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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. has arrived

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Furthermore, the focus is expanding beyond neurons to include non-neuronal cells. Astrocytes and microglia are now known to contribute to disease propagation via neuroinflammatory pathways. Therapeutic strategies that target these support cells