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1 epresents a promising therapeutic target for Machado-Joseph disease.
2 signalling is beneficial in animal models of Machado-Joseph disease.
3 as a neuroprotective therapeutic approach in Machado-Joseph disease.
4 , which causes the neurodegenerative disease Machado-Joseph disease.
5 3, a deubiquitinating enzyme associated with Machado-Joseph disease.
6 uence repeat (SSR) variation associated with Machado-Joseph disease.
7 I, dentatorubral-pallidoluysian atrophy, and Machado-Joseph disease.
8  whether ibuprofen treatment would alleviate Machado-Joseph disease.
9        Mutant ataxin-3, the genetic cause of Machado-Joseph Disease, also contains an expanded CAG re
10 increased longevity in a Drosophila model of Machado-Joseph disease and effectively reduced aggregate
11 a potentially promising therapeutic drug for Machado-Joseph disease and possibly other neurological p
12 nerative polyglutamine disease known both as Machado-Joseph disease and spinocerebellar ataxia type 3
13 cerebellar ataxia type-3 (SCA3), also called Machado-Joseph disease, and is cleaved in mammalian cell
14 ion and induces neuroprotection, alleviating Machado-Joseph disease-associated neuropathology and mot
15 nts, which correlated with preservation from Machado-Joseph disease-associated neuropathology, namely
16 spinocerebellar ataxia type 3, also known as Machado-Joseph disease, causes dendritic and synapse los
17                                Patients with Machado-Joseph disease exhibit significant motor impairm
18 -expanded neurotoxic protein (MJDtr78Q; MJD, Machado-Joseph disease) in the major timeless (tim)-expr
19                                              Machado-Joseph disease is a neurodegenerative disease wi
20                                              Machado-Joseph disease is caused by an expansion of a tr
21 ter among Jews of North African descent, and Machado-Joseph disease is particularly frequent in Yemen
22                Spinocerebellar ataxia type 3/Machado-Joseph disease is the most common autosomal domi
23 rebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease, is reported to be the most commo
24 ctive treatment of symptomatic patients with Machado-Joseph disease may require cell replacement, whi
25 transplantation into the cerebellum of adult Machado-Joseph disease mice, cerebellar neural stem cell
26                Huntington's disease (HD) and Machado Joseph Disease (MJD) are severe neurological dis
27 dentatorubral pallidoluysian atrophy (DRPLA) Machado-Joseph disease (MJD or SCA3) and SCA2.
28                                These include Machado-Joseph disease (MJD) and Huntington's disease (H
29 found to be dysregulated in blood samples of Machado-Joseph disease (MJD) carriers.
30                      Strikingly, we find the Machado-Joseph disease (MJD) class to be unappreciated n
31                                              Machado-Joseph disease (MJD) is a late-onset, progressiv
32                                              Machado-Joseph disease (MJD) is a neurodegenerative diso
33                                              Machado-Joseph disease (MJD) is a neurodegenerative diso
34                                              Machado-Joseph disease (MJD) is an autosomal dominant ne
35                                              Machado-Joseph disease (MJD) is an inherited neurodegene
36                                              Machado-Joseph disease (MJD) is one of at least six neur
37                                              Machado-Joseph disease (MJD) is the most common dominant
38                The neurodegenerative disease Machado-Joseph disease (MJD), also known as spinocerebel
39 e frequency of SCA2 compared with SCA1, SCA3/Machado-Joseph disease (MJD), and dentatorubropallidoluy
40 RPLA), spinocerebellar ataxia type 1 (SCA1), Machado-Joseph disease (MJD), and Friedreich ataxia.
41 ouped as repeat expansion SCAs, such as SCA3/Machado-Joseph disease (MJD), and rare SCAs that are cau
42 rebellar ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is an autosomal-dominant n
43 rformed in patients of Japanese descent with Machado-Joseph disease (MJD), it was reported that disea
44  (ATXN3), a deubiquitylase (DUB) involved in Machado-Joseph Disease (MJD), remains elusive.
45 nd modifier of the molecular pathogenesis of Machado-Joseph disease (MJD), the most common autosomal
46 ed protein in the neurodegenerative disorder Machado-Joseph disease (MJD).
47 ich attaches O-GlcNAc to target proteins, in Machado-Joseph disease (MJD).
48                                              Machado-Joseph disease (MJD; MIM 109150) is a late-onset
49 al data of 292 spinocerebellar ataxia type 3/Machado-Joseph disease mutation carriers.
50 T3) results in spinocerebellar ataxia type 3/Machado-Joseph disease, one of the nine polyglutamine ne
51                                              Machado-Joseph disease or spinocerebellar ataxia 3 (SCA3
52                                              Machado-Joseph disease or spinocerebellar ataxia type 3
53             Additionally, neural cultures of Machado-Joseph disease patients' induced pluripotent ste
54         Spinocerebellar ataxia type 3 (SCA3)/Machado Joseph disease results from expansion of the pol
55             Spinocerebellar ataxia type-3 or Machado-Joseph disease (SCA3/MJD) is a member of the CAG
56 n described in spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), an autosomal dominant
57 Spinocerebellar ataxia type 3, also known as Machado-Joseph disease (SCA3/MJD), is one of at least ei
58 ase protein in spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), or an unrelated green
59             In spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), the expanded cytosine
60 spinocerebellar ataxia type 3, also known as Machado-Joseph disease (SCA3/MJD), we show that the dise
61                                              Machado-Joseph disease (spinocerebellar ataxia type 3) (
62  dominant ataxias was high, particularly for Machado-Joseph disease (spinocerebellar ataxia type 3).
63 e siRNA that exclusively silenced the mutant Machado-Joseph disease/spinocerebellar ataxia type 3 all
64 aging model of spinocerebellar ataxia type 3/Machado-Joseph disease that includes a biomarker stage c
65 replacement and neuroprotective approach for Machado-Joseph disease therapy.
66 ural stem cells into the cerebellum of adult Machado-Joseph disease transgenic mice and assessed the