Pharmacological |
Reserpine |
Induces transient parkinsonian symptoms without nigral dopaminergic neurodegeneration |
Haloperidol
|
Blocks striatal dopaminergic transmission
|
Environmental |
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) |
Widespread animal models. Rapid neurodegeneration does not mirror the chronic and progressive evolution of PD |
6-hydroxydopamine (6-OHDA) |
Rotenone |
Less frequently used models. Induce dopaminergic neuron loss and Lewy bodies. The main limitations are peripheral toxicity and extent inflammation |
Paraquat |
Isoquinolines |
Methamphetamine |
Proteasome inhibitor I (PSI) |
Induce nigrostriatal neuron loss and Lewy bodies with progressive motor disability. High variability and low reproducibility. |
Epoximicin |
Lipopolysaccharide
|
Induce inflammation and related nigrostriatal neuronal loss. Does not replicate PD features.
|
Genetic |
Parkin |
Knock-out mice for these genes show motor dysfunction, but no neurodegeneration |
PTEN-induced kinase 1 (PINK1) |
Protein deglycase (DJ-1) |
Leucine-rich repeat kinase (LRRK) 2 |
Knock-in mice show alteration of dopaminergic transmission, without clear behavioral deficits |
Vacuolar protein sorting-associated protein (VPS) 35 |
Knock-out mice show a reduction in striatal dopamine level, accompanied by α-Synuclein accumulation and motor deficits |
Mitopark |
The specific loss of the gene coding for mitochondrial transcription factor A in dopaminergic neurons leads to a progressive decline of neuronal function and slow development of PD-related behavior |
α-Synuclein models |
Useful for the study of pathogenic mechanisms rather than for drug development. |