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1 reduce lethality in two Drosophila models of polyglutamine disease.
2 nd indicate a novel therapeutic strategy for polyglutamine disease.
3 Drosophila models of Alzheimer's disease and polyglutamine disease.
4  ataxia type 2 (SCA2), an autosomal dominant polyglutamine disease.
5 assay that recapitulates several features of polyglutamine disease.
6 d neurodegeneration in a Drosophila model of polyglutamine disease.
7 es a new treatment strategy for HD and other polyglutamine diseases.
8 erones as a potential therapeutic target for polyglutamine diseases.
9  an important role in the pathophysiology of polyglutamine diseases.
10 is thus regarded as the most unstable of the polyglutamine diseases.
11 ons (NIIs), a hallmark of SBMA and the other polyglutamine diseases.
12 ng therapeutic strategies for this and other polyglutamine diseases.
13 clearance might underlie the pathogenesis of polyglutamine diseases.
14 ease, reminiscent of juvenile forms of other polyglutamine diseases.
15 and Parkinson's disease, prion disorders and polyglutamine diseases.
16 n DNA repair genes have wider effects in the polyglutamine diseases.
17 o altering the progression of this and other polyglutamine diseases.
18 l intervention in SBMA and potentially other polyglutamine diseases.
19 ing factor to Huntington's disease and other polyglutamine diseases.
20 RAN translation may also contribute to other polyglutamine diseases.
21  spinocerebellar ataxia type 8, and the nine polyglutamine diseases.
22  structure/function and neurodegeneration in polyglutamine diseases.
23 inal and bulbar muscular atrophy and related polyglutamine diseases.
24 r's disease, Spinomuscular Atrophy and other polyglutamine diseases.
25 sregulation is an important early feature of polyglutamine diseases.
26 ations for the pathogenesis and treatment of polyglutamine diseases.
27 mportant for unravelling the pathogenesis of polyglutamine diseases.
28 ction, a mechanism that may apply broadly to polyglutamine diseases.
29 onal dysfunction and/or neurodegeneration in polyglutamine diseases.
30 ecular pathogenesis of SCA1 as well as other polyglutamine diseases.
31 for histone deacetylase (HDAC) inhibitors in polyglutamine diseases.
32 e pathways may be effective for treatment of polyglutamine diseases.
33 enerative disorders, such as Alzheimer's and polyglutamine diseases.
34 diseases may be much broader than HD or even polyglutamine diseases.
35 mentia, Huntington's disease (HD), and other polyglutamine diseases.
36 rse neurodegenerative diseases including the polyglutamine diseases.
37 plicing may contribute to the progression of polyglutamine diseases.
38         Hsp70 is a potent suppressor of both polyglutamine disease and Parkinson's disease in Drosoph
39 arly, largely independent, manifestations of polyglutamine disease and suggests that additional epige
40 Ggamma is not a viable therapeutic target in polyglutamine disease and that overall proteasome functi
41 s affected in Huntington's disease and other polyglutamine diseases and by discerning whether gene ex
42 etic mechanism modulates age at onset across polyglutamine diseases and could extend to other repeat
43 omparing modifiers isolated in the models of polyglutamine diseases and in a Drosophila model of tauo
44 xpanded protein is a unifying feature of CAG/polyglutamine diseases and may be initiated or catalyzed
45 gest a therapeutic approach for treatment of polyglutamine diseases and provide the potential for yea
46  similar role for glial dysfunction in other polyglutamine diseases and SCAs.
