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1 onal dystrophic swellings (a hallmark of CNS axonopathy).
2  that SFN is a non-length-dependent terminal axonopathy.
3 d their potential as therapeutic targets for axonopathy.
4 gth and evidence that ALS occurs as a distal axonopathy.
5 onal degeneration pathways leading to distal axonopathy.
6 ularly potent mediators of demyelination and axonopathy.
7  in rats similarly accelerated ganglion cell axonopathy.
8    Axon injury markers defined the burden of axonopathy.
9 on in the burden of microscopic necrosis and axonopathy.
10 ting that lack of Bcl-w results in a primary axonopathy.
11 ized by early loss of synaptic terminals and axonopathy.
12 l extension of spinal cord long-tract distal axonopathy.
13 human neurological diseases characterized by axonopathy.
14 mice developed a chronic peripheral hindlimb axonopathy.
15 luorescence signal and metabolic stress from axonopathy.
16 gy metabolism are associated with late-onset axonopathy.
17 the axon, and its dysfunction causes various axonopathies.
18 me represents a novel therapeutic target for axonopathies.
19 yndromes and link them with hereditary motor axonopathies.
20 date therapeutic targets for a wide-range of axonopathies.
21  other central nervous system (CNS) ischemic axonopathies.
22 bon disulfide exposure leads to an identical axonopathy, achieving neurofilament cross-linking throug
23 ystrophy, which manifests as the spinal cord axonopathy adrenomyeloneuropathy (AMN) in nearly all mal
24 tations ranging from progressive spinal cord axonopathy [adrenomyeloneuropathy (AMN)] to severe demye
25 he HSPs, with clear relevance for other long axonopathies affecting peripheral nerves and lower motor
26 xonal degeneration in peripheral and central axonopathies and to provide a transformational disease-m
27 egeneration and brain dysfunction by causing axonopathy and conserved transcriptomic signature found
28 neuronal death, peripheral neuropathies like axonopathy and demyelination).
29                  Spinal MNs developed distal axonopathy and formed ubiquitinated inclusions and degen
30 d1(D83G/D83G) mice also phenocopy the distal axonopathy and hepatocellular carcinoma found in Sod1 nu
31 le D2 overexpression was sufficient to cause axonopathy and inhibit mitochondria motility, reduction
32          Chronic demyelination can result in axonopathy and is associated with human neurological con
33 e for treatment of diseases characterized by axonopathy and neurodegeneration.
34 y: reversible neurotoxicity characterized by axonopathy and recovery, and irreversible neurotoxicity
35 The most sensitive indicator of toxicity was axonopathy and secondary myelin changes accompanied by a
36 ailure of the ER-endosome contact process in axonopathy and suggest that coupling of ER-mediated endo
37 60 HAT activity in the nervous system causes axonopathy and transport defects associated with epigene
38  a rapidly progressive diffuse sensory motor axonopathy, and electroencephalogram findings progressed
39                                              Axonopathies are a group of clinically diverse disorders
40                 Axonal transport defects and axonopathy are prominent in early preclinical stages of
41 axonal autophagy as a possible mechanism for axonopathy associated with neurodegeneration.
42 more, we determine pathways specific to each axonopathy by analyzing the difference of the axonopathy
43   Neuroaxonal dystrophy (NAD), a distinctive axonopathy characterized by dramatic swelling of preterm
44 CHMP2B also develop an early and progressive axonopathy characterized by numerous amyloid precursor p
45       Unbiased characterization of inherited axonopathy disease modules will provide novel candidate
46                                    Inherited axonopathies display an extreme degree of genetic hetero
47 reliminary evidence that DTS can distinguish axonopathy from other processes such as inflammation, ed
48                                        Giant axonopathy (gaxp), an autosomal recessive mouse mutation
49                    Spastin is mutated in the axonopathy hereditary spastic paraplegia.
50 hickness and abnormal extramyelin loops) and axonopathy (i.e., altered neurofilament phosphorylation,
51 ivator of sGC, potently inhibited NO-induced axonopathy (IC(50) = 3 microM).
