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1 d forms of superoxide dismutase 1 (linked to familial amyotrophic lateral sclerosis).
2 e role of mutant SOD1 in the pathogenesis of familial amyotrophic lateral sclerosis.
3 diseases," such as myofibrillar myopathy and familial amyotrophic lateral sclerosis.
4 tures of disease in this transgenic model of familial amyotrophic lateral sclerosis.
5 with mutations linked to autosomal dominant familial amyotrophic lateral sclerosis.
6 icals in motor neurons may be the culprit in familial amyotrophic lateral sclerosis.
7 velopment of novel therapeutic strategies in familial amyotrophic lateral sclerosis.
8 gain-of-function mechanism, to about 20% of familial amyotrophic lateral sclerosis.
9 sed life span in a transgenic mouse model of familial amyotrophic lateral sclerosis.
10 tia nigra degeneration in some patients with familial amyotrophic lateral sclerosis.
11 ene (SOD1) are found in 20% of kindreds with familial amyotrophic lateral sclerosis.
12 y be implicated in the pathogenesis of human familial amyotrophic lateral sclerosis.
13 patients with this mutation may suffer from familial amyotrophic lateral sclerosis.
14 , hereditary spastic paraplegia, and 1-2% of familial amyotrophic lateral sclerosis.
15 administration in patients with SOD1-related familial amyotrophic lateral sclerosis.
16 Mutations in SOD1 cause 13% of familial amyotrophic lateral sclerosis.
17 n, motor neuron and bone, and in one case of familial amyotrophic lateral sclerosis.
18 on in attenuating the disease progression of familial amyotrophic lateral sclerosis.
19 totemporal dementia, widening the concept of familial amyotrophic lateral sclerosis.
20 survival in a large cohort of patients with familial amyotrophic lateral sclerosis.
21 Cu/Zn-superoxide dismutase (SOD1) result in familial amyotrophic lateral sclerosis.
22 s implicated in the onset and progression of familial amyotrophic lateral sclerosis.
23 SOD1 are associated with autosomal dominant familial amyotrophic lateral sclerosis.
24 by TARDBP), are associated with sporadic and familial amyotrophic lateral sclerosis.
25 g virus as a viable therapy for this type of familial amyotrophic lateral sclerosis.
26 utase (SOD1) gene cause dominantly inherited familial amyotrophic lateral sclerosis.
27 the context of SOD1 evolutionary biology and familial amyotrophic lateral sclerosis.
28 iants of SOD1 that have been associated with familial amyotrophic lateral sclerosis.
29 ked to the fatal neurodegenerative disorder, familial amyotrophic lateral sclerosis.
31 ic of protein misfolding disorders including familial amyotrophic lateral sclerosis, a neurodegenerat
32 xide dismutase (SOD1) gene cause one form of familial amyotrophic lateral sclerosis, a progressive di
33 superoxide dismutase (SOD1) associated with familial amyotrophic lateral sclerosis all exhibited abe
34 ant superoxide dismutase-1 (SOD-1) linked to familial amyotrophic lateral sclerosis (ALS) against unf
35 is the most common mutation associated with familial amyotrophic lateral sclerosis (ALS) and frontot
36 f neuronal degeneration in both sporadic and familial amyotrophic lateral sclerosis (ALS) associated
37 morphology abnormalities occur in models of familial amyotrophic lateral sclerosis (ALS) associated
38 e (SOD1) are linked to motor neuron death in familial amyotrophic lateral sclerosis (ALS) by an uncle
