Akademik Veri Yönetim Sistemi
Turkiye Klinikleri, Ankara, 2025
Neuroinflammation is increasingly recognized as a complex contributor to amyotrophic lateral sclerosis (ALS) pathogenesis. Yet, whether neuroinflammation acts as a causative factor or a consequence of motor neuron degeneration remains uncertain. Neuroinflammation plays a dual role in ALS where early-stage anti-inflammatory responses promote neuronal survival, but late-stage pro-inflammatory states exacerbate neuronal damage. Key mediators include microglia, astrocytes, and peripheral immune cells, whose phenotypic shifts significantly influence disease progression. Genetic factors such as SOD1, C9orf72, TDP43, and FUS mutations further exacerbate these inflammatory pathways. This chapter comprehensively discusses neuroinflammation in ALS based on the underlying molecular and cellular mechanisms and evidence from clinical studies and drug trials. Novel interventions targeting inflammatory pathways, including immune-modulatory drugs, stem cell transplantation, and off-label treatments, hold promise but face challenges due to ALS’s heterogeneity and dynamic inflammatory states. The review also highlights innovations in preclinical models and biomarker identification, pivotal for understanding disease mechanisms and personalizing therapeutic strategies. Future research must prioritize resolving the complexities of neuroinflammatory responses, tailoring interventions to individual genetic profiles, and optimizing treatment timing to address ALS’s multifaceted pathology.