Publications by authors named "Linxin Tang"

Background: Neuroimaging has been increasingly used to assess brain structural alterations in patients with amyotrophic lateral sclerosis (ALS). We aimed to investigate alterations in brain sub-cortical structures and to identify potential neuroimaging biomarkers for disease progression for patients with ALS.

Methods: A total of 61 patients with ALS were prospectively enrolled and were divided into three subgroups according to disease progression, i.

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Objective: In this study, we aimed to investigate retinal changes in a large cohort of amyotrophic lateral sclerosis (ALS) patients and healthy controls (HCs) to further elucidate their relationship with ALS.

Methods: This was a cross-sectional observational study. We evaluated retinal layer thickness in 134 ALS patients and 66 HCs using optical coherence tomography (OCT).

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Article Synopsis
  • CLCC1 was identified as a novel gene related to ALS, prompting a study to investigate its variants in a cohort of 1005 ALS patients and 1224 healthy controls.
  • Four rare missense variants in CLCC1 were found in unrelated sporadic ALS patients, predicted to be pathogenic and linked to specific clinical features such as earlier onset and rapid disease progression.
  • Although these findings further the understanding of CLCC1-related ALS, statistical analysis did not show a significant association of the gene variants with ALS risk, indicating that more research is needed.
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Introduction: was recently identified as a novel causative gene for amyotrophic lateral sclerosis (ALS). We aimed to determine the contribution of variations in in the Chinese ALS population and to further explore the genotype-phenotype correlations.

Methods: We screened rare, putative pathogenic mutations in a large Chinese ALS cohort and performed association analysis of both rare and common variations between cases and controls.

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Astrocyte aerobic glycolysis provides vital trophic support for central nervous system neurons. However, whether and how astrocytic metabolic dysregulation contributes to neuronal dysfunction in intellectual disability (ID) remain unclear. Here, we demonstrate a causal role for an ID-associated SNX27 mutation (R198W) in cognitive deficits involving reshaping astrocytic metabolism.

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