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The precise regulation of ALS pathogenetic mechanisms is still elusive, despite the abundance of identified mechanisms mediating MN degeneration and death, including neuroinflammation, glutamate excitotoxicity, altered RNA metabolism, mitochondrial dysfunction, impaired cytoskeletal integrity, altered axonal transport dynamics, OS [71, 84, 85]

This leads to disruption in motor functions, driven by mitochondrial dysfunction, aggregation of alpha-synuclein proteins into Lewy bodies, chronic neuroinflammation, and oxidative stress 33