Parkinson’s disease (PD) is a neurodegenerative disease characterised by histopathological
and biochemical manifestations such as loss of midbrain dopaminergic (DA) neurons and decrease
in dopamine levels accompanied by a concomitant neuroinflammatory response in the affected
brain regions. Over the past decades, the use of toxin-based animal models has been crucial to
elucidate disease pathophysiology, and to develop therapeutic approaches aimed to alleviate its motor
symptoms. Analyses of transgenic mice deficient for cytokines, chemokine as well as neurotrophic
factors and their respective receptors in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
model of PD have broadened the current knowledge of neuroinflammation and neurotrophic support.
Here, we provide a comprehensive review that summarises the contribution of microglia-mediated
neuroinflammation in MPTP-induced neurodegeneration. Moreover, we highlight the contribution of
neurotrophic factors as endogenous and/or exogenous molecules to slow the progression of midbrain
dopaminergic (mDA) neurons and further discuss the potential of combined therapeutic approaches
employing neuroinflammation modifying agents and neurotrophic factors.