Publications by authors named "Xuxiong Tang"
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.
Background: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder. An increasing number of researchers have found extra motor features in ALS, which are also called ALS-plus syndromes. Besides, a great majority of ALS patients also have cognitive impairment.
View Article and Find Full Text PDFIntroduction: Although the relationship between psychiatric disorders and Parkinson's disease (PD) has attracted continuous research attention, the causal linkage between them has not reached a definite conclusion.
Methods: To identify the causal relationship between psychiatric disorders and PD, we used public summary-level data from the most recent and largest genome-wide association studies (GWASs) on psychiatric disorders and PD to conduct a bidirectional two-sample Mendelian randomization (MR). We applied stringent control steps in instrumental variable selection using the Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) method to rule out pleiotropy.
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.
Background: Amyotrophic lateral sclerosis (ALS) is a late-onset neurodegenerative disorder. Mitochondrial dysfunction is involved in the complex pathophysiology of ALS; however, the role of mitochondrial DNA (mtDNA) variants in ALS is poorly understood. We aimed to elucidate the role of mtDNA variants in the pathogenesis of ALS.
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