Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease (AD), and its pathogenesis remains obscure. Current treatment approaches mainly including levodopa and dopamine agonists provide symptomatic relief but fail to halt disease progression, and they are often accompanied by severe side effects. In this context, natural phytochemicals have received increasing attention as promising preventive or therapeutic candidates for PD, given their multitarget pharmaceutical mechanisms of actions and good safety profile. Ginger (Zingiber officinale Roscoe, Zingiberaceae) is a very popular spice used as a medicinal herb throughout the world since the ancient years, for a wide range of conditions, including nausea, diabetes, dyslipidemia, and cancer. Emerging in vivo and in vitro evidence supports the neuroprotective effects of ginger and its main pharmaceutically active compounds (zingerone, 6-shogaol, and 6-gingerol) in PD, mainly via the regulation of neuroinflammation, oxidative stress, intestinal permeability, dopamine synaptic transmission, and possibly mitochondrial dysfunction. The regulation of several transcription factors and signaling pathways, including nuclear factor kappa B (NF-κB), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol-3-kinase (PI3K)/Ak strain transforming (Akt), extracellular signal-regulated kinase (ERK) 1/2, and AMP-activated protein kinase (AMPK)/proliferator-activated receptor gamma coactivator 1 alpha (PGC1α) have been shown to contribute to the protective effects of ginger. Herein, we discuss recent findings on the beneficial role of ginger in PD as a preventive agent or potential supplement to current treatment strategies, focusing on potential underlying molecular mechanisms.