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1 anded, causes spinocerebellar ataxia type 6 (SCA6).
2 ated, suggesting a potential new therapy for SCA6.
3 ential predictor of future motor deficits in SCA6.
4 motor dysfunction at a pre-clinical stage of SCA6.
5 inocerebellar ataxias: SCA1, SCA2, SCA3, and SCA6.
6               There are few animal models of SCA6.
7 .01] per additional SARA point; p=0.0195) in SCA6.
8 DnaJ-1 as a potential therapeutic target for SCA6.
9  with SCA3, and 0.80 (0.09) in patients with SCA6.
10  potential mechanism for the pathogenesis of SCA6.
11  adjacent to the genes for Cayman ataxia and SCA6.
12 e CACNA1A protein lead to PC degeneration in SCA6.
13 reached or exceeded the pathogenic range for SCA6.
14 d autosomal dominant spinocerebellar ataxia, SCA6.
15 ive oculomotor studies in four kindreds with SCA6.
16  its receptor tropomyosin kinase B (TrkB) in SCA6.
17 cant spinal cord differences were evident in SCA6.
18 ts, we examined the endo-lysosomal system in SCA6.
19 for the importance of early intervention for SCA6.
20             Nineteen human participants with SCA6 (13 woman) and 18 healthy controls performed fast g
21 etic ataxias were Friedreich's ataxia (22%), SCA6 (14%), EA2 (13%), SPG7 (10%) and mitochondrial dise
22 arly disease stage in a mouse model of SCA6 (SCA6(84Q/84Q)).
23 ing the more prevalent SCA1, SCA2, SCA3, and SCA6 along with SCA7 and SCA17 are caused by expansion o
24               Spinocerebellar ataxia type 6 (SCA6), an autosomal dominant, progressive disease, arise
25 cal stages of spinocerebellar ataxia type 6 (SCA6), an inherited neurodegenerative disease.
26 hus both a novel locus of pathophysiology in SCA6 and a promising therapeutic target.
27 rain barrier, is a promising therapeutic for SCA6 and argue for the importance of early intervention
28 ceptors, identifying coding variants between SCA6 and NA32 which could contribute to unique capacitie
29 ao genotypes (ICS1, WFT, Gu133, Spa9, CCN51, Sca6 and Pound7) to better understand their reactions to
30 on stomatal aperture in two cacao genotypes (SCA6 and Pound7) under varying light conditions.
31 1, WFT, Gu133 and Spa9) or resistant (CCN51, Sca6 and Pound7).
32             Spinocerebellar ataxias 6 and 7 (SCA6 and SCA7) are neurodegenerative disorders caused by
33 n about the steps leading to degeneration in SCA6 and the means to protect neurons in this disease ar
34 nalysis of the disease-resistant cacao clone SCA6 and the susceptible clone NA32 to characterize basa
35 ive genetic testing for SCA1, SCA2, SCA3, or SCA6 and with progressive, otherwise unexplained ataxia
36 1A, five with spinocerebellar ataxia type 6 (SCA6) and one with episodic ataxia type 2 (EA-2).
37 oral accuracy occurs in all individuals with SCA6, and can be explained by lesser temporal variabilit
38 proteins are also responsible for SCA1-SCA3, SCA6, and SCA17; however, the converging and diverging p
39 enes have been identified: SCA1, SCA2, SCA3, SCA6, and SCA7.
40 r, the pathophysiological changes underlying SCA6 are not fully understood.
41               Spinocerebellar ataxia type 6 (SCA6) belongs to the family of CAG/polyglutamine (polyQ)
42                Invertebrate animal models of SCA6 can expand our understanding of molecular sequelae
43                               Statistically, SCA6 clustered into two distinct groups for temporal var
44                     One hypothesis regarding SCA6 disease is that a CT fragment of the Cav2.1 channel
45                                     Notably, SCA6 exhibited stomatal opening in response to P. megaka
46  can be a potential therapeutic strategy for SCA6, here we created knockin mice that exclusively expr
47                                              SCA6 individuals exhibited lower temporal endpoint error
48 invariance and more severe ataxia than other SCA6 individuals.SIGNIFICANCE STATEMENT Variability is a
49                                              SCA6 is caused by abnormal expansion in a CAG trinucleot
50               Spinocerebellar ataxia type 6 (SCA6) is a neurodegenerative disease resulting in motor
51               Spinocerebellar ataxia type 6 (SCA6) is a rare disease that is characterized by cerebel
52               Spinocerebellar ataxia type 6 (SCA6) is linked to poly-glutamine (polyQ) within the C t
53 d (Q33) as in spinocerebellar ataxia type 6 (SCA6), is toxic to cells.
54 PCs in mice reveals that only CT-long causes SCA6-like symptoms, i.e., deficits in eyeblink condition
55      Suppression of CACNA1A IRES function in SCA6 may be a potential therapeutic strategy.
56 e found that the enlarged early endosomes in SCA6 mice accumulated both BDNF and TrkB.
57 osomal compartments in the Purkinje cells of SCA6 mice.
58 CA2 flies and modest protection in exercised SCA6 models, with no benefit to SCA3 flies.
59  the P/Q-type channel is sufficient to cause SCA6 pathogenesis in mice and identifies EBC as a new di
60 ons in SCA6 patients, is associated with the SCA6 pathogenesis.
61 l transport and function could contribute to SCA6 pathophysiology through alterations to BDNF-TrkB si
62 Our results showed that Ca(2+) channels from SCA6 patients display near-normal biophysical properties
63  human CT splice variants, as predicted from SCA6 patients, in PCs of mice using viral and transgenic
64 ically in cytosolic and nuclear fractions in SCA6 patients, is associated with the SCA6 pathogenesis.
65  (BDNF) is reduced in postmortem tissue from SCA6 patients.
66 defense-associated genes could contribute to SCA6's broad-spectrum disease resistance.
67 t an early disease stage in a mouse model of SCA6 (SCA6(84Q/84Q)).
68 1ACT, mutations in which are associated with SCA6, that controls expression of genes important for ce
69                             In patients with SCA6, the number of non-ataxia symptoms increased linear
70            In spinocerebellar ataxia type 6 (SCA6), there is evidence that individuals have greater f
71 , which could be critical for the ability of SCA6 to combat infection.
72 metric abnormalities in SCA1, SCA2, SCA3 and SCA6 using a large multisite MRI dataset.
73               Spinocerebellar ataxia type 6 (SCA6) was recently identified as a form of autosomal dom
74 us, in this large study of motor features in SCA6, we provide novel evidence for the existence of sub
75 2006, 526 patients with SCA1, SCA2, SCA3, or SCA6 were enrolled.
76 tes the progressively degenerative nature of SCA6 when expressed in various fly tissues and the prese
77 sociated with spinocerebellar ataxia type 6 (SCA6), whereas MPc splices to an immediate stop codon, r
78 sive feature of SCA1, SCA2 and SCA3, but not SCA6, which can be captured using quantitative MRI.
79  the first Drosophila melanogaster models of SCA6, which express the entire human alpha1ACT protein w
80 cerebellar vermis tissue in a mouse model of SCA6, which revealed widespread dysregulation of genes a
81     We provide new evidence that a subset of SCA6 with greater loss of GM in cerebellum lobule VI exh