47 findings may be relevant to the treatment of polyglutamine diseases and, perhaps, to other neurodegen
48 es-Alzheimer's disease, Parkinson's disease, polyglutamine diseases, and amyotrophic lateral sclerosi
49                                              Polyglutamine diseases are a class of dominantly inherit
50                                              Polyglutamine diseases are a family of neurodegenerative
51                                              Polyglutamine diseases are a family of nine neurodegener
52                                              Polyglutamine diseases are a major cause of neurodegener
53                                              Polyglutamine diseases are caused by an expanded glutami
54                                              Polyglutamine diseases are caused by CAG expansions in d
55       The current working hypothesis is that polyglutamine diseases are caused by misfolding and aggr
56                                              Polyglutamine diseases are dominantly inherited neurodeg
57                                              Polyglutamine diseases are inherited neurodegenerative d
58 ease, amyotrophic lateral sclerosis, and the polyglutamine diseases, are characterized by intracellul
59 roteins may also be present in the tissue of polyglutamine diseases as a result of frameshifting of t
60  loss of neurite outgrowth and cell death in polyglutamine diseases, as these phenotypes were partial
61 ew leads for therapeutic development for the polyglutamine diseases based on their efficacy in mammal
62 ention, and may provide broader insight into polyglutamine diseases beyond SCA3.
63 into the cell specificity of pathology for a polyglutamine disease by relating SCA7-induced retinal d
64 Ggamma could contribute to UPS impairment in polyglutamine diseases by suppressing the proteasomal ca
65                                              Polyglutamine diseases comprise a class of familial neur
66 damental unanswered question in the field of polyglutamine diseases concerns the pathophysiology of n
67                                          The polyglutamine diseases consist of nine neurodegenerative
68 iously observed in a Drosophila model of the polyglutamine disease Dentatorubral-pallidoluysian atrop
69 Here, we show that, in a mouse model for the polyglutamine disease dentatorubral-pallidoluysian atrop
70    Consistently, the recovery of lifespan in polyglutamine disease fly models by TERA/VCP/p97 corresp
71                                          For polyglutamine diseases generally, the findings support a
72 ociation with age at onset when grouping all polyglutamine diseases (HD+SCAs; p = 1.43 x 10(-5) ).
73 n the striatum of various knock-in models of polyglutamine diseases highlights the role of trans-acti
74                       Experimental models of polyglutamine disease implicate the nucleus in pathogene
75            This disease is unusual among the polyglutamine diseases in that it involves lower motor a
76                                              Polyglutamine diseases include at least nine neurodegene
77                                          The polyglutamine diseases include at least nine neurodegene
78  HSP27 is also found in cell models of other polyglutamine diseases, including Huntington disease as
79                                          The polyglutamine diseases, including Huntington's disease (
80 nisms of neurodegeneration in the CAG repeat polyglutamine diseases, including Spinal and Bulbar Musc
81                                              Polyglutamine diseases, including spinocerebellar ataxia
82                                The family of polyglutamine diseases is characterized by the presence
83  A key unanswered question in SCA3 and other polyglutamine diseases is the extent to which neurodegen
84                   A pathological hallmark of polyglutamine diseases is the presence of inclusions or
85                A hallmark of these so-called polyglutamine diseases is the presence of ubiquitylated
86 tment exists for the fatal neurodegenerative polyglutamine disease known both as Machado-Joseph disea
87 egenerative diseases such as Alzheimer's and polyglutamine diseases like Huntington's disease.
88 pendent manner, suggesting that pathology in polyglutamine disease may result from cellular depletion
89                                           In polyglutamine disease models, CHIP has been considered a
90  to the selective neurodegeneration in other polyglutamine diseases or not.
91                  These studies encompass the polyglutamine diseases, Parkinson's disease, Alzheimer's
92 ion for further studies as a therapeutic for polyglutamine diseases, particularly as it is an establi
93 ate a direct role of arginine methylation in polyglutamine disease pathogenesis.
94 P-43 function may play an unexpected role in polyglutamine disease pathogenesis.
95  normal aging processes might be involved in polyglutamine disease pathogenesis.
96                                       In all polyglutamine diseases, polyglutamine-expanded proteins
97 nally blocked versions of one substrate, the polyglutamine disease protein ataxin-3, and showed that
98 regulates the activity of a DUB, ataxin-3, a polyglutamine disease protein implicated in protein qual
99 t host protein context is the key arbiter of polyglutamine disease protein toxicity.
100                  Finally, studies of a third polyglutamine disease protein, ataxin-1, reveal unexpect
101                        Here we show that the polyglutamine disease protein, ataxin-3, binds and cleav
102 ations, and reporter assays to show that the polyglutamine disease protein, ataxin-3, interacts with
103  cell-based approaches we establish that the polyglutamine disease protein, ataxin-3, is a poly-ubiqu
104 eurodegeneration induced by human pathogenic polyglutamine disease protein.
