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1 tinated inclusions, recently relabelled the 'TDP-43 proteinopathies'.
2 previously identified protective allele for TDP-43 proteinopathy.
3 ding of TDP-43 is predicted to aggravate the TDP-43 proteinopathy.
4 lation and loss of RNA binding are linked to TDP-43 proteinopathy.
5 s splicing defect could potentially underlie TDP-43 proteinopathy.
6 fication of pathogenic mechanisms underlying TDP-43 proteinopathy.
7 protein quality control is a risk factor for TDP-43 proteinopathy.
8 s could mitigate disease in a mouse model of TDP-43 proteinopathy.
9 TDP-43 may contribute to the pathogenesis of TDP-43 proteinopathy.
10 describe a Drosophila melanogaster model of TDP-43 proteinopathy.
11 cultured cells recapitulates key features of TDP-43 proteinopathy.
12 MEM106B haplotype that is protective against TDP-43 proteinopathy.
13 ected underlying TAR DNA-binding protein 43 (TDP-43) proteinopathy.
14 th transactive response DNA binding protein (TDP-43) proteinopathy.
15 o facilitate its phosphorylation, as seen in TDP-43 proteinopathies.
16 in the pathogenesis of FTLD-TDP and related TDP-43 proteinopathies.
17 th progranulin, may contribute to disease in TDP-43 proteinopathies.
18 ion may be critical for halting or reversing TDP-43 proteinopathies.
19 ch could provide new therapeutic avenues for TDP-43 proteinopathies.
20 pitulating key neuropathological features of TDP-43 proteinopathies.
21 ation of alternative therapeutic targets for TDP-43 proteinopathies.
22 the underlying mechanisms of this and other TDP-43 proteinopathies.
23 rapeutic strategy for treating ALS and other TDP-43 proteinopathies.
24 hanges that recapitulate several features of TDP-43 proteinopathies.
25 igate mechanisms of disease in ALS and other TDP-43 proteinopathies.
26 and tamoxifen) in a FTLD-U mouse model with TDP-43 proteinopathies.
27 ajor cause for neurodegeneration in ALS with TDP-43 proteinopathies.
28 e therapy of neurodegenerative diseases with TDP-43 proteinopathies.
29 or therapeutic intervention in ALS and other TDP-43 proteinopathies.
30 or neurites are collectively referred to as TDP-43 proteinopathies.
31 generation disease mechanisms underlying the TDP-43 proteinopathies.
32 major pathology observed in IBMPFD and other TDP-43 proteinopathies.
33 , which may contribute to the progression of TDP-43 proteinopathies.
34 tulating a key biochemical characteristic of TDP-43 proteinopathies.
35 uction may be a valid therapeutic target for TDP-43 proteinopathies.
36 specific for pathologic inclusions in human TDP-43 proteinopathies.
37 ses may underlie the development of abnormal TDP-43 proteinopathies.
38 l class of neurodegenerative diseases called TDP-43 proteinopathies.
39 in transactive response DNA-binding protein (TDP-43) proteinopathies.
40 isease, 230 with synucleinopathies, 157 with TDP-43 proteinopathies, 144 with tauopathies and 59 with
41 s an active mediator of neurodegeneration in TDP-43 proteinopathies, a class of disorder that include
42 ducible rNLS8 transgenic (Tg) mouse model of TDP-43 proteinopathy and found striking differences in M
44 TDP-43 mutations, we established a model of TDP-43 proteinopathies by expressing fluorescently tagge
45 escuing several cytopathological features of TDP-43 proteinopathy by increasing the turnover of patho
46 ntly, the majority of the ALS cases are with TDP-43 proteinopathies characterized with TDP-43-positiv
49 pathogenic mutation in TDP-43 and show that TDP-43 proteinopathies do not display an astrocyte non-c
51 43 that is deposited in the vast majority of TDP-43 proteinopathies, implicating other unknown factor
52 eration and provides an opportunity to study TDP-43 proteinopathies in human neurons generated from p
53 HIPK2 activation positively correlates with TDP-43 proteinopathy in NEFH-tTA/tetO-hTDP-43DeltaNLS mi
54 s joined a growing list of diseases known as TDP-43 proteinopathies, in which this protein becomes mi
55 Our studies confirm that the spectrum of TDP-43 proteinopathies includes most cases of sporadic a
56 apitulates several salient features of human TDP-43 proteinopathies, including conversion from nuclea
57 system atrophy; and 4) TDP-43 lesions in two TDP-43 proteinopathies, including frontotemporal lobar d
58 the pathogenic mechanism of a broad array of TDP-43 proteinopathies, including frontotemporal lobar d
59 pport CDC7 as a novel therapeutic target for TDP-43 proteinopathies, including FTLD-TDP and amyotroph
60 odegenerative diseases collectively named as TDP-43 proteinopathy, including amyotrophic lateral scle
61 gest that the onset of cognitive deficits in TDP-43 proteinopathies is independent of TDP-43 inclusio
64 opsy-confirmed FTLD with tauopathy (n = 31), TDP-43 proteinopathy (n = 49), or AD (n = 26) with antem
65 smic accumulation, it has been proposed that TDP-43 proteinopathies originate from either a loss-of-f
66 ion response element DNA-binding protein 43 (TDP-43) proteinopathy patients while accounting for Alzh
67 opathological and clinical features of human TDP-43 proteinopathy, providing a powerful animal model
69 TDP-43-directed therapies for ALS or related TDP-43 proteinopathies, such as frontotemporal dementia.
70 accumulation of abnormal proteins including TDP-43 proteinopathy, tauopathy and alpha-synucleinopath
71 in tissues that are uniquely susceptible to TDP-43 proteinopathies.TDP-43 aggregation is linked to v
72 of cognitive deficits in FTLD-TDP and other TDP-43 proteinopathies; thus, the TDP-25 transgenic mice
73 developed a Caenorhabditis elegans model of TDP-43 proteinopathies to study the cellular, molecular,
74 d a Caenorhabditis elegans model of neuronal TDP-43 proteinopathy to specifically interrogate the con
75 vious studies of TAR DNA-binding protein 43 (TDP-43) proteinopathies to investigate TDP-43 as a candi
76 000 community participants, we observed that TDP-43 proteinopathy was very common, frequently mixed w
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