Abstract: Deep brain stimulation (DBS) is an established therapeutic intervention for people with Parkinson’s disease (PwPD) and is increasingly being utilized for other neurological disorders. Although effective in alleviating motor symptoms and reducing medication requirements, DBS has undergone minimal conceptual evolution and still relies on continuous high-frequency electrical stimulation. In Parkinson’s disease (PD), this persistent stimulation may cause adverse effects, including dysarthria, stimulation-induced dyskinesia, impulsivity, and mood alterations. Additionally, the continuous energy demand of current DBS systems accelerates battery depletion, necessitating more frequent battery charging or battery replacement surgeries, increasing risks, burden, and costs. Basic neuroscience research has long demonstrated that exogenous electrical stimulation can induce persistent changes to synaptic connections, known as longterm plasticity. This raises the question of whether continuous DBS could be replaced by stimulation paradigms leveraging plasticity for therapeutic effects that persist even after stimulation ceases. Such approaches have recently been demonstrated in Parkinsonian rodent models (Figure 1A and C) and PwPD (Figure 1B and D). In general, the field still lacks robust bench-to-bedside translation, with limited incorporation of mechanistic insights into clinical DBS protocols. A critical re-evaluation of existing DBS strategies, with an emphasis on harnessing lasting physiologically-informed plastic changes to modulate circuit function, may yield more effective therapeutic strategies that minimize stimulation-related side effects and energy demands to reduce therapeutic burden, risks, and costs.