Looking back at the nearly 200 years of Parkinson’s disease research history, counting its step-by-step leap, in revisiting the history of the classic at the same time, we are also constantly summarizing and thinking: in the rapid development of medical level today, with the clinical understanding of Parkinson’s disease more and more in-depth, we have what new understanding and improvement for its diagnosis and treatment? First, should be based on clinical, integrated multiple means to improve the correct rate of Parkinson’s disease diagnosis Since 1817 Parkinson first described the typical clinical symptoms of Parkinson’s disease, although nearly 200 years have passed, but at present the world for the diagnosis of Parkinson’s disease still depends mainly on its clinical characteristics. Bradykinesia, myotonia, resting tremor and postural balance disorders are the four core symptoms. However, these core symptoms are not unique to Parkinson’s disease; secondary Parkinson’s syndrome and Parkinson’s superimposed syndrome can have similar clinical manifestations. Especially in the early stages of the disease, they often have a high degree of similarity and are more difficult to distinguish from each other. Therefore, the development of more valuable aids for more accurate diagnosis of Parkinson’s disease has been a hot topic of research in the field of Parkinson’s disease. Today, the diagnosis of familial Parkinson’s disease is supported by more precise causative genes. As for early-onset Parkinson’s disease, multiple susceptibility genes such as LRRK2, parkin, PINKl, DJ-1, ATPl3A2, PLA2G6, FBX07 and other genes have also been extensively probed by researchers in multiple ethnic populations. Olfactory testing should be an important aid in our diagnosis of Parkinson’s disease in 2013, as 60% to 90% of patients with Parkinson’s disease have olfactory deficits, while in patients with multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal ganglion degeneration, and idiopathic tremor, olfaction is normal or only mildly impaired in a minority of patients. The vast majority of vascular and drug-induced Parkinson’s syndromes also have a normal sense of smell. Monogenic inheritance, especially recessive Parkinson’s disease, also has a milder degree of olfactory involvement. In the differential diagnosis of Parkinson’s disease, neuroimaging techniques have highlighted their important clinical value. In addition to conventional 1.5 T MRI and diffusion sequences that can be used as imaging tools to differentiate MSA, PSP and Parkinson’s disease, cranial ultrasound diagnosis that detects hyper-echoic signals in the substantia nigra is rapidly being used in various countries as another effective tool to differentiate Parkinson’s disease from Parkinson’s superposition syndrome or secondary Parkinson’s syndrome. Functional brain imaging has also made a major breakthrough in the diagnosis of Parkinson’s. DaTscan SPECT has been approved in Europe and the United States for differentiating neurodegenerative Parkinson’s syndrome from idiopathic tremor, drug-induced Parkinson’s syndrome, or isolated unilateral postural tremor. In addition, cardiac interiodinated benzylguanidine SPECT uptake has also been used to identify Parkinson’s disease and MSA. Appropriate use of all of these clinical aids can significantly improve the correct diagnosis of Parkinson’s disease. Our clinical study also found that integrated genetic or biochemical markers, olfactory testing, cranial ultrasound, and functional brain imaging showing dopamine transporter activity and D2 dopamine receptor activity can significantly improve the correct rate of Parkinson’s disease diagnosis. The milestone in the history of Parkinson’s disease treatment is undoubtedly the application of levodopa, which revolutionized the fate of Parkinson’s disease patients. However, as the “honeymoon period” ended, the disabling motor complications associated with levodopa changed us from “worship” to “fear”. The issue of levodopa’s “neurotoxicity” also plagued us for a while. With the development of other anti-Parkinsonian drugs, including anticholinergic agents, amantadine, monoamine oxidase B (MAO-B) inhibitors, catechol monooxygenase inhibitors, and dopamine agonists, the first choice of drug therapy for Parkinson’s disease has become a hot topic of controversy. attention. The best efficacy of compounded levodopa agents is unquestioned, despite their tendency to cause “motor complications”. Receptor agonists are favored as the treatment of choice for younger patients because of their ability to prevent “motor complications” and their potential neuroprotective effects. While the debate over the drug of choice continues, what has come to light over the years is a question that has put leading experts to shame: What is the appropriate dose of levodopa for different individuals? Olanow has recently proposed that a dose of no more than 400 mg/d is the appropriate dose, clearly stating that this dose is less likely to produce exercise complications. Therefore, we should be able to overcome the “levodopa phobia” and understand and apply levodopa in a more scientific way. In the selection of drug therapy for Parkinson’s disease, we should follow the principles of existing guidelines and also focus on the principle of individualization, taking into account the financial burden, occupation and quality of life requirements of patients. In 2013, our ultimate goal for Parkinson’s disease treatment remains the same – to achieve a cure – but this is still a dream due to the lack of ideal animal models that mimic both the motor and non-motor symptoms of Parkinson’s disease. Recent findings suggest that active exercise can help prevent or delay the onset of Parkinson’s disease, and even if it does develop, symptoms are relatively mild, and for those who have developed the disease, active exercise can improve symptoms to varying degrees. This undoubtedly opens up a new avenue for the treatment of Parkinson’s disease. Although Parkinson’s disease attracts the most attention for its motor symptoms, after the motor symptoms have been actively controlled, the increasingly prominent problem is its non-motor symptoms. Pain, fatigue, sleep disturbances, autonomic dysfunction, and especially anxiety, depression, and cognitive dysfunction, severely impact the quality of life of patients. The average prevalence of Parkinson’s disease dementia (PDD) is as high as 40% in patients with Parkinson’s disease, and its prevalence is four to six times higher than that of the healthy population. The average prevalence of Parkinson’s disease mild cognitive impairment (PD-MCI) is also in the range of 20%-50%. Therefore, how to diagnose, assess and treat cognitive impairment early is significant for the quality of life of patients and their caregivers. Treatment with cholinesterase inhibitors has shown mild to moderate effects. However, research on cognitive impairment in Parkinson’s disease is just beginning, and neuroimaging including PET techniques have initially revealed cortical atrophy, hypometabolism, white matter alterations, dopaminergic and/or cholinergic dysfunction and increased amyloid load. The combination of imaging manifestations and detection of cerebrospinal fluid biomarkers such as tau protein and B-amyloid to diagnose PD-MCI and PDD will be the main research direction in the future. Parkinson’s disease is not a simple disease; it involves physical, psychological and social issues. With the peak of population aging, the socio-economic problems caused by this disease will become increasingly serious. The motor symptoms of Parkinson’s disease are actually just the tip of the iceberg, and the numerous non-motor symptoms it has may become a greater challenge for future research. The preclinical diagnosis and the foundation for subsequent neuroprotective treatment will also be a high priority for future research.