Recent Progress in Parkinson’s Disease Research

Parkinson’s disease is a common degenerative disease of the nervous system in the elderly, which can seriously affect the quality of life of patients and put great pressure on patients and families. From the global research on the aging, the prevalence of Parkinson’s disease in the population is increasing year by year, which brings heavy burden to the society. Meanwhile, the treatment of Parkinson’s disease is also one of the important research topics in the field of life and health. In this article, we sort out recent research on Parkinson’s disease.

1. The level of caffeine in the blood may diagnose people with Parkinson’s disease

Testing the level of caffeine in the blood may provide a simple way to aid the diagnosis of Parkinson’s disease, according to a study published in the January 3, 2018, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study found that people with Parkinson’s disease had significantly lower levels of caffeine in their blood than people without the disease, even if they consumed the same amount of caffeine.

2. Student finds Parkinson’s treatment could be more effective

A Binghamton University senior and her colleagues recently uncovered evidence that the current treatment for Parkinson’s disease may not be as effective as it could be. Parkinson’s disease, a neurodegenerative disorder, caused by a loss of the brain chemical dopamine. The dopamine circuit involved in motor movements consists of two receptors in the brain, the D1 and the D2 receptors. The current treatment for Parkinson’s disease is the drug L-DOPA, which acts on both of these receptors to release and replenish dopamine in the brain. The researchers in the Freshman Research Immersion program (FRI) at Binghamton provided evidence that stimulating the D2 receptor produces cognitive deficits, illustrating that L-DOPA may not be the best treatment for Parkinson’s disease.

3. Why exercise slows progression of Parkinson’s disease

While vigorous exercise on a treadmill has been shown to slow the progression of Parkinson’s disease in patients, the molecular reasons behind it have remained a mystery. But now scientists at the University of Colorado Anschutz Medical Campus may have an answer. For the first time in a progressive, age-related mouse model of Parkinson’s, researchers have shown that exercise on a running wheel can stop the accumulation of the neuronal protein alpha-synuclein in brain cells. The researchers said clumps of alpha-synuclein are believed to play a central role in the brain cell death associated with Parkinson’s disease.

4. New brainstem changes were identified in Parkinson’s disease

A pioneering study has found that patients with Parkinson’s disease have more errors in the mitochondrial DNA within the brainstem, leading to increased cell death in that area. Experts at Newcastle and Sussex universities also revealed that surviving brain cells in the brainstem have more copies of mitochondrial DNA and this has not been identified before. The study’s deeper understanding into Parkinson’s disease suggests a new target for therapies for patients with the debilitating condition.

5. Tapeworm drug could fight against Parkinson’s disease

Over the last decade or so, researchers striving to find a cure for this debilitating disease have focused their attention on a protein found in the human body known as PINK1. It’s understood that the malfunction of this protein is one of the leading causes of Parkinson’s disease. Several studies have suggested that discovering a drug which is capable of enhancing the function of PINK1 could be a significant step in halting neurodegeneration and therefore slow down or even treat Parkinson’s disease. With this knowledge in mind, researchers at Cardiff and Dundee Universities have discovered that a drug traditionally used to treat tapeworm infections, named Niclosamide, is also an effective activator of the PINK1 protein.

6. New findings point to the potential therapy for Parkinson’s disease

Parkinson’s disease is a progressive neurological disorder marked by the loss of dopaminergic neurons. There is no cure for it. Current treatments help control the symptoms of Parkinson’s disease, including tremor, slow movement and loss of balance. A new study, published in Proceedings of the National Academy of Sciences (PNAS), sheds light on a mechanism underlying Parkinson’s disease and suggests that Tacrolimus—an existing drug that targets the toxic protein interaction explored in the study—could be used as a novel treatment.

7. Restless sleep may be an early sign of Parkinson’s disease

Researchers from Aarhus University have discovered that patients with the RBD sleep behaviour disorder lack dopamine and have a form of inflammation of the brain. This means that they are at risk of developing Parkinson’s disease or dementia when they grow older. Because they already suffer from a lack of dopamine in the brain. Parkinson’s disease occurs precisely because the group of nerve cells in the brain that produce dopamine stop working.

8. Critical toxic species behind Parkinson’s disease is glimpsed at work

Researchers have glimpsed how the toxic protein clusters that are associated with Parkinson’s Disease disrupt the membranes of healthy brain cells, creating defects in the cell walls and eventually causing a series of events that induce neuronal death. The study examined what are known as toxic oligomers, clusters of protein molecules that emerge when individual proteins misfold and clump together. In the case of Parkinson’s Disease, the protein involved is called alpha synuclein, which when it is functioning normally plays an important part in signalling in the brain. The formation and spread of these clusters is thought to be a key component of the underlying molecular mechanisms of this progressive illness. Understanding how they enter and damage cells presents an opportunity to develop new and more effective treatments.

9. Changes in diet may improve life expectancy in Parkinson’s patients

New research from the University of Aberdeen shows that weight loss in people with Parkinson’s disease leads to decreased life expectancy, increased risk of dementia and more dependency on care. The team, led by Dr Angus Macleod, propose that closer monitoring for weight loss in Parkinson’s patients and interventions in those who lose weight, such as a high calorie diet, may improve life expectancy, reduce dementia and reduce dependence on carers.



Fujimaki, M., Saiki, S., Li, Y., Kaga, N., Taka, H., Hatano, T., … & Koinuma, T. (2018). Serum caffeine and metabolites are reliable biomarkers of early Parkinson disease. Neurology, 10-1212.

Zhou, W., Barkow, J. C., & Freed, C. R. (2017). Running wheel exercise reduces α-synuclein aggregation and improves motor and cognitive function in a transgenic mouse model of Parkinson’s disease. PloS one, 12(12), e0190160.

Bury, A. G., Pyle, A., Elson, J. L., Greaves, L., Morris, C. M., Hudson, G., & Pienaar, I. S. (2017). Mitochondrial Dna changes in pedunculopontine cholinergic neurons in Parkinson disease. Annals of neurology, 82(6), 1016-1021.

Barini, E., Miccoli, A., Tinarelli, F., Mulholand, K., Kadri, H., Khanim, F., … & Mehellou, Y. (2017). The Anthelmintic Drug Niclosamide and its Analogues Activate the Parkinson’s Disease Associated Protein Kinase PINK1. ChemBioChem.

Caraveo, G., Soste, M., Cappelleti, V., Fanning, S., van Rossum, D. B., Whitesell, L., … & Picotti, P. (2017). FKBP12 contributes to α-synuclein toxicity by regulating the calcineurin-dependent phosphoproteome. Proceedings of the National Academy of Sciences, 114(52), E11313-E11322.

Stokholm, M. G., Iranzo, A., Østergaard, K., Serradell, M., Otto, M., Svendsen, K. B., … & Møller, A. (2017). Assessment of neuroinflammation in patients with idiopathic rapid-eye-movement sleep behaviour disorder: a case-control study. The Lancet Neurology, 16(10), 789-796.

Fusco, G., Chen, S. W., Williamson, P. T., Cascella, R., Perni, M., Jarvis, J. A., … & Ying, L. (2017). Structural basis of membrane disruption and cellular toxicity by α-synuclein oligomers. Science, 358(6369), 1440-1443.