105 ve effects produced by expression of a human polyglutamine disease protein.
106                                    Among the polyglutamine diseases, protein folding and histone acet
107 protein (VCP)/p97 directly binds to multiple polyglutamine disease proteins (huntingtin, ataxin-1, at
108    This heterogeneity may also extend to how polyglutamine disease proteins are handled by cellular p
109 he mechanisms of pathology for the family of polyglutamine disease proteins are unknown; however, rec
110 ial differential regulation by UBQLN2 of two polyglutamine disease proteins, huntingtin (HTT) and ata
111 s reveal a selective action of UBQLN2 toward polyglutamine disease proteins, indicating that polyglut
112 (UBQLN2) selectively interacts with specific polyglutamine disease proteins.
113 ng all conditions studied (DM1, DM2, C9-ALS, polyglutamine diseases), reduction of polyglutamine prot
114 e of these inclusions in the pathogenesis of polyglutamine diseases remains unclear.
115 l sclerosis/frontotemporal dementia and with polyglutamine diseases, respectively, localize to neurit
116 sed, the neurodegeneration in SCA1 and other polyglutamine diseases selectively involves a few neuron
117 orders, such as Alzheimer's, Parkinson's and polyglutamine diseases, share a common pathogenic mechan
118  contrast to this view, we show that, in the polyglutamine disease spinal and bulbar muscular atrophy
119  We have developed a transgenic model of the polyglutamine disease spinal and bulbar muscular atrophy
120 loss in the inherited ataxias, including the polyglutamine disease spinocerebellar ataxia type 3 (SCA
121 se pathogenesis to ubiquitin pathways in the polyglutamine disease spinocerebellar ataxia type 3 (SCA
122                                       In the polyglutamine disease spinocerebellar ataxia type 7 (SCA
123 ) as a candidate mediator of toxicity in the polyglutamine disease, spinocerebellar ataxia type 1 (SC
124 ns formed in a cell culture model of another polyglutamine disease, spinocerebellar ataxia type 3.
125 may be a common mechanism of pathogenesis in polyglutamine diseases such as Huntington disease and sp
126  a primary cause of cellular pathogenesis in polyglutamine diseases such as Huntington disease; the r
127  approach may be broadly applicable to other polyglutamine diseases such as Huntington's disease and
128                                           In polyglutamine diseases such as X-linked spinobulbar musc
129                  Conditional mouse models of polyglutamine diseases, such as Huntington's disease (HD
130 ults, together with recent findings in other polyglutamine diseases, suggest that CAG repeat expansio
131  primary site of protein aggregation in many polyglutamine diseases, suggesting a central role in pat
132 de a novel common pathomechanism in multiple polyglutamine diseases that is mediated by DNA repair fu
133                    In SCA1 and several other polyglutamine diseases, the expanded protein aggregates
134                                 In all known polyglutamine diseases, the glutamine expansion confers
135 e loss in neurons modeling neurodegenerative polyglutamine diseases through injury to a single primar
136 or class of neurodegenerative disorders, the polyglutamine diseases, to show reduced polyglutamine ag
137 fer toxicity to the mRNA and, in the case of polyglutamine diseases, to the encoded protein.
138 tion can be modeled by expressing pathogenic polyglutamine disease transgenes in Drosophila neurons i
139        Therefore, in HD, as well as in other polyglutamine diseases, tTG is unlikely to play a role i
140  Drosophila model for Huntington's and other polyglutamine diseases was used to screen for genetic fa
141  important development in the study of such "polyglutamine" diseases was the realization that merely
142     Using a Drosophila melanogaster model of polyglutamine disease, we show that directed expression
143 as allowed subclassification into translated polyglutamine diseases, which are due to CAG repeat expa
144 erstanding of the role of protein folding in polyglutamine disease with emerging evidence that altera
145 G repeats are often used to create models of polyglutamine diseases yet are very rare in humans where

 
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