Maculopathy and adult‐onset ataxia in patients with biallelic MFSD8 variants

Abstract Background Biallelic variants in the major facilitator superfamily domain containing 8 gene (MFSD8) are associated with distinct clinical presentations that range from typical late‐infantile neuronal ceroid lipofuscinosis type 7 (CLN7 disease) to isolated adult‐onset retinal dystrophy. Clas...

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Main Authors: Sigurd Dobloug, Ulrika Kjellström, Glenn Anderson, Emily Gardner, Sara E. Mole, Jayesh Sheth, Andreas Puschmann
Format: Article
Language:English
Published: Wiley 2024-08-01
Series:Molecular Genetics & Genomic Medicine
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Online Access:https://doi.org/10.1002/mgg3.2505
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author Sigurd Dobloug
Ulrika Kjellström
Glenn Anderson
Emily Gardner
Sara E. Mole
Jayesh Sheth
Andreas Puschmann
author_facet Sigurd Dobloug
Ulrika Kjellström
Glenn Anderson
Emily Gardner
Sara E. Mole
Jayesh Sheth
Andreas Puschmann
author_sort Sigurd Dobloug
collection DOAJ
description Abstract Background Biallelic variants in the major facilitator superfamily domain containing 8 gene (MFSD8) are associated with distinct clinical presentations that range from typical late‐infantile neuronal ceroid lipofuscinosis type 7 (CLN7 disease) to isolated adult‐onset retinal dystrophy. Classic late‐infantile CLN7 disease is a severe, rare neurological disorder with an age of onset typically between 2 and 6 years, presenting with seizures and/or cognitive regression. Its clinical course is progressive, leading to premature death, and often includes visual loss due to severe retinal dystrophy. In rare cases, pathogenic variants in MFSD8 can be associated with isolated non‐syndromic macular dystrophy with variable age at onset, in which the disease process predominantly or exclusively affects the cones of the macula and where there are no neurological or neuropsychiatric manifestations. Methods Here we present longitudinal studies on four adult‐onset patients who were biallelic for four MFSD8 variants. Results Two unrelated patients who presented with adult‐onset ataxia and had macular dystrophy on examination were homozygous for a novel variant in MFSD8 NM_152778.4: c.935T>C p.(Ile312Thr). Two other patients presented in adulthood with visual symptoms, and one of these developed mild to moderate cerebellar ataxia years after the onset of visual symptoms. Conclusions Our observations expand the knowledge on biallelic pathogenic MFSD8 variants and confirm that these are associated with a spectrum of more heterogeneous clinical phenotypes. In MFSD8‐related disease, adult‐onset recessive ataxia can be the presenting manifestation or may occur in combination with retinal dystrophy.
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spelling doaj-art-a5dd1973fd084228a9cd7051f8edf8162025-08-20T01:59:26ZengWileyMolecular Genetics & Genomic Medicine2324-92692024-08-01128n/an/a10.1002/mgg3.2505Maculopathy and adult‐onset ataxia in patients with biallelic MFSD8 variantsSigurd Dobloug0Ulrika Kjellström1Glenn Anderson2Emily Gardner3Sara E. Mole4Jayesh Sheth5Andreas Puschmann6Department of Neurology Helsingborg General Hospital Helsingborg SwedenLund University, Skåne University Hospital, Ophthalmology Lund SwedenDepartment of Histopathology Great Ormond Street Hospital London UKGreat Ormond Street Institute of Child Health University College London London UKGreat Ormond Street Institute of Child Health University College London London UKFoundation for Research in Genetics and Endocrinology Institute of Human Genetics Ahmedabad IndiaLund University, Skåne University Hospital, Neurology Lund SwedenAbstract Background Biallelic variants in the major facilitator superfamily domain containing 8 gene (MFSD8) are associated with distinct clinical presentations that range from typical late‐infantile neuronal ceroid lipofuscinosis type 7 (CLN7 disease) to isolated adult‐onset retinal dystrophy. Classic late‐infantile CLN7 disease is a severe, rare neurological disorder with an age of onset typically between 2 and 6 years, presenting with seizures and/or cognitive regression. Its clinical course is progressive, leading to premature death, and often includes visual loss due to severe retinal dystrophy. In rare cases, pathogenic variants in MFSD8 can be associated with isolated non‐syndromic macular dystrophy with variable age at onset, in which the disease process predominantly or exclusively affects the cones of the macula and where there are no neurological or neuropsychiatric manifestations. Methods Here we present longitudinal studies on four adult‐onset patients who were biallelic for four MFSD8 variants. Results Two unrelated patients who presented with adult‐onset ataxia and had macular dystrophy on examination were homozygous for a novel variant in MFSD8 NM_152778.4: c.935T>C p.(Ile312Thr). Two other patients presented in adulthood with visual symptoms, and one of these developed mild to moderate cerebellar ataxia years after the onset of visual symptoms. Conclusions Our observations expand the knowledge on biallelic pathogenic MFSD8 variants and confirm that these are associated with a spectrum of more heterogeneous clinical phenotypes. In MFSD8‐related disease, adult‐onset recessive ataxia can be the presenting manifestation or may occur in combination with retinal dystrophy.https://doi.org/10.1002/mgg3.2505ataxiaCLN7MFSD8NCL7neuronal ceroid lipofuscinosisretinal degeneration
spellingShingle Sigurd Dobloug
Ulrika Kjellström
Glenn Anderson
Emily Gardner
Sara E. Mole
Jayesh Sheth
Andreas Puschmann
Maculopathy and adult‐onset ataxia in patients with biallelic MFSD8 variants
Molecular Genetics & Genomic Medicine
ataxia
CLN7
MFSD8
NCL7
neuronal ceroid lipofuscinosis
retinal degeneration
title Maculopathy and adult‐onset ataxia in patients with biallelic MFSD8 variants
title_full Maculopathy and adult‐onset ataxia in patients with biallelic MFSD8 variants
title_fullStr Maculopathy and adult‐onset ataxia in patients with biallelic MFSD8 variants
title_full_unstemmed Maculopathy and adult‐onset ataxia in patients with biallelic MFSD8 variants
title_short Maculopathy and adult‐onset ataxia in patients with biallelic MFSD8 variants
title_sort maculopathy and adult onset ataxia in patients with biallelic mfsd8 variants
topic ataxia
CLN7
MFSD8
NCL7
neuronal ceroid lipofuscinosis
retinal degeneration
url https://doi.org/10.1002/mgg3.2505
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