Parkinson’s disease is a complex disease with multiple treatment options, especially in the early stages of the disease. When patients are first diagnosed with PD, they need to be aware of two different treatment approaches – neuroprotective therapies and symptomatic treatments that target neurotransmitter function. In many cases, treatment strategies need to consider when to start treatment and which symptoms need to be treated. This requires a discussion of the pros and cons of treatment based on the patient’s level of disability and treatment goals. As the patient’s disease progresses, treatment endpoints may change and other medications or supplemental medications may be needed. Although studies related to drugs such as rasagiline, pramipexole and ropinirole have not yet suggested a clear neuroprotective therapeutic benefit, neuroprotective drug research continues and involves a number of different pathways, such as reducing oxidative stress, altering apoptotic pathways, inducing production of neurotrophic factors, and modulating cell signaling. Glutathione: It has been shown that increased oxidative stress may lead to the death of dopaminergic neurons, so glutathione is used as an antioxidant in PD research. Oral glutathione does not cross the blood-brain barrier, and studies have been conducted to try to increase the effect of glutathione through other mechanisms. One phase I clinical study is evaluating the safety and tolerability of transnasal glutathione administration; another study is attempting to increase glutathione concentrations through dietary supplementation. 2. Nicotine: Smokers have a lower incidence of PD, and studies have shown that nicotine may alter calcium-related signaling pathways as well as the immune response system, thereby reducing or preventing neuronal damage. An RCT is evaluating the efficacy of nicotine transdermal patches in PD patients treated for 52 weeks, with the primary endpoint being a change in UPDRS (Parkinson’s Disease Rating Scale) scores before and after treatment. 3.Pioglitazone: Studies have shown that pioglitazone can reduce microglia activation as well as oxidative stress and restore mitochondrial function. Because pioglitazone can inhibit MAO-B activity, so it is not clear whether it has a real neuroprotective effect or just reflects the effect of inhibiting MAO-B activity. 4, Granulocyte colony-stimulating factor: Although granulocyte colony-stimulating factor is commonly used in the treatment of leukopenia, a study in PD mice showed that it can play a long-term neuroprotective effect and improve the motor function of animals. Possible mechanisms of action include anti-apoptosis, reduction of inflammatory response, and induction of neurogenesis. 5, GM608: GM608 is a neuromodulatory and signaling-related peptide that appears at the endogenous human cellular stage. A phase II RCT study is currently evaluating the efficacy of intravenous GM608 as a neuroprotective drug in PD. 6. Physical exercise: Animal models have shown that exercise induces the production of brain-derived neurotrophic factor, which exerts a potential neuroprotective effect. Human studies are underway on different types of exercise, including moderate- or vigorous-intensity treadmill exercise, brisk walking, or simulated cycling. A systematic review has shown that treadmill exercise improves gait abnormalities in patients, however, the amount and duration of exercise is unclear. 7. Surgery: Animal studies have shown improved survival of dopaminergic neurons after pharmacologic ablation or DBS. Symptomatic treatment of PD: motor symptoms Gene and cellular therapies are invasive and are currently only being considered for patients with intermediate to advanced PD. In the future, once the safety, tolerability, and efficacy of potential therapies are clarified, clinicians will intervene early in the disease with both symptomatic and neuroprotective treatments.