Latest news with #PINK1


The Independent
16-03-2025
- Health
- The Independent
Scientists make major breakthrough in understanding cause of Parkinson's
Scientists have identified the structure of the PINK1 protein, a breakthrough with potential implications for Parkinson's disease treatment. PINK1 mutations are linked to Parkinson's, particularly early-onset cases, and the research reveals how these mutations disrupt normal cellular processes in the brain. The discovery paves the way for developing drugs that could potentially slow or stop Parkinson's progression by targeting PINK1. The research also looks at how PINK1 binds to mitochondria – the powerhouse of the cell – and stops it from functioning properly. This breakthrough is hailed as a significant step towards understanding Parkinson's and creating new therapeutic strategies, offering hope for those affected.
Yahoo
15-03-2025
- Health
- Yahoo
Undiscovered cause of Parkinson's found for first time by scientists in huge breakthrough
Scientists have made a potentially 'life-changing' discovery that could pave the way for new drugs to treat Parkinson's disease. Experts have known for several decades that the PINK1 protein is directly linked to Parkinson's disease – the fastest growing neurodegenerative condition in the world. Until now, no one has seen what human PINK1 looks like, how PINK1 attaches to the surface of damaged mitochondria inside of cells, or how it is activated. But scientists have now discovered how the mutation switches on and can start using this knowledge to find a way to switch it off and slow the progression of the condition down. Researchers at the Walter and Eliza Hall Institute, Parkinson's Disease Research Centre, in Australia, have solved the decades-long mystery. The findings published in the journal Science reveal for the first time ever the structure of PINK1 and how it binds to mitochondria – the powerhouse of a cell – and stops it functioning properly. Parkinson's disease can take years, sometimes decades to diagnose. Often associated with tremors, there are close to 40 symptoms including cognitive impairment, speech issues, body temperature regulation and vision problems. The neurological condition affects around 153,000 Britons. There is currently no cure for Parkinson's, although medicine, physiotherapy and surgery can help manage symptoms. One of the hallmarks of Parkinson's is the death of brain cells. Around 50 million cells die and are replaced in the human body every minute. But, unlike other cells in the body, when brain cells die, the rate at which they are replaced is extremely low. When mitochondria are damaged, they stop making energy and release toxins into the cell. In a healthy person, the damaged cells are disposed of in a process called mitophagy. In a person with Parkinson's and a PINK1 mutation, the mitophagy process no longer functions correctly and toxins accumulate in the cell, eventually killing it. Brain cells need a lot of energy and are especially sensitive to this damage. In particular, PINK1 has been linked to young-onset Parkinson's Disease, which affects people under the age of 50. Despite the known link, researchers have previously been unable to visualise the protein or how it works. 'This is a significant milestone for research into Parkinson's. It is incredible to finally see PINK1 and understand how it binds to mitochondria,' said Professor David Komander, corresponding author on the study. 'Our structure reveals many new ways to change PINK1, essentially switching it on, which will be life-changing for people with Parkinson's,' he added. Lead author on the study, Dr Sylvie Callegari, said PINK1 works in four distinct steps, with the first two steps not having been seen before. First, PINK1 senses mitochondrial damage. Then, it attaches to damaged mitochondria. Once attached, it links to a protein called Parkin so that the damaged mitochondria can be recycled. 'This is the first time we've seen human PINK1 docked to the surface of damaged mitochondria, and it has uncovered a remarkable array of proteins that act as the docking site. We also saw, for the first time, how mutations present in people with Parkinson's disease affect human PINK1,' said Dr Callegari. The idea of using PINK1 as a target for potential drug therapies has long been touted but not yet achieved because the structure of PINK1 and how it attaches to damaged mitochondria were unknown. The research team hope to use the knowledge to find a drug to slow or stop Parkinson's in people with a PINK1 mutation. Researchers in the UK also believe the discovery could lead to better drug design. Consultant neurologist Dr Richard Ellis said: 'It is a crucial step towards understanding the impact of PINK1 in Parkinson's disease. These observations may hopefully create new opportunities for developing novel strategies for slowing the progression of Parkinson's disease.' Dr Zhi Yao, research scientist, Life Arc, said: 'A robust understanding of these aspects could present a significant opportunity for accelerating drug discovery for Parkinson's disease and potentially other neurodegenerative conditions too.' Becky Jones, research communications manager at Parkinson's UK, said: 'Changes in the PINK1 have long been linked to Parkinson's, and a specific mutation in the gene that contains the instructions for making the protein are known to cause a rare inherited form of the condition. 'It's encouraging to see this research, which will help us understand how changes in PINK1 might be causing damage to dopamine-producing brain cells in people with Parkinson's. 'This knowledge unlocks future avenues for better drug design and discovery of a treatment that could slow or even stop Parkinson's progression. This is vital, as despite it being the fastest growing neurological condition in the world, we don't yet have any drug treatments that can do this.'


