Table 1.

Pre-clinical anti-inflammatory stem cell studies for Parkinson’s disease.

Citation	Model	Cell type	Dosage	Findings
Haney et al. (2013) [94]	6-OHDA mice	Modified macrophages with antioxidant plasmid	5 × 106 cells/mouse in 100 µL PBS	Macrophages released exosomes containing antioxidant genetic material prompting neurons to increase protein synthesis. Mice had improved motor function.
Ugen et al. (2015) [56]	A53T α-synuclein overexpressing cells and mice	Bone marrow-derived dendritic cells	106 cells	α-synuclein sensitized DCs induced α-synuclein antibodies, improved motor function in mice, and had lower pro-inflammatory cytokine levels.
Oh et al. (2017) [95]	A53T α-synuclein overexpressing cells and mice	Mesenchymal stem cells	1 × 106 cells in 200 µL saline in tail	Eukaryotic elongation factor 1A-2 from MSCs increased neuronal survival by improving axonal transport and monitoring α-synuclein pathological phosphorylation
Kojima et al. (2018) [96]	6-OHDA mice	Catalase mRNA in designer exosomes	Four hundred microliters of the cell/Matrigel mixture	Reduced neuroinflammation and neurotoxicity in Parkinson’s mice.
L’Episcopo et al. (2018) [97]	MPTP mice	Neural stem cells	100 × 103 cells	NSCs that became astrocytic expressed Wnt1 and prompted Wnt/ β-catenin signaling in substantia nigra pars compacta midbrain dopaminergic neurons and microglia. This allowed for dopaminergic neuron rescue and decreased microglial inflammation.
Lee et al. (2019a) [98]	MPTP mice	Human umbilical cord blood stem cells	500 µL cord blood plasma	Mice showed improved motor and GI function, ameliorated dopamine cell loss, and reduced neurological and GI inflammation.
Lee et al. (2019b) [99]	6-OHDA mice	Human umbilical cord blood stem cells	Three separate doses of 4 × 106 cells	Mice showed improved motor and GI function, ameliorated dopamine cell loss, and reduced neurological and GI inflammation.
Serapide et al. (2020) [100]	MPTP Mice	Engrafted astrocytes	150 × 103 ventral midbrain-Astrocytes	Grafted astrocytes can rescue dying dopaminergic neurons, likely via antioxidant and anti-inflammatory Nrf2/ARE/Wnt/β-catenin signaling.