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BackgroundAmyotrophic lateral sclerosis (ALS) is a relentlessly progressive neurodegenerative disease affecting the motor neurons. Although much research has been conducted in this field, few bibliometric studies have been conducted. This study aimed to provide an overview of publishing characteristics and trends in ALS research since 2000 using a bibliometric analysis.MethodsWe conducted a comprehensive literature search in the Web of Science (WOS) Core Collection database for scientific output related to ALS from 2000 to 2022. The retrieved dataset was refined using Google OpenRefine and analyzed using bibliometrix.ResultsA total of 29,391 articles published since 2000 were retrieved, with an average annual growth rate of 6.35%. Ninety-six countries and regions contributed to ALS research, among which the United States had the dominant position with the highest number of publications (n = 8,202) and citations (n = 558,561). An association analysis was performed to form networks of country collaboration and keyword co-occurrence. The evolution of topic trends was demonstrated in terms of both frequency and proportion.ConclusionThe output of ALS research has increased steadily over the years, and the United States and Western Europe are leaders in this field. There is an upgradation in the pathomechanism and clinical research on ALS.

Substantial evidence implicates abnormal protein kinase function in various aspects of Parkinson's disease (PD) etiology. Elevated phosphorylation of the PD-defining pathological protein, α-synuclein, correlates with its aggregation and toxic accumulation in neurons, whilst genetic missense mutations in the kinases PTEN-induced putative kinase 1 and leucine-rich repeat kinase 2, increase susceptibility to PD. Experimental evidence also links kinases of the phosphoinositide 3-kinase and mitogen-activated protein kinase signaling pathways, amongst others, to PD. Understanding how the levels or activities of these enzymes or their substrates change in brain tissue in relation to pathological states can provide insight into disease pathogenesis. Moreover, understanding when and where kinase dysfunction occurs is important as modulation of some of these signaling pathways can potentially lead to PD therapeutics. This review will summarize what is currently known in regard to the expression of these PD-implicated kinases in pathological human postmortem brain tissue. [ABSTRACT FROM AUTHOR]