The Independent
15-03-2025
- Health
- The Independent
Undiscovered cause of Parkinson's found for first time by scientists in huge breakthrough
Scientists have made a potentially 'life-changing' discovery that could pave the way for new drugs to treat Parkinson's disease. Experts have known for several decades that the PINK1 protein is directly linked to Parkinson's disease – the fastest growing neurodegenerative condition in the world. Until now, no one has seen what human PINK1 looks like, how PINK1 attaches to the surface of damaged mitochondria inside of cells, or how it is activated. But scientists have now discovered how the mutation switches on and can start using this knowledge to find a way to switch it off and slow the progression of the condition down. Researchers at the Walter and Eliza Hall Institute, Parkinson's Disease Research Centre, in Australia, have solved the decades-long mystery. The findings published in the journal Science reveal for the first time ever the structure of PINK1 and how it binds to mitochondria – the powerhouse of a cell – and stops it functioning properly. Parkinson's disease can take years, sometimes decades to diagnose. Often associated with tremors, there are close to 40 symptoms including cognitive impairment, speech issues, body temperature regulation and vision problems. The neurological condition affects around 153,000 Britons. There is currently no cure for Parkinson's, although medicine, physiotherapy and surgery can help manage symptoms. One of the hallmarks of Parkinson's is the death of brain cells. Around 50 million cells die and are replaced in the human body every minute. But, unlike other cells in the body, when brain cells die, the rate at which they are replaced is extremely low. When mitochondria are damaged, they stop making energy and release toxins into the cell. In a healthy person, the damaged cells are disposed of in a process called mitophagy. In a person with Parkinson's and a PINK1 mutation, the mitophagy process no longer functions correctly and toxins accumulate in the cell, eventually killing it. Brain cells need a lot of energy and are especially sensitive to this damage. In particular, PINK1 has been linked to young-onset Parkinson's Disease, which affects people under the age of 50. Despite the known link, researchers have previously been unable to visualise the protein or how it works. 'This is a significant milestone for research into Parkinson's. It is incredible to finally see PINK1 and understand how it binds to mitochondria,' said Professor David Komander, corresponding author on the study. 'Our structure reveals many new ways to change PINK1, essentially switching it on, which will be life-changing for people with Parkinson's,' he added. Lead author on the study, Dr Sylvie Callegari, said PINK1 works in four distinct steps, with the first two steps not having been seen before. First, PINK1 senses mitochondrial damage. Then, it attaches to damaged mitochondria. Once attached, it links to a protein called Parkin so that the damaged mitochondria can be recycled. 'This is the first time we've seen human PINK1 docked to the surface of damaged mitochondria, and it has uncovered a remarkable array of proteins that act as the docking site. We also saw, for the first time, how mutations present in people with Parkinson's disease affect human PINK1,' said Dr Callegari. The idea of using PINK1 as a target for potential drug therapies has long been touted but not yet achieved because the structure of PINK1 and how it attaches to damaged mitochondria were unknown. The research team hope to use the knowledge to find a drug to slow or stop Parkinson's in people with a PINK1 mutation. Researchers in the UK also believe the discovery could lead to better drug design. Consultant neurologist Dr Richard Ellis said: 'It is a crucial step towards understanding the impact of PINK1 in Parkinson's disease. These observations may hopefully create new opportunities for developing novel strategies for slowing the progression of Parkinson's disease.' Dr Zhi Yao, research scientist, Life Arc, said: 'A robust understanding of these aspects could present a significant opportunity for accelerating drug discovery for Parkinson's disease and potentially other neurodegenerative conditions too.' Becky Jones, research communications manager at Parkinson's UK, said: 'Changes in the PINK1 have long been linked to Parkinson's, and a specific mutation in the gene that contains the instructions for making the protein are known to cause a rare inherited form of the condition. 'It's encouraging to see this research, which will help us understand how changes in PINK1 might be causing damage to dopamine-producing brain cells in people with Parkinson's. 'This knowledge unlocks future avenues for better drug design and discovery of a treatment that could slow or even stop Parkinson's progression. This is vital, as despite it being the fastest growing neurological condition in the world, we don't yet have any drug treatments that can do this.'


