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Time of India
31-07-2025
- Health
- Time of India
A new drug may reduce brain damage from stroke by 60%
Globally, strokes affect 15 million individuals annually, resulting in 5 million deaths and leaving another 5 million with permanent disabilities. Recognizing the severe consequences of stroke, scientists have developed a promising new drug. This innovative treatment aims to significantly minimize brain damage caused by strokes, potentially improving patient outcomes and quality of life. 15 million people suffer a stroke every year worldwide, according to the World Health Organisation( WHO ). Of these, 5 million die, while another 5 million are left permanently disabled. What makes a stroke exceptionally dangerous, is that it could either be fatal or leave the person disabled. The latter significantly reduces the quality of life. Scientists have now developed a new drug that may significantly reduce brain damage caused by strokes. Yes, that's right! Scientists from the University of Cambridge have developed a drug that can reduce brain damage caused by strokes by 60%. The findings of the study is published in Cardiovascular Research . What is a stroke A stroke occurs when blood flow to the brain is blocked or there is sudden bleeding in the brain. There are two types of strokes. Ischemic stroke Hemorrhagic stroke Ischemic stroke is a stroke that occurs when the blood flow to the brain is blocked. Hemorrhagic strokes are those that occur when a blood vessel ruptures and bleeds into the brain. Ischemic stroke is the most common type, accounting for approximately 87% of all strokes. A stroke can be either fatal or leave devastating consequences. by Taboola by Taboola Sponsored Links Sponsored Links Promoted Links Promoted Links You May Like Mini House for 60 sqm for Seniors with Toilet and Bath (Price May Surprise You) Pre Fabricated Homes | Search Ads Search Now Undo As many as one in four people will have a stroke during their lifetime. The first few hours following a stroke are crucial. This is the time when the blood clot needs to be removed quickly so that the oxygen supply to the brain can be restored; otherwise, the brain tissue begins to die. At present, the gold standard treatment is mechanical thrombectomy. However, the outcomes are still poor, with fewer than one in 10 patients leaving the hospital with no neurological impairment. New drug offers a promise to reduce the brain damage in stroke survivors (Pic courtesy: iStock) The Cambridge scientists have developed and tested a new drug in mice that has the potential to reduce damage to the brain when blood flow is restored following a stroke . 'Stroke is a devastating disease. Even for those who survive, there is a significant risk of damage to the brain that can lead to disabilities and a huge impact on an individual's life. But in terms of treatment, once the stroke is happening, we have only limited options,' Professor Thomas Krieg from the Department of Medicine at the University of Cambridge said in a statement. Mechanical thrombectomy is a minimally invasive medical procedure where a thin tube, known as a catheter, is inserted into the blood vessel, often through the groin or arm. This is guided to the blood clot, where it is removed by a tiny device, restoring normal blood flow. However, restoring the blood flow too quickly could also backfire. This is called ischaemia-reperfusion injury, where blood rushes back into the oxygen-starved tissue (a process known as reperfusion), the damaged cells struggle to cope, leading to the production of harmful molecules called free radicals that can damage cells, proteins, and DNA. This triggers further damage and can cause an inflammatory response. A previous study by the Cambridge team showed that when the brain is starved of oxygen, it lead to the build-up of a chemical called succinate. When blood flow is restored, the succinate is rapidly oxidised to drive free radical production within mitochondria, the 'batteries' that power our cells, initiating the extra damage. This occurs within the first few minutes of reperfusion, but the researchers showed that the oxidation of succinate can be blocked by the molecule malonate. 'All of this happens very rapidly, but if we can get malonate in quickly at the start of reperfusion, we can prevent this oxidation and burst of free radicals. We discovered in our labs that we can get malonate into cells very quickly by lowering the pH a little, making it a bit more acidic, so that it can cross the blood-brain barrier better. If we inject it into the brain just as we're ready to reperfuse, then we can potentially prevent further damage,' Professor Mike Murphy from the Medical Research Council Mitochondrial Biology Unit said. The findings The new study found that treating the brain with a form of the chemical known as acidified disodium malonate (aDSM) alongside mechanical thrombectomy greatly decreased the amount of brain damage that occurs from ischaemia-reperfusion injury by as much as 60%. The researchers developed a mouse model that mimics mechanical thrombectomy, allowing the team to test the effectiveness of aDSM against ischaemia-reperfusion injury. 'This approach reduces the amount of dead brain tissue resulting from a stroke. This is incredibly important because the amount of dead brain tissue is directly correlated to the patient's recovery, to their disability, whether they can still use all their limbs, speak, and understand language, for example,' Dr Jordan Lee, a postdoctoral researcher in the group, and the one behind the mouse model, said. No more guesswork: Doctor busts common myths about women's health The researchers are now hoping to start early-stage clinical trials. 'If it's successful, this same drug could have much wider applications for other instances of ischemia-reperfusion injuries, such as heart attack, resuscitation, organ transplantation, and so on, which have similar underlying mechanisms,' Professor Murphy added.
