For more than 20 years, World Parkinson's Day takes place on April 11. On this date, the British physician James Parkinson was born in 1755. He was the first to describe the symptoms of the so-called "shaking palsy" in 1817, which was later named after him.
Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's disease. It affects approximately 1% of the world's population over the age of 60, making it a classic disease of old age. Although the disease is still incurable, there are currently many ways to make life better for Parkinson's patients. This year's Parkinson's Awareness Month in April of the Parkinson's Foundation is themed #UniteForParkinsons. The goal: to collectively raise awareness of the chronically progressive disease and call for continued research.
CECAD's social goal is to enable healthy aging. With this in mind, several CECAD research groups are investigating the basic biological mechanisms of Parkinson's as well as possible therapeutic approaches. We would like to take the opportunity of Parkinson's Awareness Month to provide insights into some of the current Parkinson's research projects at CECAD.
The research group led by Prof Peter Kloppenburg investigates which physiological properties render certain nerve cells particularly susceptible to degeneration during Parkinson's disease.
"In the course of Parkinson's disease, the nerve cells in the brain that produce dopamine, known as the happiness hormone, die in particular. We want to understand whether and how disturbances in calcium-dependent signaling pathways contribute to or are associated with the development of Parkinson's disease. In the long term, the hope is to identify new starting points for neuroprotective strategies against Parkinson's," explained Kloppenburg.
The research group led by Prof Rudolf Wiesner is studying the function of mitochondria, the so-called power plants of cells, which are also important for regulated cell death. The scientists are investigating how impaired mitochondrial function triggers the death of dopamine-producing neurons that is characteristic of Parkinson's disease.
"We know that especially in Parkinson's disease, as in many other diseases of old age, mitochondria do not function properly. That's why we're studying how mitochondrial defects specifically kill dopamine-producing neurons. The insights will open up avenues for new treatment strategies to slow the progression of the disease," Wiesner said.
Prof Thorsten Hoppe and his team are also shedding light on the role of mitochondria in the context of Parkinson's disease. They are investigating how hereditary defects in the quality control of mitochondrial proteins are linked to the disease.
"Among other things, our mitochondria control the folding and function of cellular proteins. Parkin, a key protein that regulates this process, is mutated and thus defective in many Parkinson's patients. We are investigating the role of Parkin in the quality control of mitochondria and the influence of the dysregulation on the development of Parkinson's disease in order to enable a therapeutic treatment in the long term," Hoppe summarized his work.
Prof Andreas Beyer and his team are investigating how Parkinson's disease, which progresses over a long period of time, affects many different functions of our cells. The goal is to find distinguishing features from healthy cells that appear as early as possible.
"Parkinson's disease is a highly complex neurodegenerative disorder that develops over many years. We are convinced that an early detection and treatment significantly improves prognosis and promises better outcomes. We believe that with our integrative, systems-based approaches, we can contribute significantly to a better understanding of disease mechanisms and potential treatment options. That is why we are working - together with international partners - on the development of improved molecular markers for Parkinson's disease," Beyer explained.
Which mechanisms lead to the neuropsychiatric symptoms of Parkinson's disease is the subject of Dr Marc Tittgemeyer's research. He and his colleagues are also investigating how the symptoms of affected individuals and their response to medication are influenced.
"In Parkinson's patients, nerve cells in the midbrain die. Our research is concerned with how the communication between these nerve cells is related to the patients' symptoms, such as neuropsychiatric impairments, as well as their response to drug therapy," said Tittgemeyer.