Gulf Today
15-03-2025
- Health
- Gulf Today
Scientists make life-changing discovery on treating Parkinson's disease
Scientists have made a potentially 'life-changing' discovery that could pave the way for new drugs to treat Parkinson's disease. Experts have known for several decades that the PINK1 protein is directly linked to Parkinson's disease – the fastest growing neurodegenerative condition in the world. Until now, no one has seen what human PINK1 looks like, how PINK1 attaches to the surface of damaged mitochondria inside of cells, or how it is activated. But scientists have now discovered how the mutation switches on and can start using this knowledge to find a way to switch it off and slow the progression of the condition down. Researchers at the Walter and Eliza Hall Institute, Parkinson's Disease Research Centre, in Australia, have solved the decades-long mystery. The findings published in the journal Science reveal for the first time ever the structure of PINK1 and how it binds to mitochondria – the powerhouse of a cell – and stops it functioning properly. Parkinson's disease can take years, sometimes decades to diagnose. Often associated with tremors, there are close to 40 symptoms including cognitive impairment, speech issues, body temperature regulation and vision problems. The neurological condition affects around 153,000 Britons. There is currently no cure for Parkinson's, although medicine, physiotherapy and surgery can help manage symptoms. Death of brain cells One of the hallmarks of Parkinson's is the death of brain cells. Around 50 million cells die and are replaced in the human body every minute. But, unlike other cells in the body, when brain cells die, the rate at which they are replaced is extremely low. When mitochondria are damaged, they stop making energy and release toxins into the cell. In a healthy person, the damaged cells are disposed of in a process called mitophagy. In a person with Parkinson's and a PINK1 mutation, the mitophagy process no longer functions correctly and toxins accumulate in the cell, eventually killing it. Brain cells need a lot of energy and are especially sensitive to this damage. In particular, PINK1 has been linked to young-onset Parkinson's Disease, which affects people under the age of 50. Despite the known link, researchers have previously been unable to visualise the protein or how it works. 'This is a significant milestone for research into Parkinson's. It is incredible to finally see PINK1 and understand how it binds to mitochondria,' said Professor David Komander, corresponding author on the study. 'Our structure reveals many new ways to change PINK1, essentially switching it on, which will be life-changing for people with Parkinson's,' he added. 4 steps Lead author on the study, Dr Sylvie Callegari, said PINK1 works in four distinct steps, with the first two steps not having been seen before. First, PINK1 senses mitochondrial damage. Then, it attaches to damaged mitochondria. Once attached, it links to a protein called Parkin so that the damaged mitochondria can be recycled. 'This is the first time we've seen human PINK1 docked to the surface of damaged mitochondria, and it has uncovered a remarkable array of proteins that act as the docking site. We also saw, for the first time, how mutations present in people with Parkinson's disease affect human PINK1,' said Dr Callegari. The idea of using PINK1 as a target for potential drug therapies has long been touted but not yet achieved because the structure of PINK1 and how it attaches to damaged mitochondria were unknown. The research team hope to use the knowledge to find a drug to slow or stop Parkinson's in people with a PINK1 mutation. Researchers in the UK also believe the discovery could lead to better drug design. Consultant neurologist Dr Richard Ellis said: 'It is a crucial step towards understanding the impact of PINK1 in Parkinson's disease. These observations may hopefully create new opportunities for developing novel strategies for slowing the progression of Parkinson's disease.' Dr Zhi Yao, research scientist, Life Arc, said: 'A robust understanding of these aspects could present a significant opportunity for accelerating drug discovery for Parkinson's disease and potentially other neurodegenerative conditions too.' Becky Jones, research communications manager at Parkinson's UK, said: 'Changes in the PINK1 have long been linked to Parkinson's, and a specific mutation in the gene that contains the instructions for making the protein are known to cause a rare inherited form of the condition. 