Latest news with #JaleesRehman
Japan Today
12-08-2025
- Health
- Japan Today
Vaccines hold tantalizing promise in the fight against dementia
By Anand Kumar and Jalees Rehman Over the past two centuries, vaccines have been critical for preventing infectious diseases. The World Health Organization estimates that vaccination prevents between 3 million and 5 million deaths annually from diseases like diphtheria, tetanus, influenza, measles and, more recently, COVID-19. While there has long been broad scientific consensus that vaccines prevent or mitigate the spread of infections, there is new research suggesting that the therapeutic impact might go beyond the benefit of preventing infectious diseases. An April study published in the prominent journal Nature found tantalizing evidence that the herpes zoster – or shingles – vaccine could lower the risk of dementia in the general population by as much as 20%. We are a team of physician scientists with expertise in the clinical and basic science of neurodegenerative disorders and dementia. We believe that this study potentially opens the door to other breakthroughs in understanding and treating dementia and other degenerative disorders of the brain. A role for vaccines in reducing dementia risk? One of the major challenges researchers face when trying to study the effects of vaccines is finding an unvaccinated 'control group' for comparison – a group that is similar to the vaccine group in all respects, save for the fact that they haven't received the active vaccine. That's because it's unethical to assign some patients to the control group and deprive them of vaccine protection against a disease such as shingles. The Nature study took advantage of a policy change in Wales that went into effect in 2013, stating that people born on or after September 2, 1933, were eligible for the herpes zoster vaccination for at least a year, while those born before that cutoff date were not. The vaccine was administered to prevent shingles, a painful condition caused by the same virus that causes chickenpox, which can lie dormant in the body and be reactivated later in life. The researchers used the policy change as a natural laboratory of sorts to study the effect of shingles vaccination on long-term health outcomes. In a statistically sophisticated analysis of health records, the team found that the vaccine reduced the probability of getting dementia by one-fifth over a seven-year period. This means that people who received the shingles vaccine were less likely to develop clinical dementia over the seven-year follow-up period, and women benefited more than men. The study design allowed researchers to compare two groups without actively depriving any one group of access to vaccination. The two groups were also of comparable age and had similar medical comorbidities – meaning similar rates of other medical conditions such as diabetes or high blood pressure. Results from this and other related studies raise the possibility that vaccines may have a broader role in experimental therapeutics outside the realm of infectious diseases. These studies also raise provocative questions about how vaccines work and how our immune system can potentially prevent dementia. How vaccines might be protective One scientific explanation for the reduction of dementia by the herpes zoster vaccine could be the direct protection against the shingles virus, which may play a role in exacerbating dementia. However, there is also the possibility that the vaccine may have conferred protection by activating the immune system and providing 'trained immunity,' in which the immune system is strengthened by repeated exposure to vaccines or viruses. The study did not differentiate between different types of dementia, such as dementia due to Alzheimer's disease or dementia due to stroke. Additionally, researchers cannot draw any definitive conclusions about possible mechanisms for how the vaccines could be protective from an analysis of health records alone. The next step would be a prospective, randomized, double-blind, placebo-controlled study – the 'gold standard' for clinical trials in medicine – to directly examine how the herpes zoster vaccine compares with a placebo in their ability to reduce the risk of dementia over time. Such studies are necessary before any vaccines, as well as other potential therapies, can be recommended for routine clinical use in the prevention of dementia. The challenges of untangling dementia Dementia is a major noncommunicable disease that is a leading cause of death around the world. A January 2025 study provided updated figures on lifetime dementia risk across different subsets of the U.S. population. The researchers estimate that the lifetime risk of dementia after age 55 is 42% – more than double earlier estimates. The dementia risk was 4% by age 75, and 20% by age 85, with the majority of risk occurring after 85. The researchers projected that the number of new cases of dementia in the U.S. would double over the next four decades from approximately 514,000 cases in 2020 to 1 million in 2060. Once considered a disease largely confined to the developed world, the deleterious effects of dementia are now apparent throughout the globe, as life expectancy increases in many formerly developing countries. While there are different forms of dementia with varying clinical manifestations and underlying neurobiology, Alzheimer's disease is the most common. Prospective studies that specifically test how giving a vaccine changes the risk for