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Parkinson’s disease (PD) is a chronic and progressive neurodegenerative condition characterized by motor impairments such as tremors and stiffness, along with non-motor symptoms including cognitive decline and depression. While current dopaminergic therapies help manage symptoms, they do not halt the progression of the disease, underscoring the urgent need for treatments that can modify its course. This review explores the potential of repurposing drugs from diverse therapeutic categories—such as immunomodulators, cardiometabolic agents, and anti-infectives—to treat PD. Immunomodulatory compounds such as c-Abl inhibitors (e.g., imatinib and nilotinib) and sargramostim have shown potential to reduce α-synuclein buildup and brain inflammation, though clinical outcomes have been inconsistent. Among cardiometabolic drugs, glucagon-like peptide-1 (GLP-1) receptor agonists, such as exenatide, have shown promising results in improving motor and cognitive function, with phase III trials currently investigating their ability to slow disease progression. Some anti-infective agents, including doxycycline and rifampicin, offer neuroprotective benefits through anti-inflammatory and anti-aggregation mechanisms. Despite ongoing concerns regarding their effectiveness and potential side effects, these repurposed drugs represent promising avenues for PD treatment. Moreover, emerging strategies such as gene therapy, enzyme replacement therapy, and advanced drug-delivery technologies aim to target the underlying disease mechanisms directly. Although no definitive disease-modifying treatment exists yet, the investigation of repurposed and novel therapies provides optimism for future advancements. Further large-scale clinical studies are essential to confirm their safety and therapeutic value.

Parkinson’s disease stands as the second most common neurodegenerative disorder worldwide. This study aimed to assess the impact of DMSO in a rotenone-induced rat model of Parkinson’s disease. DMSO has become a popular agent in preclinical and clinical studies due to its ability to facilitate the transport of poorly soluble drugs across the blood-brain barrier. In this investigation, we explored how a three-week treatment with rotenone, combined with DMSO, influenced hippocampal neuronal activity and the properties of neuronal responses in rats. We specifically compared the toxic effects of rotenone on hippocampal CA1 and CA3 neurons in the presence of DMSO. Our results showed that rotenone induced substantial morphological changes in hippocampal cells. Following DMSO treatment, however, there was a significant restoration of pyramidal cells and Nissl bodies within the CA1 and CA3 regions. DMSO also effectively suppressed both outward and inward currents. Additionally, we recorded spontaneous and evoked spike activity in the hippocampus of rats treated with DMSO (1 ml/kg, administered intraperitoneally for 3 weeks). While rotenone elevated TP and produced a moderate TD effect, DMSO also increased TP but produced a more pronounced TD effect. The analysis indicated inhibitory responses in the hippocampus following high-frequency stimulation (100 Hz for 1 second) of the ipsilateral entorhinal cortex.