'It's encouraging to see this research, which will help us understand how changes in PINK1 might be causing damage to dopamine-producing brain cells in people with Parkinson's. 'This knowledge unlocks future avenues for better drug design and discovery of a treatment that could slow or even stop Parkinson's progression. This is vital, as despite it being the fastest growing neurological condition in the world, we don't yet have any drug treatments that can do this.'
Yahoo
14-03-2025
- Health
- Yahoo
Key Parkinson's Protein Structure And Malfunction Revealed For First Time
Researchers have unveiled the first real look at a mitochondrial protein strongly linked to Parkinson's disease, revealing key details in how its malfunction might play a critical role in the disease's progress. Scientists have known for more than two decades that mutations in the gene for a protein called PTEN-induced putative kinase 1 (PINK1) can trigger early-onset Parkinson's, but the mechanisms at play have remained a mystery. A team of scientists from the Walter and Eliza Hall Institute of Medical Research (WEHI) in Australia used advanced imaging technology to not only determine the structure of PINK1, but to show how the protein attaches to cellular power houses and how they are activated. "This is a significant milestone for research into Parkinson's," says WEHI medical biologist David Komander. "It is incredible to finally see PINK1 and understand how it binds to mitochondria. Our structure reveals many new ways to change PINK1, essentially switching it on, which will be life-changing for people with Parkinson's." The PINK1 protein is an important maintenance worker in the body. In healthy mitochondria, the protein passes through the outer and inner membranes, where it sinks out of sight. In mitochondria that have broken down, the protein is forced to pause half way through, tagging the power house for deletion through a series of processes that release a chemical signal called ubiquitin. When mutations prevent PINK1 from doing its job, dysfunctional mitochondria aren't cleared. Brain cells are particularly energy hungry, making the replacement of inefficient power units vital in order to prevent the neurodegeneration that triggers conditions like Parkinson's disease. Here, the team used techniques including cryo-electron microscopy and mass spectrometry to study PINK1 and mitochondria close-up, finding their attachment is based on a specific protein complex called TOM-VDAC. It's still early days for this research, but if treatments to repair the functionality of the protein can be developed, that may then give us a way of reducing the risk of Parkinson's or slowing its progress. "This is the first time we've seen human PINK1 docked to the surface of damaged mitochondria and it has uncovered a remarkable array of proteins that act as the docking site," says biochemist Sylvie Callegari, from WEHI. "We also saw, for the first time, how mutations present in people with Parkinson's disease affect human PINK1." Parkinson's is a complex disease, with undoubtedly numerous contributing factors. Yet by identifying the mechanisms behind proteins like PINK1, researchers move closer to understanding what the many causes have in common. The research has been published in Science. Just 5 Days of Junk Food Can Trigger Obesity's Hold on Your Brain World-First: Man Leaves Hospital With Life-Saving Titanium Heart Experts Warn Against Slushies For Kids, After UK Hospitalizations