Table 4.

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

HD patient-derived iPSCs: genetic mutation	differentiation into cell type	differentiation marker	result	references
180 HTT CAG repeats	cortical neurons	Tuj-I	reduction in pS202 levels in differentiated cortical neurons	[80]
Q47	Q47 striatal neurons	Tuj-I	reduction of the formation of VCP-LC3-mHTT ternary complex	[81]
MSNs	striatal medium spiny neurons (MSNs), microglia	Map2, TREM2 and IBA1	striatal neurons with DARPP32+ neurons	[82,83]
	GABA+ MSNs	Map2, GABA	DARPP32 positivity; increased caspase activity	[84,85]
	TUJ1+, MAP2+ and Olig2+ neurons	TUJ1, MAP2,	ARPP-32 positivity; higher rate of DNA damage	[86]
	TUJ1+, MAP2+, neurons	TUJ1, MAP2,	elevated levels of caspase activity upon growth factor withdrawal	[87]
	GABAergic neurons	GABA	hiPSCs generated mostly GABAergic neurons	[88]