future dementia may benefit from studying patient populations with specific types of dementia because each version of dementia might require distinct treatments. Unfortunately, for the past two to three decades, the amyloid hypothesis of Alzheimer's disease – which posits that accumulation of a protein called amyloid in the brain contributes to the disorder – dominated the scientific conversation. As a result, most of the efforts in the experimental therapeutics of Alzheimer's disease have focused on drugs that lower the levels of amyloid in the brain. However, results to date have been modest and disappointing. The two recently approved amyloid-lowering therapies have only a minimal impact on slowing the decline, are expensive and have potentially serious side effects. And no drug currently approved by the Food and Drug Administration for clinical use reverses the cognitive decline. Studies based on health records suggest that past exposure to viruses increase the risk of dementia, while routine vaccines, including those against tetanus, diphtheria, pertussis, pneumonia, shingles and others, reduce the risk. Innovation and an open mind There is sometimes a tendency among scientists to cling to older, familiar models of disease and a reluctance to move in more unconventional directions. Yet the process of doing science has a way of teaching researchers like us humility, opening our minds to new information, learning from our mistakes and going where that data takes us in our quest for effective, lifesaving therapies. Vaccines may be one of those paths less traveled. It is an exciting possibility that may open the door to other breakthroughs in understanding and treating degenerative disorders of the brain. Anand Kumar is Professor and Department Head of Psychiatry, University of Illinois Chicago. Jalees Rehman is Department Chair and Professor of Biochemistry and Molecular Genetics, University of Illinois Chicago. The Conversation is an independent and nonprofit source of news, analysis and commentary from academic experts. External Link © The Conversation
Japan Today
30-07-2025
- Health
- Japan Today
Muscle weakness in cancer survivors may be caused by treatable weakness in blood vessels: new research
Poorly functioning blood vessels lead to the characteristic muscle weakness that so many cancer patients experience. By Jalees Rehman Tumors can destroy the blood vessels of muscles even when the muscles are nowhere close to the tumor. That is the key finding of a new study that my colleagues and I recently published in the journal Nature Cancer. Muscle loss in cancer patients is a major health problem, but the exact causes of how precisely tumors affect muscles remain an active area of research. Scientists in my lab were curious whether one explanation for the muscle loss in cancer patients could be that the cancer impairs the blood vessels that are necessary to supply nutrients and oxygen to muscles. Healthy blood vessels ensure that blood containing oxygen and nutrients is transported from the heart to all tissues and organs in the body, and then circulates back to the heart. Unhealthy blood vessels lose the ability to circulate sufficient blood and develop leaks, with nutrients seeping into the tissue prematurely and thereby cutting off the supply of nutrients to tissues that are further downstream. To tackle this question, my colleagues and I worked with several other scientific research teams with expertise in advanced microscopy, cancer research and metabolism. We used animal models to study several kinds of tumors – lung cancer, skin cancer, colon cancer and pancreatic cancer. We consistently observed that the blood vessels in the muscles became fewer and leakier even before the muscle weakness set in. We also found that tumors release a protein called Activin-A, which acts on blood vessels to cause the leakiness and, ultimately, loss of blood vessels in the muscle. When we used a gene therapy to restore blood vessel health by counteracting the effects of Activin-A, we were able to prevent the muscle loss. So we examined the muscles of patients who had passed away because of cancer and found that the muscles of cancer patients contained fewer blood vessels than expected. Why Activin-A matters Millions of cancer survivors struggle with muscle weakness, which can be so profound that they may have difficulties walking up a couple of flights of stairs or going shopping for groceries on their own. Severe muscle weakness and muscle loss during cancer is called cancer cachexia, which occurs in up to 80% of patients with advanced cancer. Recent research indicates that cachexia is far more common among cancer patients than previously suspected, with approximately half the patients who see their cancer doctor for the first time already showing signs of muscle weakness. Importantly, cachexia can persist even after the cancer is successfully treated and cured. This can have a devastating impact on the quality of life for cancer survivors. Our discovery that the loss of blood vessel function in the muscles occurs early on during the progression of the cancer suggests that fixing blood vessels in cancer patients and cancer survivors could be a new way to prevent or reverse cachexia. The reasons for the muscle loss in cancer are complicated and involve poor nutrition due to loss of appetite and inflammation, which are initially caused by the tumor but persist even when the tumor is removed. What other research is being done There are currently no treatments approved