Abstract Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disorder characterized by the loss of upper and lower motor neurons. Historically considered a purely motor disorder, ALS is now understood as a multisystem disease with complex genetic and environmental etiologies. This paper reviews the current state of ALS research, focusing on the molecular mechanisms of pathogenesis—including protein aggregation, RNA metabolism, and glutamate excitotoxicity—and highlights recent advancements in biomarker discovery and gene-targeted therapies that are reshaping the clinical management of the disease.
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2.2 RNA Metabolism Dysregulation of RNA metabolism is a central theme in ALS pathogenesis. Genes like TARDBP and FUS encode RNA-binding proteins. When these proteins mislocalize to the cytoplasm, they form aggregates that sequester other RNA-binding proteins, leading to widespread splicing errors and mRNA instability. The C9orf72 hexanucleotide expansion leads to the production of toxic dipeptide repeat proteins (DPRs) via an unconventional translation mechanism, further disrupting nucleocytoplasmic transport. Frontend: modal, panel, mobile adaptations — 2–3 sprint
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