Latest news with #JCIInsight
UPI
5 days ago
- Health
- UPI
'Harmless' virus might trigger Parkinson's disease, researchers say
Human Pegivirus (HPgV), was found in half the autopsied brains of patients with Parkinson's, but not in any brains from healthy people, researchers reported Tuesday in the journal JCI Insight. Photo by Thirdman/ Pexels July 9 (UPI) -- A common virus once thought harmless to humans might be linked to Parkinson's disease, a new study says. The germ, Human Pegivirus (HPgV), was found in half the autopsied brains of patients with Parkinson's, but not in any brains from healthy people, researchers reported Tuesday in the journal JCI Insight. "HPgV is a common, symptomless infection previously not known to frequently infect the brain," lead researcher Dr. Igor Koralnik, chief of neuroinfectious diseases and global neurology at Northwestern Medicine in Chicago, said in a news release. "We were surprised to find it in the brains of Parkinson's patients at such high frequency and not in the controls." The virus also appeared to prompt different responses from people's immune systems, depending on their genetics, Koralnik said. "This suggests it could be an environmental factor that interacts with the body in ways we didn't realize before," Koralnik said. "For a virus that was thought to be harmless, these findings suggest it may have important effects, in the context of Parkinson's disease. It may influence how Parkinson's develops, especially in people with certain genetic backgrounds." Parkinson's disease occurs when brain cells that produce an important hormone called dopamine begin to die off or become impaired. As dopamine levels decrease, people develop movement symptoms like shaking or stiffness, as well as problems maintaining balance and coordination. More than 1 million people in the U.S. live with Parkinson's disease, including actors Michael J. Fox and Alan Alda, singer Neil Diamond and football great Brett Favre. About 90,000 new cases are diagnosed every year, researchers said. Most cases of Parkinson's are not linked to a person's genetics, raising the question of what might trigger the death of dopamine-producing nerve cells, researchers said in background notes. For the new study, researchers autopsied the brains of 10 Parkinson's patients and 14 people not suffering from the disorder. The team found HPgV in 5 out of 10 brains from people with Parkinson's, but none of the 14 healthy brains. The virus also was present in the spinal fluid of Parkinson's patients, but not in the control group. Further, more brain damage was found in patients with HPgV, researchers said. Next, researchers tested blood samples from more than 1,000 participants in the Parkinson's Progression Markers Initiative, a biosample library available for Parkinson's research. HPgV is a blood-borne virus in the same family as hepatitis C. Only about 1% of Parkinson's patients had HPgV in their blood samples, researchers found. But people who had the virus showed different signals from their immune system, particularly those with a Parkinson's-related gene mutation called LRRK2, researchers said. "We plan to look more closely at how genes like LRRK2 affect the body's response to other viral infections to figure out if this is a special effect of HPgV or a broader response to viruses," Koralnik said. Researchers plan to continue tracking how common the virus is among Parkinson's patients, and how it might trigger the brain disorder. "One big question we still need to answer is how often the virus gets into the brains of people with or without Parkinson's," Koralnik said. "We also aim to understand how viruses and genes interact; insights that could reveal how Parkinson's begins and could help guide future therapies." More information The National Institute on Aging has more about Parkinson's disease. Copyright © 2025 HealthDay. All rights reserved.
