Latest news with #WalterandElizaHallInstituteofMedicalResearch
NDTV
12-05-2025
- Health
- NDTV
Scientists Find Molecule That Blocks Brain Cell Death In Parkinson's, Alzheimer's
Sydney: A team of Australian scientists has identified a small molecule that blocks cell death, an advance that could lead to new treatments for neurodegenerative conditions like Parkinson's and Alzheimer's. The team from the Melbourne-based Walter and Eliza Hall Institute of Medical Research (WEHI) aimed to find new chemicals that block cell death, which could help treat degenerative diseases in the future. The findings offer hope for treatments that could slow or stop the progression of neurodegenerative diseases. After screening over 100,000 chemical compounds, the team found a small molecule that targets a killer protein called BAX. By interfering with a well-understood cell death protein, the molecule effectively stopped cells from dying. "We were thrilled to find a small molecule that targets a killer protein called BAX and stops it working," said Professor Guillaume Lessene from WEHI. "While not the case in most cells, in neurons turning off BAX alone may be sufficient to limit cell death," Lessene added. While drugs that trigger cell death are transforming the treatment of certain cancers, the development of cell death blockers -- that could be similarly game-changing for neurodegenerative conditions -- has proven challenging. The new molecule targets a killer protein called BAX, which kills cells by damaging mitochondria, the powerhouse of cells. "For the first time we could keep BAX away from mitochondria and keep cells alive using this molecule," said lead author and Dewson Lab researcher Kaiming Li. "This could pave the way for next-generation cell death inhibitors to combat degenerative conditions," Li said, in the paper published in the journal Science Advances. While drugs that trigger cell death are transforming the treatment of certain cancers, the development of cell death blockers - that could be similarly game-changing for neurodegenerative conditions -- has proven challenging. The study demonstrates the potential to identify drugs that block cell death and may open a new avenue to find much-needed disease-modifying drugs for Parkinson's and Alzheimer's, said the researchers.
Hans India
12-05-2025
- Health
- Hans India
Scientists find molecule that blocks brain cell death in Parkinson's, Alzheimer's
Sydney: A team of Australian scientists has identified a small molecule that blocks cell death, an advance that could lead to new treatments for neurodegenerative conditions like Parkinson's and Alzheimer's. The team from the Melbourne-based Walter and Eliza Hall Institute of Medical Research (WEHI) aimed to find new chemicals that block cell death, which could help treat degenerative diseases in the future. The findings offer hope for treatments that could slow or stop the progression of neurodegenerative diseases. After screening over 100,000 chemical compounds, the team found a small molecule that targets a killer protein called BAX. By interfering with a well-understood cell death protein, the molecule effectively stopped cells from dying. 'We were thrilled to find a small molecule that targets a killer protein called BAX and stops it working,' said Professor Guillaume Lessene from WEHI. 'While not the case in most cells, in neurons turning off BAX alone may be sufficient to limit cell death," Lessene added. While drugs that trigger cell death are transforming the treatment of certain cancers, the development of cell death blockers -- that could be similarly game-changing for neurodegenerative conditions -- has proven challenging. The new molecule targets a killer protein called BAX, which kills cells by damaging mitochondria, the powerhouse of cells. 'For the first time we could keep BAX away from mitochondria and keep cells alive using this molecule,' said lead author and Dewson Lab researcher Kaiming Li. 'This could pave the way for next-generation cell death inhibitors to combat degenerative conditions,' Li said, in the paper published in the journal Science Advances. While drugs that trigger cell death are transforming the treatment of certain cancers, the development of cell death blockers – that could be similarly game-changing for neurodegenerative conditions -- has proven challenging. The study demonstrates the potential to identify drugs that block cell death and may open a new avenue to find much-needed disease-modifying drugs for Parkinson's and Alzheimer's, said the researchers.
Yahoo
01-04-2025
- Health
- Yahoo
Protein That Calms Waking Hair Follicles Could Lead to Alopecia Treatment
A new study has identified a protein that appears to be essential for hair growth and hair follicle protection. Called MCL‑1, it could potentially be targeted by treatments for certain kinds of baldness such as alopecia. Led by a team from the Duke‑NUS Medical School in Singapore and the Walter and Eliza Hall Institute of Medical Research in Australia, researchers found that when MCL-1 production was blocked in mice, the animals lost their hair later in life. Hair follicles go through cycles of quiescence and growth, with MCL-1 playing a critical role in the latter phase. The protein doesn't seem to affect the resting phase or the initial development of hair follicles, however. "Acute MCL‑1 deletion rapidly depletes activated hair follicle stem cells and completely blocks depilation‑induced hair regeneration in adult mice, while quiescent hair follicle stem cells remain unaffected," write the researchers in their published paper. It was already known that MCL-1 played an important role in protecting a number of different kinds of tissue from apoptosis; the programmed death of redundant or damaged cells to keep the body functioning. When it comes to hair, MCL-1 prevents follicle stem cells from being stressed and damaged as they 'reawaken' from rest. Without MCL-1 to protect them, these cells stop functioning. The team was also able to reveal new details on MCL-1's function, identifying ways it suppresses another protein called BAK and how MCL-1 is regulated by a signaling pathway called ERBB. These details could be useful in developing new methods of hair loss treatments. "These findings suggest that ERBB signaling modulates MCL‑1 expression through translational control mechanisms, particularly during periods of heightened apoptosis and regression in the hair cycle," the researchers write. The study was based solely on mice, so while there's good reason to think the same processes are happening on the top of our own heads, the findings will need to be replicated in clinical research on humans. It's also worth bearing in mind that there are several different kinds of