Table 2.

Potential anti-inflammatory agents for treating and/or preventing PD and/or MDD [78, 89–95]

Potential therapeutic agent	Study	Empirically derived effect
Lenalidomide	[78]	Targets NOX2 activation to inhibit microglial activation and cytokine release, reducing dopaminergic neurodegeneration in transgenic mice
Diphenyleneiodonium	[91]	Targets NOX2 activation to reduce microglial activation, reducing dopaminergic neurodegeneration and α-syn aggregation in mice
Taurine	[92]	Targets NOX2 activation to reduce microglial activation, reducing dopaminergic neurodegeneration and α-syn aggregation in mice
α-Mangostin	[93]	Reduces NOX2 signalling and release of pro-inflammatory agents, including iNOS and ROS, by microglia in primary microglial cultures prepared from rats
Dimethyl fumarate	[90]	Reduces α-syn aggregation, reverses oxidative stress in neurons, reduces levels of COX2 and IL-1β, and induces natural antioxidant response in mice
AZD480	[94]	Inhibits JAK1/2 in the JAK/STAT pathway (a cytokine signalling pathway) that can activate in response to α-syn overexpression to produce a neuroinflammatory response
Semapimod	[89]	Inhibits MAPK, attenuating microglial activation and dopaminergic neuron degeneration
Fluoxetine olanzapine amitriptyline	[95]	Antidepressants that attenuate astrocyte reduction and hence limit impairment in glymphatic clearance

MDD, major depressive disorder; PD, Parkinson's disease; ROS, reactive oxygen species; IL, interleukin; MAPK, mitogen-activated protein kinase.