New York Post
6 days ago
- Health
- New York Post
Seemingly harmless, symptomless virus may actually cause Parkinson's disease: study
While some cases of Parkinson's disease are genetic, the vast majority have no known cause. Now, scientists have discovered that a virus that has flown under the radar for years might be a potential contributor to the neurodegenerative disorder. 'We wanted to investigate potential environmental factors – such as viruses – that might contribute to Parkinson's disease,' Igor Koralnik, the lead author of the study and chief of neuroinfectious diseases and global neurology at Northwestern Medicine, said in a press release. Advertisement 3 Researchers at Northwestern Medicine have discovered that a virus that has flown under the radar for years might be a potential contributor to the neurodegenerative disorder. Laura Brown 'Using a tool called 'ViroFind', we analyzed post-mortem brain samples from individuals with Parkinson's and from those who died of other causes. We searched for all known human-infecting viruses to identify any differences between the two groups.' What they found was that the Human Pegivirus (HPgV) — a blood-borne, symptomless virus from the same family as hepatitis C — was present in the brains and spinal fluid of 50% of people with Parkinson's but not in those without it. The findings — published Tuesday in the journal JCI Insight — could be a major breakthrough in unlocking some of the factors that lead to this tricky disease and provide new insight into a virus that was previously considered benign. Advertisement 'HPgV is a common, symptomless infection previously not known to frequently infect the brain,' Dr. Koralnik said. 'We were surprised to find it in the brains of Parkinson's patients at such high frequency and not in the controls. Even more unexpected was how the immune system responded differently, depending on a person's genetics.' 'This suggests it could be an environmental factor that interacts with the body in ways we didn't realize before. Advertisement 'For a virus that was thought to be harmless, these findings suggest it may have important effects, in the context of Parkinson's disease. It may influence how Parkinson's develops, especially in people with certain genetic backgrounds.' 3 What they found was that the Human Pegivirus (HPgV) — a blood-borne, symptomless virus from the same family as hepatitis C — was present in the brains and spinal fluid of 50% of people with Parkinson's but not in those without it. C Davids/ – Blood samples from more than 1,000 people enrolled in the Parkinson's Progression Markers Initiative, a project launched by The Michael J. Fox Foundation, showed that people with HPgV had unique immune system 'signals' — patterns that appeared both in the bloodstream and the brain. Advertisement 'With the blood samples, we observed similar immune-related changes, mirroring those found in the brain,' Dr. Koralnik said. 'People who had the virus showed different signals from the immune system than those who didn't, and this pattern was the same, no matter the genetics. But as we followed each person over time, we saw a more complicated picture.' In people with a Parkinson's-linked mutation in the LRRK2 gene, the immune system reacted to the virus differently than in those without the mutation — suggesting the virus may interact with certain genes to help set the disease in motion. 3 Blood samples from more than 1,000 people enrolled in the Parkinson's Progression Markers Initiative, a project launched by The Michael J. Fox Foundation. Getty Images 'We plan to look more closely at how genes like LRRK2 affect the body's response to other viral infections to figure out if this is a special effect of HPgV or a broader response to viruses,' added Dr. Koralnik. Now, the team wants to go bigger, examining more brains to determine how often HPgV sneaks past the blood-brain barrier. 'One big question we still need to answer is how often the virus gets into the brains of people with or without Parkinson's,' said Dr. Koralnik. 'We also aim to understand how viruses and genes interact; insights that could reveal how Parkinson's begins and could help guide future therapies.'
Business Wire
08-05-2025
- Health
- Business Wire
n-Lorem Foundation Identifies New, Important Roles of JIP3, Offering Critical Insights into Therapeutic Approaches for Nano-rare Patients