alopecia, all with a variety of contributing causes: if treatments are one day developed that focus on boosting MCL-1, they're not going to work for all types of hair loss. Those limitations aside, this one protein's handiwork is a significant revelation concerning hair follicles' ability to grow hair. The findings could also inform future studies into other processes affected by MCL-1, including cancer cell death. "This study advances our understanding of the molecular mechanisms underlying hair follicle regeneration and offers new insights into how stem cell survival and tissue regeneration are orchestrated," write the researchers. "These findings may have broader implications for controlling the survival of stem and progenitor cells in tissue regeneration and cancer expansion." The research has been published in Nature Communications. Woman's Brain Implant Turns Her Thoughts Into Speech in Real Time Sometimes Alzheimer's Strikes Early. This Experimental Drug May Help. Dangerous Fungal Infection Sees a Dramatic Increase in US Hospitals
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
New York Times
04-03-2025
- Health
- New York Times
James Harrison, Whose Antibodies Helped Millions, Dies at 88
James Harrison did not much care for needles. Whenever he donated plasma, he would look away as the tip went into his arm. But Mr. Harrison, an Australian who died last month at 88, was one of the most prolific donors in history, extending his arm 1,173 times. He may have also been one of the most important: Scientists used a rare antibody in his plasma to make a medication that helped protect an estimated 2.4 million babies in Australia from possible disease or death, medical experts say. 'He just kept going, and going, and going,' his grandson Jarrod Mellowship, 32, said in an interview on Monday. 'He didn't feel like he had to do it. He just wanted to do it.' Mr. Harrison — who was affectionately known as 'The Man with the Golden Arm' — died in his sleep at age 88 on Feb. 17, at a nursing home about an hour's drive north of his regular donation center in Sydney, Mr. Mellowship said. Mr. Harrison's plasma contained a rare antibody, anti-D. Scientists used it to make a medication for pregnant mothers whose immune systems could attack their fetuses' red blood cells, according to Australian Red Cross Lifeblood. It helps protect against problems that can occur when babies and mothers have different blood types, most often if the fetus is 'positive' and the mother is 'negative,' according to the Cleveland Clinic. (The positive and negative signs are called the Rhesus factor, or Rh factor.) In such cases, a mother's immune system might react to the fetus as if it were a foreign threat. That can lead babies to develop a dangerous and potentially fatal condition, hemolytic disease of the fetus and newborn, which can cause anemia and jaundice. The condition is uncommon: Only about 276 out of 100,000 live births have complications related to this type of blood incompatibility, the Cleveland Clinic said. But doctors cannot predict whether such an incompatibility will lead to serious problems. So, in Australia, the practice is to offer the medication to all pregnant women with negative antibodies as a preventative measure, according to Lifeblood. In Australia, that's about 17 percent of the population, or about 45,000 women a year. In the United States, it's about 15 percent, according to the Cleveland Clinic. In Australia, scientists from the Walter and Eliza Hall Institute of Medical Research in Melbourne are working to create a synthetic version of the drug using what some have called 'James in a Jar,' an antibody that can be made in a lab. But for now, human donors are essential: The anti-D shots are made with donated plasma, and Mr. Harrison was one of about 200 donors among the 27 million people in Australia, Lifeblood said. 'It wasn't one big heroic act,' Ms. Falkenmire said in an interview as she reflected on Mr. Harrison's 64 years of donations, from 1954 to 2018. 'It was just a lifetime of being there and doing these small acts of good bit by bit.' Mr. Harrison sometimes met some of the women he helped, although most were strangers. But two he knew well indeed. His daughter, Tracey Mellowship, received an anti-D injection made with Mr. Harrison's plasma. So did his granddaughter-in-law, Rebecca Mellowship, who is married to Mr. Mellowship. 'It was special that I received dad's anti-D,' Tracey Mellowship, 58, wrote in an email. But his rare antibodies were only part of the puzzle. Mr. Harrison's commitment was key. He donated about every two weeks from age 18 to age 81, first his blood and then his plasma. Vacations did not stop him: He would stop in clinics across Australia when he and his wife, Barbara Harrison, traveled in their camper van. She was a prolific blood donor, too. Neither did old age: He rode the train for more than an hour each way to get from his home outside Sydney to his regular donation center. And he never missed an appointment, said Ms. Falkenmire, the Lifeblood spokeswoman, who talked to him during donations. Partially, she said, they just enjoyed chatting. But he also welcomed the distraction: 'He was petrified of needles,' she said. 'He hated them.' Mr. Harrison knew the importance of his work firsthand. At 14, he needed a lot of blood transfusions during a major lung surgery. The experience inspired him to donate and encourage others to donate, too. 'He would walk up to people who were donating for the first time and congratulate them, and tell them they were important and special,' Ms. Falkenmire said, 'without revealing anything about his own donations.' James Christopher Harrison was born on Dec. 27, 1936, in Junee, a small town in New South Wales, to Peggy and Reginald Harrison. After he recovered from lung surgery, Mr. Harrison met his wife, the former Barbara Lindbeck, when he was a teenager. She was a teacher who died in 2005, Ms. Falkenmire said. He worked as a clerk in the regional railway authority and received the Medal of the Order of Australia in 1999 for his donations. Mr. Harrison is survived by his daughter, Tracey, and her husband, Andrew Mellowship; his grandsons Scott and Jarrod Mellowship; and Jarrod's family: Rebecca, his wife, and their four children. And also, maybe, 2.4 million babies — which Mr. Harrison never quite knew how to comprehend. 'Saving one baby is good,' he said, after his final donation in 2018. 'Saving two million is hard to get your head around, but if they claim that's what it is, I'm glad to have done it.' Mr. Harrison's wish, he liked to say, was that people would keep donating. Maybe even more than he did, Mr. Mellowship said: 'Because then it means the world's going in the right place.'
