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1 s a promising therapeutic target for Machado-Joseph disease.
2 ng is beneficial in animal models of Machado-Joseph disease.
3 roprotective therapeutic approach in Machado-Joseph disease.
4 causes the neurodegenerative disease Machado-Joseph disease.
5 biquitinating enzyme associated with Machado-Joseph disease.
6 peat (SSR) variation associated with Machado-Joseph disease.
7 torubral-pallidoluysian atrophy, and Machado-Joseph disease.
8 ibuprofen treatment would alleviate Machado-Joseph disease.
9 utant ataxin-3, the genetic cause of Machado-Joseph Disease, also contains an expanded CAG repeat.
10 d longevity in a Drosophila model of Machado-Joseph disease and effectively reduced aggregated ATXN3
11 ially promising therapeutic drug for Machado-Joseph disease and possibly other neurological proteinop
13 ar ataxia type-3 (SCA3), also called Machado-Joseph disease, and is cleaved in mammalian cells, trans
14 induces neuroprotection, alleviating Machado-Joseph disease-associated neuropathology and motor impai
15 ch correlated with preservation from Machado-Joseph disease-associated neuropathology, namely reducti
16 ebellar ataxia type 3, also known as Machado-Joseph disease, causes dendritic and synapse loss in cul
18 d neurotoxic protein (MJDtr78Q; MJD, Machado-Joseph disease) in the major timeless (tim)-expressing c
21 g Jews of North African descent, and Machado-Joseph disease is particularly frequent in Yemenite Jews
23 ataxia type 3 (SCA3), also known as Machado-Joseph disease, is reported to be the most common type o
24 eatment of symptomatic patients with Machado-Joseph disease may require cell replacement, which we in
25 ntation into the cerebellum of adult Machado-Joseph disease mice, cerebellar neural stem cells differ
39 ncy of SCA2 compared with SCA1, SCA3/Machado-Joseph disease (MJD), and dentatorubropallidoluysian atr
41 repeat expansion SCAs, such as SCA3/Machado-Joseph disease (MJD), and rare SCAs that are caused by n
42 ataxia type 3 (SCA3), also known as Machado-Joseph disease (MJD), is an autosomal-dominant neurodege
43 in patients of Japanese descent with Machado-Joseph disease (MJD), it was reported that disease allel
45 ier of the molecular pathogenesis of Machado-Joseph disease (MJD), the most common autosomal dominant
50 lts in spinocerebellar ataxia type 3/Machado-Joseph disease, one of the nine polyglutamine neurodegen
53 Additionally, neural cultures of Machado-Joseph disease patients' induced pluripotent stem cells-
54 Spinocerebellar ataxia type 3 (SCA3)/Machado Joseph disease results from expansion of the polyglutami
55 Spinocerebellar ataxia type-3 or Machado-Joseph disease (SCA3/MJD) is a member of the CAG/polyglu
56 bed in spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), an autosomal dominant ataxia
57 ebellar ataxia type 3, also known as Machado-Joseph disease (SCA3/MJD), is one of at least eight inhe
58 ein in spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), or an unrelated green fluores
59 In spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), the expanded cytosine adenine
60 ebellar ataxia type 3, also known as Machado-Joseph disease (SCA3/MJD), we show that the disease prot
63 that exclusively silenced the mutant Machado-Joseph disease/spinocerebellar ataxia type 3 allele whil
64 del of spinocerebellar ataxia type 3/Machado-Joseph disease that includes a biomarker stage character
66 m cells into the cerebellum of adult Machado-Joseph disease transgenic mice and assessed the effect o