SAN DIEGO--(BUSINESS WIRE)-- n-Lorem, a nonprofit foundation, announced today the publication of new research characterizing a nano-rare mutation in a gene that is pivotal to normal cell signaling and cellular homeostasis. The mitogen-activated protein kinase 8 interacting protein 3 (MAPK8IP3) gene encodes for c-Jun N-terminal kinase-interacting (JNK-interacting) protein 3 (JIP3). Mutations in the MAPK8IP3 gene have been linked to severe neurodevelopmental disorders, however, the mechanisms of JIP3 underlying these deleterious effects were poorly understood. In this publication, n-Lorem scientists identified several significant roles JIP3 could play in the body, characterized a mutation in MAPK8IP3 and identified a path forward to use antisense oligonucleotide (ASO) medicines to address mutations in the MAPK8IP3 gene. The study, authored by n-Lorem scientist Wei Zhang, et al was published today in JCI Insights (JCI Insight. 10(8):e187199). 'The work described in this manuscript is exemplary of some of the challenges in defining a therapeutic strategy for nano-rare patients who have de novo mutations in genes,' said Stanley Crooke, M.D., Ph.D., Chairman, Founder and CEO of n-Lorem. 'As is often the case, the nature of the MAPK8IP3 mutation, whether loss-of-function or toxic gain-of-function, was not clearly proven before we started this. Since ASOs can be designed to carry out a variety of actions, we must know at the onset of the program if we need to alter mRNA splicing or increase or decrease protein expression. Additionally, it is often unclear what the proximal molecular events are. This information is essential to know if we are likely to correct the phenotype and potentially improve the condition.' 'At The Wolverine Foundation, our focus is to turn cutting-edge science into tangible hope for the children affected by MAPK8IP3-related neurodevelopmental disorders,' said Amy McCooe, Executive Director of The Wolverine Foundation. 'The study published in JCI Insight points to antisense oligonucleotides as a promising avenue worth pursuing. Although much remains to be learned about the therapeutic potential of this approach, we are encouraged by these findings and grateful to n-Lorem's scientists for moving us a meaningful step forward.' The study, titled 'A toxin gain-of-function variant in MAPK8IP3 provides insights into JIP3 cellular roles,' investigated a patient with a missense mutation in the MAPK8IP3 gene (c. 1714 C > T, Arg578Cys) linked to dystonia, gross motor dysfunction and developmental delays. Aimed at uncovering the molecular mechanisms driving the cytotoxicity of MAPK8IP3 mutations the research sheds new light on the cellular functions of JIP3 and its role in neurodevelopmental disorders. The study revealed, for the first time, that the Arg578Cys mutation in JIP3 was shown to trigger cellular abnormalities that culminate in cell death and neurodegenerative disease in patients with this mutation. Funded by the Wolverine Foundation, the study also revealed that this toxic gain-of-function variant disrupts JIP3's molecular interactions, selectively impairing dopamine receptor 1 signaling while sparing dopamine receptor 2 pathways. Since disruptions in dopamine signaling are closely linked to movement disorders like Parkinson's disease, these findings may explain the motor symptoms observed in the patient. 'The significance of JIP3 has been unfolding over the last few years, but a comprehensive understanding of its functioning has been incomplete,' Crooke said. 'This research has offered us new insight into the role of JIP3 and how mutations in the protein can contribute to neurodegenerative disorders. This work could not have been completed without support from the Wolverine Foundation, and we want to thank them for their confidence and patience as we embarked on this work together.' The Wolverine Foundation is dedicated to advancing research and discover novel therapeutic approaches to treat the neuro-developmental disease caused by genetic variations in the gene MAPK8IP3. The organization investigates disease mechanisms and encourages scientific collaboration between academic research, drug discovery and clinical development. About n-Lorem n-Lorem Foundation is a non-profit organization established to apply the efficiency, versatility and specificity of antisense technology to charitably provide experimental antisense oligonucleotide (ASO) medicines to treat nano-rare patients diagnosed with diseases that are the result of a single genetic defect unique to only one or very few individuals. Nano-rare patients describe a very small group of patients (1-30 worldwide) who, because of their small numbers, have few if any treatment options. n-Lorem Foundation was created to provide hope to these nano-rare patients by developing individualized ASO medicines, which are short strands of modified DNA that can specifically target the transcripts of a defective gene to correct the abnormality. The advantage of experimental ASO medicines is that they can be developed rapidly, inexpensively and are highly specific. To date, n-Lorem received over 330 applications for treatment with more than 160 nano-rare patients approved and more than 25 patients on active treatment. n-Lorem was founded by Stanley T. Crooke, M.D., Ph.D., former chairman and CEO of Ionis Pharmaceuticals, who founded Ionis Pharmaceuticals in 1989 and, through his vision and leadership, established the company as the leader in RNA-targeted therapeutics. Follow us on Twitter, Facebook, LinkedIn and YouTube. To learn more about n-Lorem's mission at and please consider giving to n-Lorem to bring hope, possibility and treatment options to these patients and families in need.