52 sence of the Wld(S) mutation ameliorates the axonopathy, implying a Wallerian degeneration-like patho
53  analysis of nerve sections, we characterize axonopathies in the phrenic and hypoglossal (XII) nerves
54  of molsidomine-prevents vincristine-induced axonopathy in both motor and sensory neurons without com
55 otif containing 1 (SARM1) is responsible for axonopathy in CIPN.
56                                          The axonopathy in CMT2A is caused by mutations in Mitofusin
57           We demonstrate a progressive motor axonopathy in these mice and show that Sod1(-/-) primary
58 ation in human cell cultures and ameliorates axonopathy in zebrafish, via its interaction with SOD1 t
59 human cell cultures and promotes synergistic axonopathy in zebrafish.
60                              Thus, the "long axonopathy" in early-onset SPG3A may result from abnorma
61 holds great promise for neural repair of CNS axonopathies, including glaucoma.
62   Neuroaxonal dystrophy (NAD), a distinctive axonopathy involving distal axons and synapses, represen
63  of corneas was performed with antibodies to axonopathy marker SMI-32.
64                       This Mutation in NAMPT Axonopathy (MINA) syndrome is the first human hereditary
65 xonopathy by analyzing the difference of the axonopathy modules.
66 s: adrenomyeloneuropathy, a non-inflammatory axonopathy mostly in adults, and an intensely inflammato
67 ilament may contribute to the distal sensory axonopathy observed in diabetes.
68  organization and function contribute to the axonopathies of myelin and other neurologic disorders.
69  to treat neurodegeneration characterized by axonopathies of the peripheral and central nervous syste
70 weakness and spasticity and length-dependent axonopathy of corticospinal motor neurons.
71 mity spasticity, owing to a length-dependent axonopathy of corticospinal motor neurons.
72 akness due to a length-dependent, retrograde axonopathy of corticospinal motor neurons.
73 akness due to a length-dependent, retrograde axonopathy of corticospinal motor neurons.
74 es that induce human paralysis due to severe axonopathy of large neurons.
75 ogical hallmark is a length-dependent distal axonopathy of nerve fibers in the corticospinal tract.
76 s characterized by a length-dependent distal axonopathy of the corticospinal tracts, resulting in low
77 e genetic conditions characterized by distal axonopathy of the longest corticospinal tract axons, and
78 ins and pathways likely central to inherited axonopathy pathogenesis, including protein processing in
79                             The finding that axonopathy precedes soma loss resembles pathology observ
80 rapy approach for traumatic and degenerative axonopathies, prevented axonal beading, while destabiliz
81 ry spastic paraplegia, which is a retrograde axonopathy primarily characterized pathologically by the
82 nd supports the role of NTE abnormalities in axonopathy produced by neuropathic OP compounds.
83  suggest that ALS2 is predominantly a distal axonopathy, rather than a neuronopathy in the central ne
84                                    Inherited axonopathies represent a spectrum of disorders unified b
85                             However, whether axonopathy represents an early pathogenic event or an ep
86 ts directly implicate a reticulon protein in axonopathy, show that this protein participates in a net
87  and behavioral effects of aging, as well as axonopathies such as multiple sclerosis, Alzheimer's dis
88                 In an animal model of distal axonopathy, systemic EPO administration prevents axonal
89 , we investigate 'gene modules' in inherited axonopathies through a network-based analysis of the Hum
90 environmental toxicants can result in distal axonopathies through reaction with various components of
91 deficiency causes an early-onset progressive axonopathy, which we also observe in global and tamoxife
92 ce lacking the KLC1 protein (KLC1-/-) led to axonopathies with cytoskeletal disorganization and abnor
93 ing, dysmorphic facies, optic atrophy, leuko-axonopathy with hypomyelination, and neurodegenerative f
94 m of predominantly motor distal neuronopathy/axonopathy with mild to moderate sensory involvement tha
95                      Kernicterus presents as axonopathy with myelination deficits at different brain
96 umn dysfunction, and is considered a primary axonopathy with secondary demyelination.
97 ted intraepidermal nerve fibers and produced axonopathy, with a secondary disruption in myelin struct
98 , which have been implicated in HSP, lead to axonopathy within the corticospinal tract, but it remain
99                     Synaptic dysfunction and axonopathy would thus be the hallmark of presymptomatic
100 The hallmark of vincristine neurotoxicity is axonopathy, yet its underpinning mechanisms remain uncer