Table 2.

iPSC-derived in vitro studies to model PD and analyse disease-related mechanisms and phenotypes.

PD patient-derived iPSCs: genetic mutation	differentiation into cell type	differentiation marker	result	references
Parkin	midbrain dopaminergic neurons	Parkin	elevated transcription of monoamine oxidases, inducing oxidative stress	[50]
LRRK2	dopaminergic neurons	dopamine LRRK2	the increased generation of alpha-synuclein protein and increased expression of oxidative stress-response genes	[51–54]
SNCA triplication mutation	midbrain dopaminergic neurons	alpha-synuclein	aggressive form of PD with dementia	[55–57]
glucocerebrosidase and SNCA mutation	functional loss of glucocerebrosidase in iPSC-derived neurons	glucocerebrosidase	the pathogenesis of sporadic synucleinopathies including idiopathic PD	[50]
SNCA triplication	accumulation of alpha-synuclein in iPSC-derived neurons	peroxide	a major phenotype of PD including oxidative stress	[55–57]