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Table 4 Different animal models and their applications in PD research. LB-Lewy bodies, IFC-impaired fear conditioning, CD-cognitive deficits, MD-mitochondrial, deficits, RA-reduced anxiety, ASP-affected synaptic plasticity, RD-reduced dopamine level

From: Current understanding of the molecular mechanisms in Parkinson's disease: Targets for potential treatments

Category Models Mechanism NS loss Inclusions Motor deficit Non-motor deficit Applications Demerits Refs.
Environ mental toxins 6-OHDA Complex I inhibition +++ _ +++ Cognitive, psychiatric,
and GI disorders 		Screen therapies for PD, study mechanisms
of cell death 		Degeneration non-progressive [283]
MPTP Complex I inhibition ++ -, presence of SNCA at SNpc +++ Numerous Screen therapies for PD, study mechanisms
of cell death 		Non-progressive rare inclusions [284, 285]
Rotenone Complex I inhibition, ↑ROS ++ Presence of SNCA at SNpc +++ Decrease GI motility Test neuroprotective
compounds 		morbidity, mortality, time consuming & laborious [286]
Paraquat Complex I inhibition, ↑ROS +++ No inclusions at SNpc _ Not detected Test neuroprotective
compounds 		Substantial morbidity, mortality, time consuming & laborious [287, 288]
Maneb Impairment of glutamate and DA uptake + _ + Not detected Study glutamate uptake in DA neurons No inclusion, less DA neuronal damage [287, 288]
Others SHH, Nurr1, Pitx3, EN1 Impaired protein synthesis in DA-neurons ++ _ +/− Not known Study the mechanism of Translation in DA neurons No SNCA [289,290,291]
MitoPark Mitochondrial deficit ++ +/− + Not known Study the role of mitochondria in PD Less motor deficit [292, 293]
PDC EAATs blockade, excitotoxicity, ↑ROS ++ _ + Not known To study excitotoxicity and Oxidative pathway in PD No SNCA [293, 294]
Genetic Parkin (PARK2) Loss of ubiquitin E3- ligase activity +/− +/− +/− _ Study the role of E3 ligase in PD No inclusion, less DA neuronal damage [239, 295]
LRRK2
(PARK 8) 		Loss of enzymatic activity _ _ Drosophila
+ 		Not detected Study the role of
LRRK2 mutations
related to PD 		No SNCA nor no DA degeneration [296, 297]
PINK (PARK6) Mitochondrial damage +/− +/− +/− Not detected Study the role of mitochondria in PD No SNCA or no DA degeneration [298, 299]
DJ-1(PARK 7) Increase ROS, Mito. dysfunction +/− +/− +/− Not detected Study oxidative stress & mitochondrial dysfunction in PD Less inclusion & DA neuronal damage [300, 301]
SNAC mutation and animal models of PD
Models Promoter Background SNCA Motor signs Nonmotor signs TH neurons loss Disease progression Ref
WT, A53T PDGF-b C57BL/6 9 DBA2 + + – + – [302,303,304]
A53T Mouse Thy-1 C57BL/6 LB + – – – [305]
WT, A30P, A53T Mouse Thy-1 C57BL/6 + + + – + [306, 307]
WT, (A30P) Mouse Thy-1 C57BL/6 x DBA2 + + IFC + + [303, 308]
Y39C Mouse Thy-1 FVB/N + + CD – + [309]
A30P + A53T Human Thy-1 C57BL/6 x DBA2 + + – + + [310]
(WT), (A30P), A53T Mouse prion C3H/HeJ 9 C57BL/6 J
backcrossed into C57BL/6 J
PARKIN KO 		+ + MD – + [311, 312]
WT, A53T Mouse prion C57BL/6 x C3H + + RA – + [313, 314]
(WT), A53T Mouse prion FVB/N, FVB 9129, SNCA-KO – + – – + [315]
(WT), A30P Mouse prion C57BL/6 J 9 DBA2
backcrossed into C57BL/6 J 		– + ASP – – [316]
WT, A30P, A53T Hamster prion C57BL/6 J x SJL – + – – + [317, 318]
WT, A30P, A53T Rat THP Swiss Webster x C57BL/DBA – – – – – [287]
WT, A30P ± A53T Rat THP C57BL/6 – + – – + [319]
WT, A30P, A53T CaM-tTA (tet-off) C57BL/6 (WT and A30P),
C57BL/CH3 (WT and A53T) 		– + CD – + [320, 321]
A30P KI in endogenous SNCA C57BL/6 – + – RD + [322]
WT, A30P, A53T Endogenous SNCA (BAC) FVB/N 9129S6 / SvEvTac – + + – + [323]
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Translational Neurodegeneration

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