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1 ons may contribute to the pathophysiology of cerebellar degeneration.
2 rning of individuals with severe ataxia from cerebellar degeneration.
3 volved in the pathogenesis of paraneoplastic cerebellar degeneration.
4  motor incoordination because of progressive cerebellar degeneration.
5 sponse to visuomotor training in people with cerebellar degeneration.
6 ward control with spared feedback control in cerebellar degeneration.
7 in EMC1 lead to neurodevelopmental delay and cerebellar degeneration.
8 y postural abnormalities, motor deficits and cerebellar degeneration.
9 ectrin causes progressive motor deficits and cerebellar degeneration.
10 l dominant spinocerebellar ataxias (SCAs) is cerebellar degeneration.
11 essive cerebellar ataxia and marked isolated cerebellar degeneration.
12 the anti-Tr immune response in patients with cerebellar degeneration.
13 n improve motor performance of patients with cerebellar degeneration.
14 neuronal excitability in the pathogenesis of cerebellar degeneration.
15 fferent cell types to fully recapitulate the cerebellar degeneration.
16 ere described 10 years ago in paraneoplastic cerebellar degeneration.
17 ce develop a strong ataxia in the absence of cerebellar degeneration.
18  mice exhibit neither Dpl overexpression nor cerebellar degeneration.
19 ssociated with tumor immunity and autoimmune cerebellar degeneration.
20 entified as an autoantigen in a patient with cerebellar degeneration.
21 ovarian and breast, can cause paraneoplastic cerebellar degeneration.
22  cognitive and motor dysfunctions arise from cerebellar degeneration.
23 clerosis, hereditary spastic paraplegia, and cerebellar degenerations.
24 otrophic lateral sclerosis (0.5%; n = 1) and cerebellar degeneration (0.5%; n = 1).
25     Twenty-five patients with paraneoplastic cerebellar degeneration (44%) had high titres of HuAb, f
26                                              Cerebellar degeneration, a hallmark of A-T, is character
27 in ataxia-telangiectasia, is associated with cerebellar degeneration, abnormal proliferation of small
28 ural-specific deletion of FIP200 resulted in cerebellar degeneration accompanied by progressive neuro
29 forward and feedback control associated with cerebellar degeneration across motor domains, we evaluat
30 of death of 65% HuAb positive paraneoplastic cerebellar degeneration and 10% HuAb negative paraneopla
31  training in 40 patients with mild to severe cerebellar degeneration and 40 age- and sex-matched heal
32 essive disorder characterized by progressive cerebellar degeneration and a greatly increased incidenc
33         A man in his 30s with paraneoplastic cerebellar degeneration and anti-Tr underwent treatment
34 esent a patient who developed paraneoplastic cerebellar degeneration and anti-Yo antibody response in
35 sidered in patients presenting with subacute cerebellar degeneration and anti-Yo antibody response in
36 eveloped neurological disease, and exhibited cerebellar degeneration and BG process loss.
37 with progressive loss of miRNAs, followed by cerebellar degeneration and development of ataxia.
38 ed normally but acquired severe ataxia, with cerebellar degeneration and gliosis.
39 e response is associated with paraneoplastic cerebellar degeneration and Hodgkin lymphoma (HL).
40  in a number of clinical symptoms, including cerebellar degeneration and increased cancer predisposit
41 , comparing the performance of patients with cerebellar degeneration and matched controls.
42            Nineteen human subjects with pure cerebellar degeneration and matched healthy controls wer
43 ion in human participants of both sexes with cerebellar degeneration and neurobiologically healthy co
44 we studied the cerebellum of 9 patients with cerebellar degeneration and of 9 age-matched normal cont
45                       SCA2 is accompanied by cerebellar degeneration and progressive motor decline.
46     Affected brain tissue showed substantial cerebellar degeneration and tau deposition.
47 oplastic encephalomyelitis, 1 paraneoplastic cerebellar degeneration, and 1 opsoclonus-myoclonus synd
48  with disrupted motor behaviors, progressive cerebellar degeneration, and abnormal auditory processin
49 elangiectasia-like disorder (ATLD) featuring cerebellar degeneration, and cancer-predisposition in ce
50 inemia of infancy, cardiac long QT syndrome, cerebellar degeneration, and certain ataxias.