39 Two decades after the discovery that 20% of familial amyotrophic lateral sclerosis (ALS) cases were
42 Cu,Zn-superoxide dismutase (SOD1) that cause familial amyotrophic lateral sclerosis (ALS) exhibit tox
45 OD1) gene cause motor neuron degeneration in familial amyotrophic lateral sclerosis (ALS) is unknown.
46 Cu/Zn superoxide dismutase (SOD1) linked to familial amyotrophic lateral sclerosis (ALS) make the mu
47 xome-wide rare variant analysis in unrelated familial amyotrophic lateral sclerosis (ALS) patients as
48 ismutase (SOD1) have been reported in 20% of familial amyotrophic lateral sclerosis (ALS) patients, t
49 .15.1.1) are responsible for a proportion of familial amyotrophic lateral sclerosis (ALS) through acq
50 used in sarcoma (FUS) gene cause a subset of familial amyotrophic lateral sclerosis (ALS), a fatal mo
51 utase (SOD1) gene produce an animal model of familial amyotrophic lateral sclerosis (ALS), a fatal ne
52 inherited degenerative neurological disease familial amyotrophic lateral sclerosis (ALS), a non-cell
53 uperoxide dismutase (SOD1) cause one form of familial amyotrophic lateral sclerosis (ALS), and metals
54 43 were recently identified in patients with familial amyotrophic lateral sclerosis (ALS), and TDP-43
55 rf72 gene represent the most common cause of familial amyotrophic lateral sclerosis (ALS), but the me
56 which corresponds to a mutation observed in familial amyotrophic lateral sclerosis (ALS), display pr
57 onds to a mutation that has been observed in familial amyotrophic lateral sclerosis (ALS), display pr
58 utosomal dominant neurodegenerative disorder familial amyotrophic lateral sclerosis (ALS), is a major
59 superoxide dismutase 1 (SOD1), which causes familial amyotrophic lateral sclerosis (ALS), self-propa
60 spirin in A4V apo-SOD1-a variant that causes familial amyotrophic lateral sclerosis (ALS)-delayed amy
78 th mutations corresponding to those found in familial amyotrophic lateral sclerosis (ALS; also known
79 human homolog ubiquilin 2 is associated with familial amyotrophic lateral sclerosis, also contributes
80 he C9orf72 gene are the most common cause of familial amyotrophic lateral sclerosis and frontotempora
81 repeat located at C9orf72 is associated with familial amyotrophic lateral sclerosis and frontotempora
82 sed in sarcoma gene have been shown to cause familial amyotrophic lateral sclerosis and fused in sarc
83 ns in superoxide dismutase cause a subset of familial amyotrophic lateral sclerosis and provoke progr
84 s localized in mitochondria of patients with familial amyotrophic lateral sclerosis and transgenic mo
85 ng superoxide dismutase mutations in causing familial amyotrophic lateral sclerosis are discussed, as
86 s of Cu/Zn-superoxide dismutase (SOD1) cause familial amyotrophic lateral sclerosis are not clearly u
87 he clinical characteristics of patients with familial amyotrophic lateral sclerosis arising from SOD1
88 ays an important role in the pathogenesis of familial amyotrophic lateral sclerosis associated with "
89 loci has been established for other forms of familial amyotrophic lateral sclerosis, but no new genes
90 A) develop a motor neuron disease similar to familial amyotrophic lateral sclerosis, but transgenic m
91 dismutase (SOD1) cause approximately 20% of familial amyotrophic lateral sclerosis by a toxic gain o
92 nalysed phenotype data for 141 index Italian familial amyotrophic lateral sclerosis cases (21 of Sard
93 ently reported to be responsible for ~40% of familial amyotrophic lateral sclerosis cases of European
96 ide dismutase gene responsible for a form of familial amyotrophic lateral sclerosis, delayed both dea
97 D and several of the mutants associated with familial amyotrophic lateral sclerosis (FALS) (Ala(4) --
98 e (SOD1) is the best characterized subset of familial amyotrophic lateral sclerosis (FALS) and accoun
99 proteins are the likely cause of SOD1-linked familial amyotrophic lateral sclerosis (fALS) and may be
100 ently been identified as causing a subset of familial amyotrophic lateral sclerosis (fALS) and more r
102 ought to cause approximately 20% of cases of familial amyotrophic lateral sclerosis (FALS) because it
103 Cu/Zn superoxide dismutase (SOD1) gene cause familial amyotrophic lateral sclerosis (FALS) by gain of
104 superoxide dismutase (CuZnSOD) cause 25% of familial amyotrophic lateral sclerosis (FALS) cases.
