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1 d 34 years) and labelled as having 'juvenile parkinsonism'.
2 nd 16 [3.5%] of multiple system atrophy with parkinsonism).
3 Bank criteria, without exclusion of familial parkinsonism.
4 tients with Gaucher disease with and without parkinsonism.
5 erated in cortical-basal ganglia circuits in parkinsonism.
6 he study of progressive neurodegeneration in parkinsonism.
7 ing of iMSNs characterize symptomatic rodent parkinsonism.
8 lear, is essential to understand its role in parkinsonism.
9 erturbed endosomal cargo sorting in atypical parkinsonism.
10 nition of patients with Gaucher disease with parkinsonism.
11 (DAT) cause a syndrome of infantile dystonia/parkinsonism.
12 he development of familial manganese-induced parkinsonism.
13 ulness as a diagnostic tool in patients with parkinsonism.
14 in a 6-hydroxydopamine (6-OHDA) rat model of parkinsonism.
15 ive diseases of the motor system or atypical parkinsonism.
16 eurological deficits, including dystonia and parkinsonism.
17 ltiple deletions, and altered mitophagy with parkinsonism.
18 w-up, patients were assessed for dementia or parkinsonism.
19 logous to some symptoms reported in INCL and parkinsonism.
20 ting the pathological firing associated with parkinsonism.
21 ning mitochondrial integrity and suppressing Parkinsonism.
22 erns include the potential for akathisia and Parkinsonism.
23 the majority of autosomal recessive juvenile Parkinsonism.
24 ith autosomal recessive early-onset dystonia-parkinsonism.
25 te a role for PPTg in the pathophysiology of parkinsonism.
26 rders, including cerebral palsy and juvenile parkinsonism.
27 dentified in family members with adult-onset parkinsonism.
28 at higher risk to develop neurodegenerative parkinsonism.
29 nts in our case series presented symptoms of parkinsonism.
30 e mutations to neurodegenerative early-onset parkinsonism.
31 extrapyramidal clinical disorders, including parkinsonism.
32 ity and is implicated in the pathogenesis of parkinsonism.
33 model for co-morbid depressive disorder and parkinsonism.
34 have a role in LID severity in experimental Parkinsonism.
35 have been implicated in late-onset familial parkinsonism.
36 se positron emission tomography for atypical parkinsonism.
37 c intracellular GPR37 aggregates observed in parkinsonism.
38 e most common cause of recessively inherited parkinsonism.
39 ith iron accumulation and prominent dystonia-parkinsonism.
40 ease or earlier onset spasticity followed by parkinsonism.
41 igher incidence than women for most types of parkinsonism.
42 he network, is also affected in experimental parkinsonism.
43 mal recessive juvenile-onset and young-onset parkinsonism.
44 his pathway is compromised in a rat model of Parkinsonism.
45 n some cases of frontotemporal dementia with parkinsonism.
46 syndrome of infantile/juvenile dystonia and parkinsonism.
47 gerated throughout basal ganglia circuits in parkinsonism.
48 individuals classified as having subclinical parkinsonism.
49 ning is associated with an increased risk of parkinsonism.
50 0), a gene that is associated with recessive Parkinsonism.
51 role of the lysosome in the pathogenesis of parkinsonism.
52 AP) in a cohort of patients with early-stage parkinsonism.
53 re discovered to be associated with atypical parkinsonism.
54 .0%), 1 had amyotrophic lateral sclerosis in parkinsonism (0.2%), 1 had parkinsonism secondary to sur
55 the 2000 subcohort, we observed 28 cases of parkinsonism (10 with PD) during 22,307 person-years.
56 were 128 nondemented patients with new-onset parkinsonism (104 with PD, 11 with multiple system atrop
59 .6-22.2 and 15.0%, 12.5-17.6, respectively), parkinsonism (12.5%, 10.1-15.0), and seizures (20.3%, 17
60 , aripiprazole was also associated with more Parkinsonism (15 [17%] of 86 vs two [2%] of 81 participa
61 ssing TTBK1 and frontotemporal dementia with parkinsonism-17-linked P301L (JNPL3) tau mutant (TTBK1/J
62 severe form of SCS and controls in rates of parkinsonism (19% vs 17%; odds ratio, 1.09 [95% CI, 0.28
63 induced parkinsonism (6.6%), 11 had vascular parkinsonism (2.0%), 1 had amyotrophic lateral sclerosis
70 the 1990 subcohort, there were 182 cases of parkinsonism (84 of which were PD) during 57,052 person-
71 s of the disorder were identified, including parkinsonism (95.2% of patients), depression/apathy (71.
