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@ARTICLE{Traschuetz:156023,
author = {Traschuetz, Andreas and Cortese, Andrea and Reich, Selina
and Dominik, Natalia and Faber, Jennifer and Jacobi, Heike
and Hartmann, Annette M and Rujescu, Dan and Montaut,
Solveig and Echaniz-Laguna, Andoni and Erer, Sevda and
Schütz, Valerie Cornelia and Tarnutzer, Alexander A and
Sturm, Marc and Haack, Tobias B and Vaucamps-Diedhiou,
Nadège and Puccio, Helene and Schöls, Ludger and
Klockgether, Thomas and van de Warrenburg, Bart P and
Paucar, Martin and Timmann, Dagmar and Hilgers, Ralf-Dieter
and Gazulla, Jose and Strupp, Michael and Moris, German and
Filla, Alessandro and Houlden, Henry and Anheim, Mathieu and
Infante, Jon and Basak, A Nazli and Synofzik, Matthis and
Barut, Banu Özen and Bilgic, Basar and Boz, Cavit and
Cauquil, Cécile and Deininger, Natalie and Dufke, Claudia
and Elibol, Bülent and Erbas, Furkan and Ertan, Sibel and
Genc, Fatma and Giegling, Ina and Parman, Yesim and Rossi,
Salvatore and Salcin, Celal and Tan, Meliha and Taştekin,
Hilal and Tranchant, Christine and Uygun, Günes and Yassa,
Özge Yagcioglu},
collaboration = {Group, RFC1 Study},
title = {{N}atural {H}istory, {P}henotypic {S}pectrum, and
{D}iscriminative {F}eatures of {M}ultisystemic {RFC}1
{D}isease.},
journal = {Neurology},
volume = {96},
number = {9},
issn = {1526-632X},
address = {[S.l.]},
publisher = {Ovid},
reportid = {DZNE-2021-01155},
pages = {e1369 - e1382},
year = {2021},
abstract = {To delineate the full phenotypic spectrum, discriminative
features, piloting longitudinal progression data, and sample
size calculations of replication factor complex subunit 1
(RFC1) repeat expansions, recently identified as causing
cerebellar ataxia, neuropathy, vestibular areflexia syndrome
(CANVAS).Multimodal RFC1 repeat screening (PCR, Southern
blot, whole-exome/genome sequencing-based approaches)
combined with cross-sectional and longitudinal deep
phenotyping in (1) cross-European cohort A (70 families)
with ≥2 features of CANVAS or ataxia with chronic cough
(ACC) and (2) Turkish cohort B (105 families) with
unselected late-onset ataxia.Prevalence of RFC1 disease was
$67\%$ in cohort A, $14\%$ in unselected cohort B, $68\%$ in
clinical CANVAS, and $100\%$ in ACC. RFC1 disease was also
identified in Western and Eastern Asian individuals and even
by whole-exome sequencing. Visual compensation, sensory
symptoms, and cough were strong positive discriminative
predictors $(>90\%)$ against RFC1-negative patients. The
phenotype across 70 RFC1-positive patients was mostly
multisystemic $(69\%),$ including dysautonomia $(62\%)$ and
bradykinesia $(28\%)$ (overlap with cerebellar-type multiple
system atrophy [MSA-C]), postural instability $(49\%),$ slow
vertical saccades $(17\%),$ and chorea or dystonia $(11\%).$
Ataxia progression was ≈1.3 Scale for the Assessment and
Rating of Ataxia points per year (32 cross-sectional, 17
longitudinal assessments, follow-up ≤9 years [mean 3.1
years]) but also included early falls, variable nonlinear
phases of MSA-C-like progression (SARA points 2.5-5.5 per
year), and premature death. Treatment trials require 330
(1-year trial) and 132 (2-year trial) patients in total to
detect $50\%$ reduced progression.RFC1 disease is frequent
and occurs across continents, with CANVAS and ACC as highly
diagnostic phenotypes yet as variable, overlapping clusters
along a continuous multisystemic disease spectrum, including
MSA-C-overlap. Our natural history data help to inform
future RFC1 treatment trials.This study provides Class II
evidence that RFC1 repeat expansions are associated with
CANVAS and ACC.},
keywords = {Adult / Aged / Ataxia / Bilateral Vestibulopathy / Cohort
Studies / DNA Repeat Expansion / Disease Progression /
Europe / Exome / Female / Genetic Testing / Humans /
Magnetic Resonance Imaging / Male / Middle Aged / Multiple
System Atrophy: diagnosis / Multiple System Atrophy:
diagnostic imaging / Multiple System Atrophy: genetics /
Phenotype / Predictive Value of Tests / Replication Protein
C: genetics / Turkey / Vestibular Diseases / RFC1 protein,
human (NLM Chemicals) / Replication Protein C (NLM
Chemicals)},
cin = {AG Gasser / Patient Studies Bonn / AG Klockgether},
ddc = {610},
cid = {I:(DE-2719)1210000 / I:(DE-2719)1011101 /
I:(DE-2719)1011001},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:33495376},
pmc = {pmc:PMC8055326},
doi = {10.1212/WNL.0000000000011528},
url = {https://pub.dzne.de/record/156023},
}