<p>Parkinson’s disease (PD) is the second most prevalent brain disorder affecting the old age population and causes motor abnormalities such as shaking, stiffness, difficulty in walking balance, and coordination due to degeneration of dopaminergic neurons in the striatum. The current therapeutic strategies focus either on enhancing dopamine release or on slowing the progression of dopaminergic degeneration. This review focuses on finding the relationship between AMP-activated protein kinase (AMPK) and c-Jun N-terminal kinase (JNK) with PD and also targets their role against PD. The AMPK acts as a key regulator of metabolism, which participates in a wide range of activities like protecting mitochondrial dysfunction, autophagy, and degeneration of dopaminergic neurons. The JNK is responsible for coordinating several pathogenic mechanisms in PD, including neuronal apoptosis, excitotoxicity, and neuroinflammation. Hence, targeting AMPK and JNK as a therapeutic approach in PD by halting the progression of neurodegeneration and thereby increasing the life expectancy of patients.</p>