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The Evolving Landscape of Amyotrophic Lateral Sclerosis: Pathophysiology, Biomarkers, and Therapeutic Horizons

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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2.3 Glutamate Excitotoxicity Glutamate is the primary excitatory neurotransmitter in the central nervous system. In ALS, impaired function of the EAAT2 transporter on astrocytes leads to excess glutamate in the synaptic cleft. This results in overstimulation of AMPA and NMDA receptors on motor neurons, causing an influx of calcium ions and triggering apoptotic pathways. This mechanism remains one of the few targets for approved pharmacotherapy. an ASO targeting SOD1 mRNA

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3.1 Antisense Oligonucleotides (ASOs) ASOs are short, synthetic strands of nucleotides that can bind to mRNA and modulate protein expression. Tofersen, an ASO targeting SOD1 mRNA, was recently approved for SOD1-ALS. Clinical trials have shown that reducing SOD1 protein levels can slow disease progression. Similarly, trials are underway for ASOs targeting C9orf72 and ATXN2. amoytoge new