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1  loss, which is consistent with 'dying-back' neuronopathy.
2  leukoencephalopathy and of JCV granule cell neuronopathy.
3 utant FUS may contribute to dying-back motor neuronopathy.
4 in rats paralyzed with a virus-induced motor neuronopathy.
5 e subject (I. W.) with a large-fibre sensory neuronopathy.
6 nsions is a major cause of inherited sensory neuronopathy.
7 al partners in relation to unexplained motor neuronopathies.
8 ateral Sclerosis and distal hereditary motor neuronopathies.
9 predominantly or pure motor neuropathies and neuronopathies.
10 f late-onset ataxia, particularly if sensory neuronopathy and bilateral vestibular areflexia coexist.
11 on in the central nervous system, peripheral neuronopathy and diluted pigmentation in the 'pale tremo
12 otor phenotypes, muscle pathology, and motor neuronopathy and dramatically extended survival.
13 ical disorders such as JC virus granule cell neuronopathy and JC virus encephalopathy, and might also
14 distinct clinical entities: JCV granule cell neuronopathy and JCV encephalopathy.
15 ifocal leukoencephalopathy, JCV granule cell neuronopathy, and JCV encephalopathy.
16     Childhood onset motor neuron diseases or neuronopathies are a clinically heterogeneous group of d
17                               Paraneoplastic neuronopathies are presumed to be the result of an autoi
18 s group of disorders, paraneoplastic sensory neuronopathies are the most frequent; many of these pati
19 This syndrome resulted from JCV granule cell neuronopathy associated with a novel JCV mutation.
20 ical continuum of predominantly motor distal neuronopathy/axonopathy with mild to moderate sensory in
21 dition to the core CANVAS phenotype (sensory neuronopathy, cerebellar syndrome and vestibular impairm
22 s, selected based on the presence of sensory neuronopathy confirmed by EMG.
23 mutated in one dominant form of distal motor neuronopathy (DHMN7A).
24                      Distal hereditary motor neuronopathies (dHMNs) are a clinically and genetically
25 manifested predominantly as subacute sensory neuronopathy did not improve after prednisone treatment
26 ated with JCV infection include granule cell neuronopathy, encephalopathy, and meningitis.
27 n dysfunction occurs in a variety of sensory neuronopathies for which there are currently no satisfac
28 indings of a case of cerebellar granule cell neuronopathy (GCN), a JCV-associated CNS disease, so far
29 al leukoencephalopathy (PML) or granule cell neuronopathy (GCN).
30 ravel the mechanisms underpinning peripheral neuronopathy in autosomal recessive polymerase gamma-rel
31 ominantly a distal axonopathy, rather than a neuronopathy in the central nervous system of the mouse
32 suggest that neurodegeneration may occur as "neuronopathy" in patients with ALS-FTD.
33 h multiple sclerosis exhibit primary retinal neuronopathy, in the absence of retrograde degeneration
34          Our results suggest that SBMA motor neuronopathy involves altered expression of VEGF, consis
35  the JC polyomavirus (JCV); JCV granule cell neuronopathy is caused by infection with a mutated form
36                   Since a sensory neuropathy/neuronopathy is identified in all patients with genetica
37                                   Peripheral neuronopathy is often part of the clinical syndrome and
38 rmining the likelihood a given neuropathy or neuronopathy is related to an underlying malignancy.
39 to call this novel syndrome JCV granule cell neuronopathy (JCV GCN).
40 ne defect underlying late onset spinal motor neuronopathy (LOSMoN/SMAJ; Online Mendelian Inheritance
41 enance in motoneurons from progressive motor neuronopathy mutant mice, a mouse model of motoneuron di
42 euronal nuclear antibody type 1 with sensory neuronopathy (n = 7), K(+)-channel antibody with limbic
43 ellar degeneration or paraneoplastic sensory neuronopathy, neither removal of the autoantibody nor tr
44 ve implications for the treatment of sensory neuronopathies of diverse etiologies.
45             First, some PNSs such as sensory neuronopathy or Lambert-Eaton myasthenic syndrome rarely
46 his, the molecular mechanisms underlying the neuronopathy remain to be elucidated and treatment strat
47 xb) into Hexb-deficient mice, a model of the neuronopathy Sandhoff disease.
48 quent motor neuron involvement and different neuronopathy subtypes.
49 re syndrome (8%) and mixed motor and sensory neuronopathy syndromes (20%, only in SLC52A2 patients).
50              In most cases of familial motor neuronopathy, the disease is caused by either gain-of-ad
51                      Mixed motor and sensory neuronopathy was observed in 19% of patients.
52                Unexpected discovery of motor neuronopathy, which may be useful for the definition of