ArticleActa neuropathologica2015
A truncating SOD1 mutation, p.Gly141X, is associated with clinical and pathologic heterogeneity, including frontotemporal lobar degeneration.
Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Cognitive and Behavioural Profile of SOD1-ALS Across the ALS-FTD Spectrum: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Updated Genetic Analysis of Japanese Familial ALS Patients CarryingNeurology. Genetics · 2024Article
- ALS-plus related clinical and genetic study from China.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
- The landscape of cognitive impairment in superoxide dismutase 1-amyotrophic lateral sclerosis.Neural regeneration research · 2023Review
- Loss of hypothalamic MCH decreases food intake in amyotrophic lateral sclerosis.Acta neuropathologica · 2023Article
- Behavioral and Cognitive Phenotypes of Patients With Amyotrophic Lateral Sclerosis Carrying SOD1 Variants.Neurology · 2022Article
- Modelling amyotrophic lateral sclerosis in rodents.Nature reviews. Neuroscience · 2022Review
- MRI Volumetric Analysis of the Thalamus and Hypothalamus in Amyotrophic Lateral Sclerosis.Frontiers in aging neuroscience · 2021Article
- Cell Cycle Deficits in Neurodegenerative Disorders: Uncovering Molecular Mechanisms to Drive Innovative Therapeutic Development.Aging and disease · 2020Review
- Neuronal intermediate filament inclusion disease may be incorrectly classified as a subtype of FTLD-FUS.Free neuropathology · 2020Article
- Clinicopathological characteristics of patients with amyotrophic lateral sclerosis resulting in a totally locked-in state (communication Stage V).Acta neuropathologica communications · 2016Article
- From animal models to human disease: a genetic approach for personalized medicine in ALS.Acta neuropathologica communications · 2016Review
- ADNP: in search for molecular mechanisms and innovative therapeutic strategies for frontotemporal degeneration.Frontiers in aging neuroscience · 2015Review
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a degenerative disorder affecting upper and lower motor neurons, but it is increasingly recognized to affect other systems, with cognitive impairment resembling frontotemporal dementia (FTD) in some patients. We report clinical and pathologic findings of a family with ALS due to a truncating mutation, p.Gly141X, in copper/zinc superoxide dismutase (SOD1). The proband presented clinically with FTD and later showed progressive motor neuron disease, while all other family members had early-onset and rapidly progressive ALS without significant cognitive deficits. Pathologic examination of both the proband and her daughter revealed degeneration of corticospinal tracts and motor neurons in brain and spinal cord compatible with ALS. On the other hand, the proband also had neocortical and limbic system degeneration with pleomorphic neuronal cytoplasmic inclusions. Extramotor pathology in her daughter was relatively restricted to the hypothalamus and extrapyramidal system, but not the neocortex. The inclusions in the proband and her daughter were immunoreactive for SOD1, but negative for TAR DNA-binding protein of 43 kDa (TDP-43). In the proband, a number of the neocortical inclusions were immunopositive for α-internexin, initially suggesting a diagnosis of atypical FTLD, but there was no evidence of fused in sarcoma (FUS) immunoreactivity, which is often detected in atypical FTLD. Analogous to atypical FTLD, neuronal inclusions had variable co-localization of SOD1 and α-internexin. The current classification of FTLD is based on the major constituent protein: FTLD-tau, FTLD-TDP-43, and FTLD-FUS. The proband in this family indicates that SOD1, while rare, can also be the substrate of FTLD, in addition to the more common presentation of ALS. The explanation for clinical and pathologic heterogeneity of SOD1 mutations, including the p.Gly141X mutation, remains unresolved.
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