by the Food and Drug Administration for cachexia, but new therapies are on the horizon. One such therapy is an antibody drug that targets the molecule GDF-15, a protein that is thought to suppress appetite. Other studies are using a combination of targeted nutrition and exercise programs to help patients with cancer cachexia regain muscle mass and muscle strength. All these studies suggest that we will need a combination of approaches to enhance exercise, nutrition, appetite, muscle regeneration and – as we propose – blood vessel health. What's next We are now evaluating drugs and exercise programs that are known to improve blood vessel health. Repurposing these treatments that are traditionally designed for cardiovascular patients could be a rapid way to help cancer patients regain muscle strength. We hope that our work highlights how important it is for cancer patients to receive comprehensive medical care, which includes improving cardiovascular health and overall quality of life. Jalees Rehman is Department Chair and Professor of Biochemistry and Molecular Genetics, University of Illinois Chicago. The Conversation is an independent and nonprofit source of news, analysis and commentary from academic experts. External Link © The Conversation
Indian Express
13-07-2025
- Health
- Indian Express
Muscle weakness in cancer survivors may be caused by treatable weakness in blood vessels — new research
By Jalees Rehman Tumours can destroy the blood vessels of muscles even when the muscles are nowhere close to the tumour. That is the key finding of a new study that my colleagues and I recently published in the journal Nature Cancer. Muscle loss in cancer patients is a major health problem, but the exact causes of how precisely tumours affect muscles remain an active area of research. Scientists in my lab were curious whether one explanation for the muscle loss in cancer patients could be that the cancer impairs the blood vessels that are necessary to supply nutrients and oxygen to muscles. Healthy blood vessels ensure that blood containing oxygen and nutrients is transported from the heart to all tissues and organs in the body, and then circulates back to the heart. Unhealthy blood vessels lose the ability to circulate sufficient blood and develop leaks, with nutrients seeping into the tissue prematurely and thereby cutting off the supply of nutrients to tissues that are further downstream. To tackle this question, my colleagues and I worked with several other scientific research teams with expertise in advanced microscopy, cancer research and metabolism. We used animal models to study several kinds of tumours – lung cancer, skin cancer, colon cancer and pancreatic cancer. We consistently observed that the blood vessels in the muscles became fewer and leakier even before the muscle weakness set in. We also found that tumours release a protein called Activin-A, which acts on blood vessels to cause the leakiness and, ultimately, loss of blood vessels in the muscle. When we used a gene therapy to restore blood vessel health by counteracting the effects of Activin-A, we were able to prevent the muscle loss. So we examined the muscles of patients who had passed away because of cancer and found that the muscles of cancer patients contained fewer blood vessels than expected. Millions of cancer survivors struggle with muscle weakness, which can be so profound that they may have difficulties walking up a couple of flights of stairs or going shopping for groceries on their own. Severe muscle weakness and muscle loss during cancer is called cancer cachexia, which occurs in up to 80% of patients with advanced cancer. Recent research indicates that cachexia is far more common among cancer patients than previously suspected, with approximately half the patients who see their cancer doctor for the first time already showing signs of muscle weakness. Importantly, cachexia can persist even after the cancer is successfully treated and cured. This can have a devastating impact on the quality of life for cancer survivors. Our discovery that the loss of blood vessel function in the muscles occurs early on during the progression of the cancer suggests that fixing blood vessels in cancer patients and cancer survivors could be a new way to prevent or reverse cachexia. The reasons for the muscle loss in cancer are complicated and involve poor nutrition due to loss of appetite and inflammation, which are initially caused by the tumour but persist even when the tumour is removed. There are currently no treatments approved by the Food and Drug Administration for cachexia, but new therapies are on the horizon. One such therapy is an antibody drug that targets the molecule GDF-15, a protein that is thought to suppress appetite. Other studies are using a combination of targeted nutrition and exercise programs to help patients with cancer cachexia regain muscle mass and muscle strength. All these studies suggest that we will need a combination of approaches to enhance exercise, nutrition, appetite, muscle regeneration and – as we propose – blood vessel health. We are now evaluating drugs and exercise programmes that are known to improve blood vessel health. Repurposing these treatments that are traditionally designed for cardiovascular patients could be a rapid way to help cancer patients regain muscle strength. We hope that our work highlights how important it is for cancer patients to receive comprehensive medical care, which includes improving cardiovascular health and overall quality of life.
