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As with other neurodegenerative diseases such as Alzheimers disease, Parkinsons disease, and Huntingtons disease, a significant number of fundamental studies have demonstrated that energy metabolism disorders resulting from mitochondrial dysfunction represent the primary pathophysiological phenotypes of amyotrophic lateral sclerosis (Sassani et al., 2020

In monocyte-derived TAMs exposed to excessive amounts of oxysterols, failed compensatory cholesterol export triggers mitochondrial dysfunction and the upregulation of Siglec-10 and PD-1 expression, thereby suppressing phagocytosis capacity [101]

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