72 nit gene (ATP1A3) cause rapid-onset dystonia-parkinsonism, a rare movement disorder characterized by
73 more than 90 days, atypical or drug-induced parkinsonism, a Unified Parkinson's Disease Rating Scale
74 the clinical and pathological correlates of parkinsonism across birth cohorts in relation to critica
77 cts were classified as level I indeterminate parkinsonism and 4 more subjects as level II indetermina
78 n DCTN1; or a family history of the disease, parkinsonism and a mutation in DCTN1; or the presence of
80 K(+)-ATPase, cause both rapid-onset dystonia parkinsonism and alternating hemiplegia of childhood.
83 in 62 isolated individuals with early-onset parkinsonism and confirmed consanguinity followed by dat
87 f each individual to confirm the presence of parkinsonism and determine the type of synucleinopathy.
88 3,4-dihydroxyphenylalanine (DOPA)-responsive parkinsonism and drug-resistant gait and balance disorde
90 of Guam is a neurodegenerative disease with parkinsonism and early-onset Alzheimer-like dementia ass
92 involved in the onset of a familial form of parkinsonism and highlight the possibility of using enha
93 3 modifies age of onset for LRRK2 Gly2019Ser parkinsonism and informs disease-relevant translational
94 displaying clinical features of early-onset parkinsonism and intellectual disability identified a ap
95 c transmission, but its role in experimental Parkinsonism and l-DOPA responses has been neglected.
97 opathological subtypes: MSA with predominant parkinsonism and MSA with predominant cerebellar ataxia,
99 These alpha-synucleinopathies have in common parkinsonism and non-motor features including orthostati
100 le-onset movement disorder (including severe parkinsonism and nonambulation), mood disturbance, auton
101 We investigated trends in the incidence of parkinsonism and Parkinson disease (PD) by comparing dat
103 Our study suggests that the incidence of parkinsonism and PD may have increased between 1976 and
105 DAT binding for differentiating symptomatic parkinsonism and relevant tremor syndromes from neurodeg
106 hydropyridine-treated macaques with advanced parkinsonism and reproducible LID received a range of na
109 r neuropathies, spinal muscular atrophy with parkinsonism and the later stages can resemble amyotroph
110 o screened positive to determine the type of parkinsonism and the presumed proteinopathy using specif
111 f (18)F-FDG PET for diagnostic evaluation of parkinsonism and the promising role of (18)F-FDG PET for
112 To study how glucocerebrosidase impacts parkinsonism and to evaluate new therapeutics, we genera
113 s used to identify all persons who developed parkinsonism and, in particular, DLB or PDD from 1991 th
116 istinct association profiles for symptoms of parkinsonism and/or dementia, respectively, toward the 3
117 of gait is a major risk factor for falls in parkinsonism, and a source of disability to patients.
118 derivations of this) to identify subclinical parkinsonism, and association of risk estimates with MDS
119 sease include progressive autonomic failure, parkinsonism, and cerebellar ataxia leading to significa
121 of an endolysosomal genetic defect linked to Parkinsonism, and highlight the presence of alpha-synucl
122 c) Gaucher disease, two with and two without parkinsonism, and one patient with Type 2 (acute neurono
123 k for Lewy body accumulation, progression of parkinsonism, and PD, but not dementia, AD, neuritic pla
124 ; P = .004) loci were associated with global parkinsonism, and these associations remained after excl
125 nsorineural deafness, peripheral neuropathy, parkinsonism, and/or cognitive impairment, in most cases
126 nce to differentiate between PD and atypical parkinsonism (AP) in a cohort of patients with early-sta
127 are mutated in autosomal-recessive juvenile Parkinsonism (AR-JP) and work together in the disposal o
129 early onset of autosomal-recessive juvenile parkinsonism (AR-JP), although the mechanisms by which a
130 netic changes specific for X-linked dystonia-parkinsonism are common in the Philippines, the epigenet
131 esting that signs of depressive disorders in parkinsonism are related to altered stress vulnerability
134 revalence and genetic causes of dystonia and parkinsonism as well as radiological findings in the con
135 everal genes whose mutation causes inherited parkinsonism, as well as risk loci for sporadic PD.
