Table 1.

A comparison of some of the most common toxin-based animal models of Parkinson's disease.

Toxin model	Mode of action	Advantages	Disadvantages
6-OHDA	(i) DAT substrate (ii) Cytotoxic quinone and ROS formation	(i) Full DA depletion (ii) Mimics late-stage PD	(i) Does not cross BBB (ii) DA degeneration is not progressive (iii) No Lewy body-like inclusions (iv) Lacks external validity
MPTP	(i) Converted into MPP+ (ii) DAT substrate (iii) Inhibits mitochondrial complex I (iv) Strong inflammatory component	(i) Highly reproducible (ii) Induces substantial DA loss and motor impairment	(i) DA degeneration is not progressive (ii) Does not provoke Lewy body-like inclusions (iii) Systemic toxicity (iv) Lacks external validity
Paraquat	(i) Potent redox cycler (ii) Neuroinflammatory component	(i) Progressive loss of DA neurons (ii) Lewy-body like α-synuclein inclusions (iii) Potential ecological validity	(i) Inconsistent striatal DA loss and motor impairment (ii) Induces only moderate DA cell loss when administered alone (ii) Systemic toxicity
Rotenone	(i) Readily crosses DA neuron membrane (ii) Inhibits mitochondrial complex I (iii) Neuroinflammatory component	(i) Progressive loss of DA neurons (ii) Lewy body-like inclusions (iii) Potential ecological validity	(i) Variable reproducibility (ii) Systemic toxicity (iii) Nonspecific accumulation within the CNS
LPS	Immune system activation	(i) Progressive loss of DA neurons (ii) Strong inflammatory component (iii) Sensitizes DA neurons to later treatment with LPS or other toxins	No Lewy body-like inclusions