ArticleActa neurologica Scandinavica2019
Glucose metabolism in the brain in LMNB1-related autosomal dominant leukodystrophy.
Article in Acta neurologica Scandinavica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 6 citations in OpenAlex.
- PET imaging of microglia in Alzheimer's disease using copper-64 labeled TREM2 antibodies.Theranostics · 2024Article
- Adult-onset leukodystrophy with vanishing white matter: a case series of 19 patients.Journal of neurology · 2023Observational
- Image reconstruction methods affect software-aided assessment of pathologies of [NeuroImage. Clinical · 2020Article
- Glucose metabolism in the brain in LMNB1-related autosomal dominant leukodystrophy.Acta neurologica Scandinavica · 2019Article
- LMNB1-Related Adult-Onset Autosomal Dominant Leukodystrophy Presenting as Movement Disorder: A Case Report and Review of the Literature.Frontiers in neuroscience · 2019Article
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7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveLMNB1-related autosomal dominant leukodystrophy is caused by an overexpression of the protein lamin B1, usually due to a duplication of the LMNB1 gene. Symptoms start in 5
methodsWe examined 8 patients, aged 48-64 years, in varying stages of clinical symptomatology. Two patients were investigated with quantitative PET on clinical indications after which six more patients were recruited. Absolute glucose metabolism was analyzed with the PVElab software in 6 patients and 18 healthy controls. A semiquantitative analysis using the CortexID software was performed in seven investigations, relating local metabolism levels to global glucose metabolism.
resultsThe clinical quantitative PET revealed low global glucose metabolism, with the most marked reduction in the cerebellum. In the PVElab analysis, patients presented low mean glucose metabolism in the cerebellum, brainstem and global grey matter. In the semiquantitative analysis, 2 patients showed a decreased metabolism in the cerebellum and 4 patients a relatively higher metabolism in parts of the temporal lobes. Since none of the patients showed an increased metabolism in the quantitative analysis, we interpret these increases as "pseudo-increases" related to a globally reduced metabolism.
conclusionsGlobal reduction of grey matter glucose metabolism in this white matter disease most likely depends on a combination of cortical afferent dysfunction and, in later stages, neuronal loss. The lowest metabolism in the cerebellum is consistent with histopathological findings and prominent cerebellar symptoms.
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