136 disease, three frontotemporal dementia with parkinsonism associated with chromosome 17, three unclas
137 nant early amnesia and behavioural change or parkinsonism associated with the 'missing' +15 mutation
142 al DA-related disorders, including infantile parkinsonism, attention-deficit/hyperactivity disorder a
144 y, mutations in SLC30A10 that cause familial parkinsonism blocked the ability of the transporter to t
145 gression models to compare the incidences of parkinsonism, both overall and by cause (PD and secondar
146 algorithm to classify subjects with clinical parkinsonism but uncertain diagnosis based on the expres
147 discharge before and after the induction of parkinsonism by administration of MPTP (1-methyl-4-pheny
149 -localized manganese efflux transporter, and parkinsonism-causing mutations block its trafficking and
150 inant disorder characterized by weight loss, parkinsonism, central hypoventilation, and psychiatric d
151 of autonomic failure, levodopa-unresponsive parkinsonism, cerebellar ataxia and pyramidal symptoms.
153 ommon and disabling symptom in patients with parkinsonism, characterised by sudden and brief episodes
154 sociated with a distinct form of early-onset parkinsonism characterized by rapid and severe disease p
155 idered in families where amnesia or atypical parkinsonism coexists with behavioural disturbance early
157 ndividuals with multiple system atrophy with parkinsonism, dementia with Lewy bodies, and Parkinson d
158 sociated with amyotrophic lateral sclerosis, parkinsonism, dementia, and related neurodegenerative sy
161 e cause of the amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC), or Alzheimer's
162 i of amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia complex (PDC) exist in Japanese on
164 eurotoxins possibly responsible for atypical Parkinsonism/dementia clusters, via the consumption of e
167 Vanoxerine has been in clinical trials for Parkinsonism, depression and cocaine addiction but lacke
168 disorder characterised by clinical signs of parkinsonism, depression/apathy, weight loss, respirator
170 city of data on cognitive functioning before parkinsonism diagnosis, a stage at which patients may st
172 ort presented with classical infantile-onset parkinsonism dystonia, with one surviving into adulthood
175 redefined extrapyramidal movement disorders (parkinsonism, dystonia, tremor, chorea, and restless leg
176 sults in rapidly progressive childhood-onset parkinsonism-dystonia with distinctive brain magnetic re
180 the proof or exclusion of neurodegenerative parkinsonism, for its early and preclinical diagnosis, a
183 isease', 'Paradoxical kinesia', 'Psychogenic parkinsonism', 'Functional somatic syndromes', 'Chronic
185 analysis model to indicate that all forms of parkinsonism had elevated free-water in the substantia n
186 with Type 2 and Type 1 Gaucher disease with parkinsonism had reduced dopamine storage and dopamine t
187 rrelated the core features of DLB (dementia, parkinsonism, hallucinations, and fluctuations) with str
188 hich is mutated in some types of early-onset Parkinsonism, has been suggested as a regulator of the a
191 associated with a higher hazard of incident parkinsonism (hazard ratio [HR], 1.79; 95% CI, 1.37-2.33
192 Patients with multiple system atrophy with parkinsonism (hazard ratio, 10.51; 95% CI, 2.92-37.82) h
194 a well-known toxic agent causing symptoms of parkinsonism in employees of certain branches of industr
195 These findings suggest that the incidence of parkinsonism in general, and of PD in particular, decrea
197 type tag for which the median onset of LRRK2 parkinsonism in GG carriers was 12.5 years younger than
200 ss induced reversible symptoms that resemble parkinsonism in humans and in animal models raise the qu
202 ify incidence cases of PD and other types of parkinsonism in Olmsted County, Minnesota, from 1976 to
203 isorder years or decades before the onset of parkinsonism in people who develop Parkinson's disease.
204 ail to excrete Mn and may develop Mn-induced parkinsonism in the absence of exposure to elevated Mn.
206 romosome inactivation is the likely cause of parkinsonism in this heterozygous mutation carrier.
207 f PPTg in gait, developed a refined model of parkinsonism including partial loss of the PPTg with bil
209 en implicated in neurological disorders with parkinsonism, including Parkinson's disease and Dementia
211 y for the potential management of Mn-induced parkinsonism, including that occurring as a result of mu
215 excluding non-DLB dementias, especially when parkinsonism is the only "core feature" exhibited by the
216 ly believed to be a common cause of atypical parkinsonism, is now recognised as a range of motor and
217 h experiments in humans and animal models of Parkinsonism, it is unclear how the pattern regularizati
218 c lateral sclerosis and rapid-onset dystonia parkinsonism, knowledge of their contribution to motor n
220 MAPT gene cause frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), characte
221 rders, including frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), which is
223 ein bearing two frontotemporal dementia with Parkinsonism linked to chromosome 17 pathogenic mutation
224 d p.S170P), and frontotemporal dementia with parkinsonism linked to chromosome-17 (FTDP-17; n = 2; MA
226 ite recessive inheritance, X-linked dystonia-parkinsonism (Lubag disease) has also been described in
228 (multiple-system atrophy with predominantly parkinsonism [MSA-P], n = 9), cerebellar type MSA (MSA-C
229 (multiple-system atrophy with predominantly parkinsonism [MSA-P], n = 9), cerebellar type MSA (MSA-C
230 yndrome; they showed a combination of severe parkinsonism, near mutism, dysphagia with choking, verti
231 y), play a role in differential diagnosis of parkinsonism (not well), and investigate pathology under
232 most stringent published cut-off for subtle parkinsonism of three definitions examined (p=0.027).
