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By whole-exome sequencing, we found the heterozygous POLG variant c.3542G>A; p.Ser1181Asn in a family of four affected individuals, presenting with a mixed neuro-myopathic phenotype. The variant is located within the active site of polymerase gamma, in a cluster region associated with an autosomal dominant inheritance. In adolescence, the index developed distal atrophies and weakness, sensory loss, afferent ataxia, double vision, and bilateral ptosis. One older sister presented with Charcot-Marie-Tooth-like symptoms, while the youngest sister and father reported exercise-induced muscle pain and proximal weakness. In none of the individuals, we observed any involvement of the central nervous system. Muscle biopsies obtained from the father and the older sister showed ragged-red fibers, and electron microscopy confirmed mitochondrial damage. We conclude that this novel POLG variant explains this family's phenotype.
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http://dx.doi.org/10.1186/s42466-022-00169-w | DOI Listing |
Introduction: We recently identified variants in 10 genes that are members of either the p53 pathway or Fanconi Anemia Complex (FAC), regulators of the DNA repair (DNA damage response; DDR) in 17 cases with Pediatric Acute-Onset Neuropsychiatry Syndrome (PANS) or regression in autism spectrum disorder (ASD) and other neurodevelopmental disorders (NDD). We aimed to identify additional cases with genetic vulnerabilities in DDR and related pathways.
Methods: Whole exome sequencing (WES) data from 32 individuals were filtered and analyzed to identify ultrarare pathogenic or likely pathogenic variants.
J Neurol
August 2025
Department of Pathophysiology and Transplantation, "Dino Ferrari" Center, Università Degli Studi Di Milano, Milan, Italy.
Background: Primary Lateral Sclerosis (PLS) is a rare, adult-onset neurodegenerative disease that predominantly affects upper motor neurons. Despite being considered mostly sporadic, familial cases and rare genetic variants in genes associated with amyotrophic lateral sclerosis, hereditary spastic paraplegia and other neurological disorders have been reported in some PLS cases. Due to its rare prevalence among general population, large genetic studies of PLS are lacking.
View Article and Find Full Text PDFMol Genet Metab
July 2025
Service de Neurophysiologie Pédiatrique, Centre de référence des pathologies neuromusculaires, AP-HP, Hôpital Necker-Enfants Malades, Université Paris Cité, Paris, France; CNRS, Laboratoire de Chimie et de Biochimie Pharmacologiques et Toxicologiques UMR8601, F-75006 Paris, France.
Pathogenic variants in POLG are involved in a large spectrum of neurological, gastrointestinal and liver impairments. Children affected with POLG-related disorders rarely exhibit peripheral neuropathy, the latter being most often described in adults as axonal polyneuropathy. Our aim was to focus on electrophysiological findings in young children affected with POLG-related disorder.
View Article and Find Full Text PDFMitochondrion
July 2025
Department of Pediatric Neurology, National Institute of Neurology Mongi-Ben Hamida, Tunis, Tunisia; Research Laboratory LR18SP04, Tunisia; Tunis El Manar University, Tunis, Tunisia. Electronic address:
Mitochondrial Neuro-Gastro-Intestinal Encephalopathy (MNGIE) is a rare and fatal mitochondrial disorder caused by biallelic mutations in the TYMP gene. In rare cases, it can be caused by pathogenic variants in the POLG gene, with a clinical presentation similar to that of TYMP-related MNGIE, except for the absence of leukoencephalopathy. Here we report the cases of six Tunisian patients presenting with a homogeneous clinical MNGIE-like phenotype, characterized by an early infantile onset.
View Article and Find Full Text PDFActa Neuropathol
May 2025
Mitochondrial Research Group, Faculty of Medical Sciences, Translational and Clinical Research Institute, Newcastle University, Newcastle Upon Tyne, NE2 4HH, UK.
Cerebellar ataxia is a frequent, debilitating neurological manifestation of primary mitochondrial disease and is associated with extensive neurodegeneration of the cerebellar cortical circuitry. However, the precise neuropathological mechanisms resulting in cerebellar degeneration in paediatric and adult forms of mitochondrial disease remain unclear. We therefore sought to perform a comparative neuropathological study using post-mortem cerebellar tissues from 28 paediatric and adult patients with pathogenic bi-allelic POLG variants and pathogenic mitochondrial DNA variants (m.
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