The Interplay Between Neuroinflammatory Pathways and Insights into Deep Brain Stimulation Mechanisms in Parkinson's Disease

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the gradual degeneration of the nigrostriatal dopaminergic pathway, leading to neuronal loss within the substantia nigra pars compacta (SNpc) and

dopamine depletion. While the primary cause of PD is the loss of dopaminergic neurons, the precise mechanisms

behind this loss remain incompletely understood. However, current evidence indicate that this process is influenced b y v arious m olecular f actors, i ncluding neuroinflammation, impaired protein homeostasis, and mitochondrial dysfunction. Further exploration of the intricate interplay between neuroinflammation and mitochondrial dysfunction is warranted to advance our understanding of PD pathogenesis. Deep brain stimulation (DBS), a neuromodulation technique involving electric current delivered through stereotactically implanted electrodes, represents a transformative intervention in neurosurgery, offering precise and minimally invasive treatments for various neurological and movement disorders. While the exact mechanism of action is not fully elucidated for DBS, it is acknowledged as a successful therapeutic choice for PD. A growing body of evidence suggests its potential for anti- neuroinflammatory and neuroprotective effects, although contrasting perspectives exist. Contrary to initial concerns, DBS demonstrates anti-inflammatory effects, impacting cytokine release, glial activation, and neuronal survival. Comprehending the potential influence o f D BS o n inflammatory processes holds substantial ramifications for addressing neurological and neuropsychiatric conditions marked by neuroinflammation, such as PD. Such insights may lead to the development of novel therapeutic strategies that combine DBS with anti- inflammatory approaches, opening new avenues for managing complex neurological disorders.