233 individuals received a diagnosis of incident parkinsonism; of these, 57 (72.2%) received a diagnosis
235 st-stroke movement disorders can manifest in parkinsonism or a wide range of hyperkinetic movement di
236 found in patients with rapid-onset dystonia parkinsonism or alternating hemiplegia of childhood caus
237 tcomes were a quantitative measure of global parkinsonism or component measures of bradykinesia, rigi
240 patients manifested Perry syndrome, isolated parkinsonism, or a predominant behavioral variant of fro
241 mentia, psychiatric disturbances, associated parkinsonism, or an autosomal dominant disorder is prese
249 enes that are mutated in autosomal recessive parkinsonism, PINK1 and Parkin, normally work together i
250 2%), often in the context of Leigh syndrome; parkinsonism predominated in 13 adult patients (43%), am
251 , cause forms of frontotemporal dementia and parkinsonism, proving that dysfunction of tau is suffici
253 (PARK9) and characterized by juvenile-onset parkinsonism, pyramidal signs, and cognitive decline.
254 t nigral cell counts correlate strongly with parkinsonism ratings may explain discordant results betw
255 of childhood (AHC), and rapid-onset dystonia parkinsonism (RDP) are caused by mutations of Na(+),K(+)
256 lysis, we previously derived and validated a parkinsonism-related metabolic pattern (PRP) in nonhuman
257 significantly over 30 years in men for both parkinsonism (relative risk [RR], 1.17 per decade; 95% C
259 These results suggest that DJ-1-associated Parkinsonism results from excessive protein glycation an
260 or older, incidence rates increased for both parkinsonism (RR, 1.24 per decade; 95% CI, 1.07-1.44) an
261 eral sclerosis in parkinsonism (0.2%), 1 had parkinsonism secondary to surgery (0.2%), and 84 remaine
263 obable multiple system atrophy-of either the parkinsonism subtype (MSA-P) or the cerebellar ataxia su
264 dopaminergic neurons from the patients with parkinsonism, suggesting that noninhibitory small-molecu
265 patients (patients without neurodegenerative parkinsonism syndromes and normal SPECT imaging) were in
266 ased, prospective cohort study of idiopathic parkinsonism that included patients diagnosed between Ja
268 m of 10 years and monitored for the onset of parkinsonism, the onset of dementia, or death, until Jan
269 c nervous system function and often signs of parkinsonism; the neuropathological hallmark of MSA is g
271 d up until January 1, 2015, for the onset of parkinsonism through serial in-person examinations and c
273 the association of a severe DOPA-responsive parkinsonism together with DOPA-unresponsive gait disord
274 bute to the skewing of the sex prevalence of parkinsonism toward women in this country, warranting fu
275 e following search terms: Parkinson disease, parkinsonism, tremor, postural instability and gait diff
277 ncluded in vivo behavioral measures of motor parkinsonism using a validated nonhuman primate rating s
278 uding motor subtype (multiple system atrophy-parkinsonism versus multiple system atrophy-cerebellar a
279 ienced a more rapid decline in her gait with parkinsonism, visual difficulties with restricted vertic
282 e overall age- and sex-adjusted incidence of parkinsonism was lower in the 2000 subcohort (incidence
287 onally relevant morphological alterations in parkinsonism, we used a combination of light and electro
289 of DBS in the refined and standard model of parkinsonism were very different despite minimal behavio
290 ng of the pathways is altered in symptomatic parkinsonism, where iMSNs fire significantly more and ea
292 6) scores were each associated with incident parkinsonism, whereas the association with word learning
293 ke in 7 non-DLB subjects (3 with concomitant parkinsonism) who had normal (123) I-MIBG myocardial upt
295 s a cause of autosomal-recessive early-onset parkinsonism with a distinctive phenotype of rapid and s
296 syndrome (KRS), characterized by early-onset Parkinsonism with additional neurological features.
298 at kinase 2 (LRRK2) cause autosomal-dominant Parkinsonism with pleomorphic pathology including deposi
302 y are to determine the relationship of motor parkinsonism with the degree of injury to nigrostriatal
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