Scientists have discovered that new drugs could potentially pave the way for Parkinson’s disease.
Experts have known for decades that Pink1 protein is directly linked to Parkinson’s disease. This is the world’s fastest growing neurodegenerative state.
Until now, no one has seen what Human Pink1 looks like, how it adheres to the surface of damaged mitochondria within cells, or how it is activated.
However, scientists can now discover how the mutation is switching on and use this knowledge to find ways to turn it off and slow the progression of the state.
Researchers at the Walter and Eliza Hall Institute at the Australian Center for Parkinson’s Disease Research have solved decades of mystery.
Research results published in the journal Science It will first reveal the structure of Pink1 and how it binds to mitochondria, a cell-powerful nation, and stop it from functioning properly.
Diagnosis of Parkinson’s disease can take decades. There are almost 40 symptoms associated with tremors, including cognitive impairment, speech problems, thermoregulation, and vision problems.
Neurological conditions affect approximately 153,000 British people. Currently, there are no treatments for Parkinson’s disease, but medication, physical therapy and surgery can help you manage your symptoms.
One characteristic of Parkinson’s disease is the death of brain cells. Approximately 50 million cells die and are replaced by the human body every minute. However, unlike other cells in the body, when brain cells die, the rate at which they are exchanged is very low.
When mitochondria are damaged, they stop making energy and release toxins into the cells. In healthy people, damaged cells are discarded in a process called mitophagy.
In people with Parkinson’s disease and Pink 1 mutations, the mitophagy process no longer functions properly, and toxins accumulate in the cells, which ultimately kills them. Brain cells require a lot of energy and are particularly sensitive to this damage.
In particular, Pink1 is associated with young onset Parkinson’s disease and affects people under the age of 50. Despite known links, researchers were unable to visualize the protein or its mechanisms previously.
“This is an important milestone for the study of Parkinson’s disease. Professor David Commander, author of the study, said:
“Our structure reveals many new ways to change Pink1 and essentially turns it on. This will be life-changing for people with Parkinson’s disease,” he added.
Dr. Sylvie Karegali, the lead author of the study, said Pink1 works in four different steps, and the first two steps were not seen previously.
First, Pink1 senses mitochondrial damage. It then attaches to damaged mitochondria. When connected, it links to a protein called parkin so that it can recycle damaged mitochondria.
“This is the first time that human Pink1 has been docked on the surface of damaged mitochondria, revealing an incredible protein that acts as a docking site, and it is the first time we’ve seen how it exists in Parkinson’s disease patients.
The idea of using Pink1 as a potential drug therapy target has long been touted, but it has not yet been achieved as its structure and how it attaches to damaged mitochondria.
The researchers hope to use their knowledge to find drugs to slow or stop Parkinson’s disease in people with Pink1 mutations.
British researchers also believe the findings could lead to better drug design.
Consultant neurologist Dr. Richard Ellis said: “This is an important step in understanding the effects of Pink 1 in Parkinson’s disease. We hope that these observations will create new opportunities for developing new strategies to slow the progression of Parkinson’s disease.”
Dr. Zhi Yao, research scientist at Life Arc, said: “A robust understanding of these aspects may present important opportunities to promote creation due to Parkinson’s disease and potentially other neurodegenerative conditions.”
“We are pleased to announce that Becky Jones, Research Communications Manager at Parkinson’s UK, said: “Modifications in Pink1 have long been associated with Parkinson’s disease, and certain mutations in genes, including instructions to make proteins, are known to cause rare hereditary conditions.
“It’s encouraging to see this study. This helps us understand the possibility that changes in Pink1 can cause damage to dopamine-producing brain cells in people with Parkinson’s disease.
“This knowledge unlocks future measures, improves drug design, and discovers treatments that may slow or stop the progression of Parkinson’s disease. This is essential. Despite being the fastest growing neurological condition in the world, there is no drug treatment that can do this yet.”
