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1 layed oligodendrocyte maturation, leading to dysmyelination.
2 (LPS) administration to mothers and eventual dysmyelination.
3 ropathy mice that cannot be accounted for by dysmyelination.
4 posed regarding how the lack of QKI leads to dysmyelination.
5 everity from early embryonic death to viable dysmyelination.
6     Loss of mature OLs results in severe CNS dysmyelination.
7 ity, and its absence leads to late-onset CNS dysmyelination.
8 eurodevelopmental disorders characterized by dysmyelination.
9 ratum oriens SST cells display severe axonal dysmyelination and a reduced excitability.
10              Loss of OPTN led to progressive dysmyelination and axonal degeneration through engagemen
11           Failure in this interaction causes dysmyelination and axonal degeneration.
12 rized by severe central nervous system (CNS) dysmyelination and demyelination, a conspicuous action t
13 m in the MD rat at this age showed extensive dysmyelination and downregulation of NMDA and to a lesse
14 Thus, Mtmr13(-/-) mice show both the initial dysmyelination and later degenerative pathology of CMT4B
15 phological studies show evidence for primary dysmyelination and myelin instability in affected animal
16 avan disease, neuroimaging shows early-onset dysmyelination and progressive brain atrophy.
17 lin basic protein that results in severe CNS dysmyelination and subsequent demyelination during devel
18 ssive pathology in the PNS, characterized by dysmyelination and swelling of the periaxonal space at t
19                          The consequences of dysmyelination are poorly understood and vary widely in
20 deficient (md) rats, which have profound CNS dysmyelination associated with oligodendrocyte cell deat
21 lipid protein and is characterized by severe dysmyelination attributable to oligodendrocyte death.
22 stribution of other myelin proteins, causing dysmyelination, axonal damage, or both.
23 integrity of macromolecules such as myelin ('dysmyelination') can be studied by applying multiple mod
24 ology, indicated a complex disease involving dysmyelination, demyelination and axonal degeneration.
25 rs persist after oligodendrocyte cell death; dysmyelination does not alter the expression of differen
26 mpanied by peripheral neuropathy and central dysmyelination has been recognized recently in associati
27 ng with life-threatening cerebral oedema and dysmyelination in affected individuals.
28 aracterized by severe central nervous system dysmyelination in affected males, and myelin mosaicism i
29  in oligodendrocytes results in differential dysmyelination in specific areas of the CNS, with the gr
30 hibit delayed axon myelination and increased dysmyelination in the central nervous system.
31 normal numbers of Schwann cells and profound dysmyelination in the central nervous system.
32  in muscle degeneration and peripheral nerve dysmyelination in the dy2J dystrophic mouse.
33 nctive patterns of axon degeneration and de-/dysmyelination in the neurodegenerative brain, highlight
34  that underlie oligodendroglial deficits and dysmyelination in the progression of the disease, highli
35 d reveal key insights into the mechanisms of dysmyelination in the quakingviable mutant.
36                    Our findings suggest that dysmyelination in visual processing regions is present i
37                                              Dysmyelination is evident in Mtmr13-deficient nerves at
38                         We conclude that: 1) dysmyelination is less severe in the shk PNS than in the
39                                 In addition, dysmyelination led to a decreased synaptic quantal conte
40         St3gal2/3 double-null mice displayed dysmyelination marked by a 40% reduction in major myelin
41  associated with both peripheral and central dysmyelination may affect pathology through a dominant-n
42                            In conclusion, AN dysmyelination may be of fundamental importance in audit
43 n in Schwann cells leads to hypermyelination/dysmyelination, mimicking some features present in neuro
44     quaking (qk), one of the classical mouse dysmyelination mutants, is defective for the expression
45        Quakingviable (qk(v)) is a well known dysmyelination mutation.
46 myelin-deficient rats, which have severe CNS dysmyelination, node-like clusters of Kv3.1b and Na+ cha
47 litis (EAE), in contrast with the non-lethal dysmyelination observed in Galc-ablated mice without the
48 ical disorders, in which complete or partial dysmyelination occurs in either the central nervous syst
49 analysis of the sciatic nerve showed de- and dysmyelination of fibers, with massive outfoldings and a
50    We documented that Msh2 deficiency causes dysmyelination of the axonal projections in the corpus c
51 MD) is an X-linked disorder characterized by dysmyelination of the central nervous system (CNS) cause
52 ed genetic disorder that is characterized by dysmyelination of the central nervous system resulting p
53 sive neurological mouse mutation with severe dysmyelination of the CNS and spermiogenesis failure.
54 ng Evans shaker (les) rat that causes severe dysmyelination of the CNS.
55 ults suggest that the primary abnormality is dysmyelination of the optic nerve in early development.
56 n events along the nerve trunk but developed dysmyelination of the preterminal segment associated wit
57  results indicate a class-specific effect of dysmyelination on the excitability of hippocampal intern
58       Previous observations of the effect of dysmyelination or demyelination on axonal survival in th
59 le for the severe reduction of MBPs in qk(v) dysmyelination, presumably because of the lack of intera
60 the white matter of FCD IIb was related to a dysmyelination process associated with severe fiber loss
61 attenuated injury-induced ROS production and dysmyelination processes of peripheral nerves.
62  quakingviable mutants, which display severe dysmyelination, QKI-6 and QKI-7 are absent exclusively f
63 cks large diameter axons, suggesting primary dysmyelination, rather than a demyelinating process.
64  spike upstroke and downstroke kinetics, but dysmyelination reduces the after-depolarization and enha
65 nd genetic mouse models of demyelination and dysmyelination, respectively, we find that loss of compa
66 regulation of sphingolipid synthesis, severe dysmyelination results.
67 h we can begin to understand the early onset dysmyelination seen in patients with R98C and similar mu
68 ding poor growth, developmental delay, brain dysmyelination, sensorineural hearing loss, nystagmus, p
69 also reveal significantly less demyelination/dysmyelination than in the null alleles.
70 fatal, connatal disease, including extensive dysmyelination, tremors, ataxia, and death at approximat
71    We compare mice with different degrees of dysmyelination using acute multiunit recordings in the a
72 n and blood-brain barrier disruption without dysmyelination were the major neuropathological alterati
73 o normal birth weight, growth failure, brain dysmyelination with calcium deposits, cutaneous photosen
74 o-normal birth weight; growth failure; brain dysmyelination with calcium deposits; cutaneous photosen
75 w, GJC2 mutations were only thought to cause dysmyelination, with primary expression of Cx47 limited