51 bations of speech to show that patients with cerebellar degeneration are impaired in adapting feedfor
52 that the hemiplegic migraine attacks and the cerebellar degeneration are linked genetically and that
53 ikingly similar ocular motility findings and cerebellar degeneration are reported in both FHM and a g
54 teract observed target errors, patients with cerebellar degeneration are surprisingly unable to compe
55 volves endosome dysfunction leading to early cerebellar degeneration, as well as later-onset cortical
56 spinal fluid of patients with paraneoplastic cerebellar degeneration associated with cancer of the ov
57 ibit three distinct defects: (1) progressive cerebellar degeneration associated with severe ataxia, (
58 rataxin (APTX) deficiency causes progressive cerebellar degeneration, ataxia and oculomotor apraxia i
59 ral forms of inherited SCAs characterized by cerebellar degeneration because of polyglutamine expansi
60 .1 restricted epitopes of the paraneoplastic cerebellar degeneration breast/ovarian cancer antigen cd
61 n did not alter the course of paraneoplastic cerebellar degeneration, but improved Lambert-Eaton myas
62                      Mutations in TG6 induce cerebellar degeneration by an unknown mechanism.
63 h the same tumour can develop paraneoplastic cerebellar degeneration by different immunological mecha
64 ssive, multisystem disorder characterized by cerebellar degeneration, cancer predisposition, and immu
65 nts afflicted with varying degrees of global cerebellar degeneration caused by hereditary, idiopathic
66 irments in male and female participants with cerebellar degeneration (CD) or Parkinson's disease (PD)
67 ent evidence has shown that individuals with cerebellar degeneration (CD) show a reduced reaction tim
68             Here, we tested individuals with cerebellar degeneration (CD), using sensory perturbation
69                     Focal rather than global cerebellar degeneration characterises ALS.
70 ffered from the HuAb negative paraneoplastic cerebellar degeneration cohort, HuAb positive patients w
71  that with vision of the hand, patients with cerebellar degeneration could also switch to an aiming s
72 t the C3H/HeSnJ inbred strain has late onset cerebellar degeneration due to this mutation.
73 ne expression and delayed ATXN1[82]-mediated cerebellar degeneration during mid-stage disease progres
74                     Second, individuals with cerebellar degeneration failed to modulate their behavio
75 s with presenting symptoms of paraneoplastic cerebellar degeneration for the presence of HuAb and P/Q
76 nine patients (16%) from both paraneoplastic cerebellar degeneration groups developed electrophysiolo
77 es from 5 other patients with paraneoplastic cerebellar degeneration, HL, and anti-Tr.
78 iectasia (A-T) is a genetic disorder causing cerebellar degeneration, immune deficiency, cancer predi
79 cessive disease characterized by progressive cerebellar degeneration, immunodeficiencies, genomic ins
80 omplex phenotype of A-T includes progressive cerebellar degeneration, immunodeficiency, gonadal atrop
81 asia (AT) is a recessive syndrome, including cerebellar degeneration, immunologic defects and cancer
82 enerative disease primarily characterized by cerebellar degeneration in children leading to motor imp
83                                    We tested cerebellar degeneration in human patients in a task desi
84  to the distinct ages of onset and timing of cerebellar degeneration in infant- and adult-onset SCA13
85 s of ATM protein is not sufficient to induce cerebellar degeneration in mice.
86  protein (PrPC) rescues doppel (Dpl)-induced cerebellar degeneration in mice.
87 r late onset SCA13, which typically produces cerebellar degeneration in middle age.
88 mal membrane permeabilization contributes to cerebellar degeneration in NPC disease.
89                Even though we found no gross cerebellar degeneration in older Atm(y/y) animals, ectop
90 ne whether gluten sensitivity contributes to cerebellar degeneration in patients with hereditary cere
91 expectedly poor performance by patients with cerebellar degeneration in visuomotor adaptation tasks.
92 xpression improves motor function and delays cerebellar degeneration, indicating that BK channels are
93                          This indicates that cerebellar degeneration is not primarily triggered by lo
94 APT is a subtype of SPT in which progressive cerebellar degeneration is the most symptomatic feature.
95 hanges functional brain networks affected by cerebellar degeneration is unknown.
