Table 1.

Modeling ALS using iPSCs-derived motor neurons, astrocytes and microglia.

Cell Type	ALS Subtypes	Key Findings
Motor neurons (or neurons)	SOD1 mutation	Neurofilament aggregation; disorders in mitochondria; decreased survival rate
	C9orf72 mutation	RNA foci formation; accumulation of RAN translation products; stress granule formation; excitotoxicity
	TARDBP mutation	TDP-43 protein aggregation; shorter neurites; mitochondrial Ca2+ uptake disorder
	FUS mutation	FUS protein aggregation; DNA damage; cytoplasmic mislocation
	sporadic ALS	TDP-43 aggregation; higher neurofilament inclusion; mitochondria distribution impairment
Astrocytes	SOD1 mutation	Impair autophagy
	C9orf72 mutation	Increased oxidative stress and neurotoxicity
	sporadic ALS	Autophagy-mediated inflammatory cytokine secretion
Microglia	FUS mutation	Disrupt intracellular calcium signaling
	sporadic ALS	Influence neurofilament deposition