulnerable to d

22 the middle cerebellar peduncles and adjacent cerebellar white matter are thought to be highly sensiti

23 ense white matter voxels was performed using cerebellar white matter as the intensity reference.

24 ltinuclear globoid cells in the cerebral and cerebellar white matter associated with severe gliosis.

25 /-5.7 pg.mL-1 vs 11.1+/-5.9, p<0.0001), more cerebellar white matter atrophy (1.44+/-0.12 % of total

26 connections as well as projection fibers and cerebellar white matter being among the affected tracts.

27 rain, especially in left temporoparietal and cerebellar white matter, but did not differ between read

28 acteristics are (i) significant cerebral and cerebellar white matter disease, (ii) associated astrocy

29 dered: caudate, pallidum, putamen, thalamus, cerebellar white matter, hemispheric white matter, and c

30 cerebellar atrophy (aOR = 3.34, p = 0.013), cerebellar white matter hyperintensity (aOR = 3.33, p =

31 e increases in anisotropy within the midline cerebellar white matter in the second study correlated w

32 also optic radiation, brainstem tracts, and cerebellar white matter, in combination with delayed mye

33 of Purkinje cells, Bergmann gliosis and deep cerebellar white matter inflammatory infiltrates.

34 ion tensor MRI abnormalities consistent with cerebellar white matter injury in 3 of 4 subjects.

35 SFV vectors injected into cerebellar white matter labelled transitional OL ((T)OL)

36 nje cells and spongiform degeneration of the cerebellar white matter may be important factors in the

37 Thus, dividing progenitors in the cerebellar white matter migrate through the white matter

38 We investigated GABAergic signaling to cerebellar white matter NG2 cells in a mouse model of DW

39 ot NAA, evokes an inward membrane current in cerebellar white matter oligodendrocytes, which is reduc

40 core (p=0.002), and higher total creatine in cerebellar white matter (p=0.026).

41 he whole cerebellum, cerebellar gray matter, cerebellar white matter, pons, and subcortical white mat

42 The three receptors were also detected in cerebellar white matter, primarily during myelination.

43 h less severe Purkinje cell loss also showed cerebellar white matter thinning and demyelination.

44 n larger human brains, while subcortical and cerebellar white matter tracts responsible for unimodal

45 Pons and cerebellar white matter volumes decreased and deviated f

46 3q29Del participants also had larger cerebellar white matter volumes than controls following

47 formed there, be readily transported to the cerebellar white matter where PrPSc is found.

48 ar streams: a dorsal pathway into developing cerebellar white matter, where the migrating cells dispe