96 isorder in which patients show a progressive cerebellar degeneration leading to ataxia, abnormal eye
97  with small-cell lung cancer, paraneoplastic cerebellar degeneration may occur with or without Hu ant
98  (ALC), 8 with (ACD) and 9 without alcoholic cerebellar degeneration (non-ACD).
99 ion does not mirror the localized pattern of cerebellar degeneration observed in tg(la) mice, providi
100                        Because patients with cerebellar degeneration often show substantial atrophy o
101  These results suggest there is an effect of cerebellar degeneration on primary auditory function.
102 ecifically, we examined the effect of global cerebellar degeneration on primary auditory sensory func
103 cal developments, focusing on paraneoplastic cerebellar degeneration, opsoclonus-myoclonus, and encep
104   In other disorders, such as paraneoplastic cerebellar degeneration or paraneoplastic sensory neuron
105 g the motor command in perturbed trials, and cerebellar degeneration participants were not.
106 ual information about hand position affected cerebellar degeneration patients (N = 12) and age-matche
107 eration and 10% HuAb negative paraneoplastic cerebellar degeneration patients (P < 0.001).
108 ddition, 20% of HuAb negative paraneoplastic cerebellar degeneration patients without clinically iden
109 tive and 20% of HuAb negative paraneoplastic cerebellar degeneration patients, the tumour was either
110 eral blood of two HLA-A2.1(+) paraneoplastic cerebellar degeneration patients.
111    For example, patients with paraneoplastic cerebellar degeneration (PCD) appear to suppress the gro
112 r described autoantibodies in paraneoplastic cerebellar degeneration (PCD) combined with Hodgkin lymp
113                    Except for paraneoplastic cerebellar degeneration (PCD) in HL and dermato/ polymyo
114                               Paraneoplastic cerebellar degeneration (PCD) is a disorder in which bre
115                               Paraneoplastic cerebellar degeneration (PCD) is believed to be an autoi
116 e pathogenesis of Yo-mediated paraneoplastic cerebellar degeneration (PCD) is unclear.
117                 Patients with paraneoplastic cerebellar degeneration (PCD) offer the opportunity to e
118                 Patients with paraneoplastic cerebellar degeneration (PCD) provide an opportunity to
119 n NPC1-deficient animals did not prevent the cerebellar degeneration phenotype, but further deteriora
120 n in the speech domain that individuals with cerebellar degeneration produce larger online correction
121 axis of CDR1as and its antisense transcript, cerebellar degeneration related protein 1 (CDR1).
122 sera was used previously to identify several cerebellar degeneration-related (cdr) genes encoding put
123                   We identified silencing of cerebellar degeneration-related 1 antisense (CDR1as), a
124 icted to thymic stromal cells that expressed cerebellar degeneration-related Ag 1 and lacked expressi
125 ochemical and cell-based assays, we identify cerebellar degeneration-related protein 2 (CDR2) and its
126 esults also show that to develop progressive cerebellar degeneration requires expressing ATXN1 with a
127 ts with Hodgkin's disease and paraneoplastic cerebellar degeneration resulted in the isolation of MAZ
128  characterized by ataxia, severe progressive cerebellar degeneration, seizures, uncontrollable moveme
129                                  People with cerebellar degeneration show characteristic ataxic motor
130 ich's ataxia as well as those with intrinsic cerebellar degeneration showed the above abnormalities,
131                  Furthermore, paraneoplastic cerebellar degeneration sometimes occurs in association
132  (Parkinson's disease, n = 9), patients with cerebellar degeneration [spinocerebellar ataxia (SCA) ty
133 ed with different cancers and paraneoplastic cerebellar degeneration suggests that several immunologi
134  how ATM deficiency leads to the early-onset cerebellar degeneration that is common in all individual
135 us animals, which show no signs of ataxia or cerebellar degeneration up to 2 years of age.
136          A-T is characterized by progressive cerebellar degeneration, variable immunodeficiency, and
137  of these disorders present with progressive cerebellar degeneration, whereas the third presents with
138                 Patients with paraneoplastic cerebellar degeneration who were HuAb positive were comp

 
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