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@ARTICLE{Rattay:140899,
author = {Rattay, Tim W and Lindig, Tobias and Baets, Jonathan and
Smets, Katrien and Deconinck, Tine and Söhn, Anne S and
Hörtnagel, Konstanze and Eckstein, Kathrin N and Wiethoff,
Sarah and Reichbauer, Jennifer and Döbler-Neumann, Marion
and Krägeloh-Mann, Ingeborg and Auer-Grumbach, Michaela and
Plecko, Barbara and Münchau, Alexander and Wilken, Bernd
and Janauschek, Marc and Giese, Anne-Katrin and De Bleecker,
Jan L and Ortibus, Els and Debyser, Martine and Lopez de
Munain, Adolfo and Pujol, Aurora and Bassi, Maria Teresa and
D'Angelo, Maria Grazia and De Jonghe, Peter and Züchner,
Stephan and Bauer, Peter and Schöls, Ludger and Schüle,
Rebecca},
title = {{FAHN}/{SPG}35: a narrow phenotypic spectrum across disease
classifications.},
journal = {Brain},
volume = {142},
number = {6},
issn = {0006-8950},
address = {Oxford},
publisher = {Oxford Univ. Press},
reportid = {DZNE-2020-07221},
pages = {1561-1572},
year = {2019},
abstract = {The endoplasmic reticulum enzyme fatty acid 2-hydroxylase
(FA2H) plays a major role in the formation of 2-hydroxy
glycosphingolipids, main components of myelin. FA2H
deficiency in mice leads to severe central demyelination and
axon loss. In humans it has been associated with phenotypes
from the neurodegeneration with brain iron accumulation
(fatty acid hydroxylase-associated neurodegeneration, FAHN),
hereditary spastic paraplegia (HSP type SPG35) and
leukodystrophy (leukodystrophy with spasticity and dystonia)
spectrum. We performed an in-depth clinical and
retrospective neurophysiological and imaging study in a
cohort of 19 cases with biallelic FA2H mutations. FAHN/SPG35
manifests with early childhood onset predominantly lower
limb spastic tetraparesis and truncal instability,
dysarthria, dysphagia, cerebellar ataxia, and cognitive
deficits, often accompanied by exotropia and movement
disorders. The disease is rapidly progressive with loss of
ambulation after a median of 7 years after disease onset and
demonstrates little interindividual variability. The hair of
FAHN/SPG35 patients shows a bristle-like appearance;
scanning electron microscopy of patient hair shafts reveals
deformities (longitudinal grooves) as well as plaque-like
adhesions to the hair, likely caused by an abnormal sebum
composition also described in a mouse model of FA2H
deficiency. Characteristic imaging features of FAHN/SPG35
can be summarized by the 'WHAT' acronym: white matter
changes, hypointensity of the globus pallidus,
ponto-cerebellar atrophy, and thin corpus callosum. At least
three of four imaging features are present in $85\%$ of FA2H
mutation carriers. Here, we report the first systematic,
large cohort study in FAHN/SPG35 and determine the
phenotypic spectrum, define the disease course and identify
clinical and imaging biomarkers.},
keywords = {Child / Cohort Studies / Demyelinating Diseases: genetics /
Female / Heredodegenerative Disorders, Nervous System:
genetics / Humans / Male / Mixed Function Oxygenases:
genetics / Mutation: genetics / Pedigree / Phenotype /
Retrospective Studies / Spastic Paraplegia, Hereditary:
classification / Spastic Paraplegia, Hereditary: genetics},
cin = {AG Gasser 1 / Tübingen Pre 2020 / AG Maetzler},
ddc = {610},
cid = {I:(DE-2719)1210000 / I:(DE-2719)6000018 /
I:(DE-2719)5000024},
pnm = {345 - Population Studies and Genetics (POF3-345) / 344 -
Clinical and Health Care Research (POF3-344)},
pid = {G:(DE-HGF)POF3-345 / G:(DE-HGF)POF3-344},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:31135052},
pmc = {pmc:PMC6536916},
doi = {10.1093/brain/awz102},
url = {https://pub.dzne.de/record/140899},
}