Table 2.

Summary of the main studies relating the impact of vitamin A pathway alterations (dietary intake, receptors or ALDH1A1) in Parkinson’s disease rodent models. VAD, vitamin A deficient; D1R, dopamine D1 receptor; D2R, dopamine D2 receptor; TH, tyrosine hydroxylase; DA, dopamine; DOPAC, 3,4-dihydroxyphenylacetic acid; 5HT, serotonine; HVA, homovanillic acid: A53T mice, transgenic mice that overexpress human α-synuclein with a PD-associated mutation (A53T)

Model	Behavioral tests	Motor behavior*	Striatal changes*	Survival of SNc neurons*	α-synuclein aggregation*	Study
A53T/aldh1a1 KO mice	Rotarod, open field	↘	↗ α-synuclein	↘	↗	[73]
RAR/RXR KO mice	Rotarod, open field	↘↘	D1R; D2R ↘↘			[76]
VAD rats	Rotarod, motor activity	↘↘	D1R, D2R, TH, DA/DOPAC = ChAT ↘↘			[84]
VAD rats	EEG recording, motor activity, open field	↘	DA and 5HT = DOPAC ↘			[85]
RARβ antagonist in mice	EEG recording	↘ wake periods	DOPAC and HVA = TH, D1R ↘ ratio HVA/DA ↘			[113]
aldh1a1 KO mice			baseline DA ↗ evoked DA ↘ DOPAC ↘	More TH+ neurons		[133]
aldh1a1/aldh2 KO mice	Rotarod, open field, actimetry, gait, Y-maze	↘↘	DA, DOPAC, DOPAC/DA ↘ DOPAL ↗	↘		[134]

^*compared to control group.