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@ARTICLE{Schmitz:271969,
author = {Schmitz, Anne S and Raju, Janani and Köhler, Wolfgang and
Klebe, Stephan and Cheheb, Khaled and Reschke, Franziska and
Biskup, Saskia and Haack, Tobias B and Röben, Benjamin and
Kellner, Melanie and Rahner, Nils and Bloch, Thomas and
Lemke, Johannes and Bender, Benjamin and Schöls, Ludger and
Hengel, Holger and Hayer, Stefanie},
title = {{N}ovel variants in {CSF}1{R} associated with adult-onset
leukoencephalopathy with axonal spheroids and pigmented glia
({ALSP}).},
journal = {Journal of neurology},
volume = {271},
number = {9},
issn = {0367-004X},
address = {Heidelberg},
publisher = {Springer},
reportid = {DZNE-2024-01111},
pages = {6025 - 6037},
year = {2024},
abstract = {The CSF1R gene, located on chromosome 5, encodes a 108 kDa
protein and plays a critical role in regulating myeloid cell
function. Mutations in CSF1R have been identified as a cause
of a rare white matter disease called adult-onset
leukoencephalopathy with axonal spheroids and pigmented glia
(ALSP, also known as CSF1R-related leukoencephalopathy),
characterized by progressive neurological dysfunction. This
study aimed to broaden the genetic basis of ALSP by
identifying novel CSF1R variants in patients with
characteristic clinical and imaging features of ALSP.
Genetic analysis was performed through whole-exome
sequencing or panel analysis for leukodystrophy genes.
Variant annotation and classification were conducted using
computational tools, and the identified variants were
categorized following the recommendations of the American
College of Medical Genetics and Genomics (ACMG). To assess
the evolutionary conservation of the novel variants within
the CSF1R protein, amino acid sequences were compared across
different species. The study identified six previously
unreported CSF1R variants (c.2384G>T, $c.2133_2919del,$
c.1837G>A, c.2304C>A, c.2517G>T, c.2642C>T) in seven
patients with ALSP, contributing to the expanding knowledge
of the genetic diversity underlying this rare disease. The
analysis revealed considerable genetic and clinical
heterogeneity among these patients. The findings emphasize
the need for a comprehensive understanding of the genetic
basis of rare diseases like ALSP and underscored the
importance of genetic testing, even in cases with no family
history of the disease. The study's contribution to the
growing spectrum of ALSP genetics and phenotypes enhances
our knowledge of this condition, which can be crucial for
both diagnosis and potential future treatments.},
keywords = {Humans / Female / Leukoencephalopathies: genetics /
Leukoencephalopathies: pathology / Male / Receptors,
Granulocyte-Macrophage Colony-Stimulating Factor: genetics /
Adult / Middle Aged / Mutation / Neuroglia: pathology / Aged
/ Receptor, Macrophage Colony-Stimulating Factor / ALSP
(Other) / CSF1R (Other) / CSF1R-related leukoencephalopathy
(Other) / Genetic diagnostics (Other) / CSF1R protein, human
(NLM Chemicals) / Receptors, Granulocyte-Macrophage
Colony-Stimulating Factor (NLM Chemicals) / Receptor,
Macrophage Colony-Stimulating Factor (NLM Chemicals)},
cin = {AG Jucker / AG Schöls},
ddc = {610},
cid = {I:(DE-2719)1210001 / I:(DE-2719)5000005},
pnm = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC11377666},
pubmed = {pmid:39031193},
doi = {10.1007/s00415-024-12557-0},
url = {https://pub.dzne.de/record/271969},
}