ライフサイエンスコーパス: axonopathy

1 onal dystrophic swellings (a hallmark of CNS axonopathy).

2 ularly potent mediators of demyelination and axonopathy.

3 in rats similarly accelerated ganglion cell axonopathy.

4 Axon injury markers defined the burden of axonopathy.

5 on in the burden of microscopic necrosis and axonopathy.

6 ting that lack of Bcl-w results in a primary axonopathy.

7 ized by early loss of synaptic terminals and axonopathy.

8 that SFN is a non-length-dependent terminal axonopathy.

9 l extension of spinal cord long-tract distal axonopathy.

10 human neurological diseases characterized by axonopathy.

11 mice developed a chronic peripheral hindlimb axonopathy.

12 d their potential as therapeutic targets for axonopathy.

13 gth and evidence that ALS occurs as a distal axonopathy.

14 me represents a novel therapeutic target for axonopathies.

15 yndromes and link them with hereditary motor axonopathies.

16 date therapeutic targets for a wide-range of axonopathies.

17 other central nervous system (CNS) ischemic axonopathies.

18 bon disulfide exposure leads to an identical axonopathy, achieving neurofilament cross-linking throug

19 ystrophy, which manifests as the spinal cord axonopathy adrenomyeloneuropathy (AMN) in nearly all mal

20 he HSPs, with clear relevance for other long axonopathies affecting peripheral nerves and lower motor

21 Spinal MNs developed distal axonopathy and formed ubiquitinated inclusions and degen

22 d1(D83G/D83G) mice also phenocopy the distal axonopathy and hepatocellular carcinoma found in Sod1 nu

23 Chronic demyelination can result in axonopathy and is associated with human neurological con

24 e for treatment of diseases characterized by axonopathy and neurodegeneration.

25 y: reversible neurotoxicity characterized by axonopathy and recovery, and irreversible neurotoxicity

26 The most sensitive indicator of toxicity was axonopathy and secondary myelin changes accompanied by a

27 ailure of the ER-endosome contact process in axonopathy and suggest that coupling of ER-mediated endo

28 60 HAT activity in the nervous system causes axonopathy and transport defects associated with epigene

29 a rapidly progressive diffuse sensory motor axonopathy, and electroencephalogram findings progressed

30 Axonopathies are a group of clinically diverse disorders

31 Axonal transport defects and axonopathy are prominent in early preclinical stages of

32 axonal autophagy as a possible mechanism for axonopathy associated with neurodegeneration.

33 Neuroaxonal dystrophy (NAD), a distinctive axonopathy characterized by dramatic swelling of preterm

34 CHMP2B also develop an early and progressive axonopathy characterized by numerous amyloid precursor p

35 reliminary evidence that DTS can distinguish axonopathy from other processes such as inflammation, ed

36 Giant axonopathy (gaxp), an autosomal recessive mouse mutation

37 Spastin is mutated in the axonopathy hereditary spastic paraplegia.

38 hickness and abnormal extramyelin loops) and axonopathy (i.e., altered neurofilament phosphorylation,

39 ivator of sGC, potently inhibited NO-induced axonopathy (IC(50) = 3 microM).

40 The axonopathy in CMT2A is caused by mutations in Mitofusin

41 We demonstrate a progressive motor axonopathy in these mice and show that Sod1(-/-) primary

42 Thus, the "long axonopathy" in early-onset SPG3A may result from abnorma

43 Neuroaxonal dystrophy (NAD), a distinctive axonopathy involving distal axons and synapses, represen

44 of corneas was performed with antibodies to axonopathy marker SMI-32.

45 s: adrenomyeloneuropathy, a non-inflammatory axonopathy mostly in adults, and an intensely inflammato

46 ilament may contribute to the distal sensory axonopathy observed in diabetes.

47 organization and function contribute to the axonopathies of myelin and other neurologic disorders.

48 weakness and spasticity and length-dependent axonopathy of corticospinal motor neurons.

49 mity spasticity, owing to a length-dependent axonopathy of corticospinal motor neurons.

50 akness due to a length-dependent, retrograde axonopathy of corticospinal motor neurons.

51 akness due to a length-dependent, retrograde axonopathy of corticospinal motor neurons.

52 es that induce human paralysis due to severe axonopathy of large neurons.

53 ogical hallmark is a length-dependent distal axonopathy of nerve fibers in the corticospinal tract.

54 s characterized by a length-dependent distal axonopathy of the corticospinal tracts, resulting in low

55 e genetic conditions characterized by distal axonopathy of the longest corticospinal tract axons, and

56 ry spastic paraplegia, which is a retrograde axonopathy primarily characterized pathologically by the

57 nd supports the role of NTE abnormalities in axonopathy produced by neuropathic OP compounds.

58 suggest that ALS2 is predominantly a distal axonopathy, rather than a neuronopathy in the central ne

59 However, whether axonopathy represents an early pathogenic event or an ep

60 ts directly implicate a reticulon protein in axonopathy, show that this protein participates in a net

61 In an animal model of distal axonopathy, systemic EPO administration prevents axonal

62 environmental toxicants can result in distal axonopathies through reaction with various components of

63 ce lacking the KLC1 protein (KLC1-/-) led to axonopathies with cytoskeletal disorganization and abnor

64 m of predominantly motor distal neuronopathy/axonopathy with mild to moderate sensory involvement tha

65 Kernicterus presents as axonopathy with myelination deficits at different brain

66 ted intraepidermal nerve fibers and produced axonopathy, with a secondary disruption in myelin struct

67 Synaptic dysfunction and axonopathy would thus be the hallmark of presymptomatic