106 A) mutation found in patients who succumb to familial amyotrophic lateral sclerosis (FALS) develop a
109 ng C-terminal truncation mutations linked to familial amyotrophic lateral sclerosis (FALS) have begun
110 dismutase 1 (Cu/Zn-SOD1) mutants that cause familial amyotrophic lateral sclerosis (FALS) have heigh
114 tions in superoxide dismutase 1 (SOD1) cause familial amyotrophic lateral sclerosis (fALS) is propose
115 mutants lead to motor neuron degeneration in familial amyotrophic lateral sclerosis (FALS) is unknown
117 to the selective death of motor neurones in familial amyotrophic lateral sclerosis (FALS) remain inc
118 nt Cu,Zn-superoxide dismutase (SOD1)-related familial amyotrophic lateral sclerosis (FALS) results fr
119 tase (SOD1) account for approximately 20% of familial amyotrophic lateral sclerosis (FALS) through so
120 dismutase enzyme produce an animal model of familial amyotrophic lateral sclerosis (FALS), a fatal d
122 human Cu,Zn superoxide dismutase (SOD) cause familial amyotrophic lateral sclerosis (FALS), a fatal n
123 in Cu,Zn-superoxide dismutase (mtSOD1) cause familial amyotrophic lateral sclerosis (FALS), a neurode
124 s in Cu,Zn superoxide dismutase (SOD1) cause familial amyotrophic lateral sclerosis (FALS), a rapidly
125 gene have been linked to the pathogenesis of familial amyotrophic lateral sclerosis (FALS), yet the m
126 It has been reported that expression of familial amyotrophic lateral sclerosis (FALS)-associated
143 he RNA/DNA binding protein FUS are linked to familial amyotrophic lateral sclerosis (FALS); however,
144 n patients carrying SOD1 mutations linked to familial amyotrophic lateral sclerosis (fALS/SOD1).
145 ith inherited amyotrophic lateral sclerosis (familial amyotrophic lateral sclerosis, FALS) associated
146 es an overview of transgenic mouse models of familial amyotrophic lateral sclerosis, familial Alzheim
147 e (SOD1) cause the neurodegenerative disease familial amyotrophic lateral sclerosis from an as-yet-un
148 n some strains of transgenic mouse models of familial amyotrophic lateral sclerosis harbouring the G9
150 nts of SOD1 (A4V, G93R, and H48Q) that cause familial amyotrophic lateral sclerosis have been studied
151 e in survival in a transgenic mouse model of familial amyotrophic lateral sclerosis having a point mu
153 e (SOD1) protein is a pathologic hallmark of familial amyotrophic lateral sclerosis linked to mutatio
155 for investigating the peroxidase activity of familial Amyotrophic Lateral Sclerosis-linked SOD mutant
157 romyces cerevisiae of a broad range of human familial amyotrophic lateral sclerosis-linked SOD1 mutan
158 regation inhibitor (designated HTB1M) of two familial amyotrophic lateral sclerosis-linked SOD1 mutan
159 superoxide dismutase (SOD1) associated with familial amyotrophic lateral sclerosis may involve oxida
160 utation in our large cohort of patients with familial amyotrophic lateral sclerosis of Italian, Sardi
161 utants causing the neurodegenerative disease familial amyotrophic lateral sclerosis or Lou Gehrig's d
162 s in the membrane protein VAPB implicated in familial amyotrophic lateral sclerosis perturb a defined
163 We identified a shared property of these familial amyotrophic lateral sclerosis-related SOD1 vari
164 easuring the peroxidase activity of SOD1 and familial amyotrophic lateral sclerosis SOD1 mutants and
165 man superoxide dismutase I (SOD1) that cause familial amyotrophic lateral sclerosis (SOD1-G85R, which
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