Yahoo
19-07-2025
- Health
- Yahoo
New study reveals single dietary factor that increases risk for heart disease: 'Our findings strengthen the importance'
New study reveals single dietary factor that increases risk for heart disease: 'Our findings strengthen the importance' An international study found that diets low in fiber may contribute to a higher risk of heart attacks, offering another reason to eat more plants. Researchers analyzed heart scans from nearly 1,400 people across Europe and Australia and discovered a clear link between low fiber intake and the buildup of dangerous plaques in the arteries. These plaques were more likely to rupture and lead to serious cardiac events. The study was published in the journal Cardiovascular Research and focused on people with existing coronary artery disease. "Our findings strengthen the importance of cardioprotective dietary recommendations," the researchers noted in the study's conclusion. The benefits of fiber were consistent even among those already taking heart medications or cholesterol-lowering drugs. While fiber has long been associated with improved digestion, reduced inflammation, and better blood sugar control, this study is among the first to directly connect fiber intake to the makeup of arterial plaques. Specifically, people who ate less fiber were more likely to have lipid-rich plaques, which are softer and more prone to rupture than fibrous or calcified plaques. That rupture risk can trigger heart attacks, even in people already on medication, making fiber an important yet often overlooked part of long-term heart care. A 2025 report from the American College of Cardiology linked plant-based eating patterns to a reduced risk of heart disease and stroke, indicating that other researchers have come to similar conclusions. And a long-term study from the Harvard T.H. Chan School of Public Health found that replacing red meat with legumes, nuts, or whole grains significantly lowered the risk of heart-related death, especially in younger adults. There are several health benefits. Fiber-rich diets are tied to reduced inflammation, improved cholesterol control, and more stable blood sugar, all of which can help prevent artery damage over time. Heart-healthy eating patterns such as the Mediterranean and DASH diets emphasize whole grains, vegetables, and legumes not only for weight control but also because they support long-term cardiovascular health. These findings align with other recent research that shows how dietary changes, even small ones, can lower the risk of chronic illness. Why do you eat plant-based foods? The health benefits It's cheaper It's good for the planet I prefer the taste Click your choice to see results and speak your mind. Join our free newsletter for easy tips to save more and waste less, and don't miss this cool list of easy ways to help yourself while helping the planet. Solve the daily Crossword


Medscape
05-06-2025
- Business
- Medscape
New Hyperkalemia Risk Model for CKD and Diabetes
A new risk model may help identify which patients with chronic kidney disease (CKD) and diabetes are more likely to develop hyperkalemia, granting physicians more confidence in prescribing medications like finerenone. However, researchers caution that further validation is needed. The model is based on pooled data from two phase 3 trials of finerenone: FIDELIO-DKD (Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease) and FIGARO-DKD (Finerenone in Reducing Cardiovascular Mortality and Morbidity in Diabetic Kidney Disease). The combined dataset, known as FIDELITY, includes 6355 patients in the placebo groups. Researchers used this dataset to develop the risk score, identifying seven factors independently associated with the primary outcome of new onset of hyperkalemia (incident serum potassium level > 5.5 mmol/L): Serum potassium > 4.5 mmol/L Prior history of hyperkalemia No use of sodium-glucose co-transporter 2 inhibitor Urine albumin-to-creatinine ratio > 1000 mg/g Hemoglobin < 12 g/dL No use of thiazide-type diuretics Estimated glomerular filtration rate < 45 mL/min/1.73 m2 The model was subsequently validated using data from the finerenone groups in FIDELITY. In their paper, published online in the European Heart Journal , João Pedro Ferreira, MD, PhD, of the Cardiovascular Research and Development Center at the University of Porto, Porto, Portugal, and coauthors noted that the model could be used to reduce the risk for hyperkalemia among high-risk patients receiving finerenone. 'This could include tailoring of individualized treatment and follow-up strategies (eg, frequency of visits and serum potassium assessments, and use of potassium binders), thus optimizing patient management and potentially improving outcomes,' they noted. Welcome Results, Validation Required CKD, which affects more than 800 million people worldwide, is a common complication of diabetes. An estimated 15%-40% of people with CKD in the setting of diabetes may have hyperkalemia, noted Bernard G. Jaar, MD, MPH, clinical director for Nephrology at Johns Hopkins School of Medicine, Baltimore, who was not involved in the study. In an email exchange with Medscape Medical News , Jaar described the study as 'welcome and much needed.' He noted that hyperkalemia poses a challenge for clinicians, as many medications required for optimal care in CKD — including renin-angiotensin-aldosterone system (RAAS) blockade agents and finerenone — can raise serum potassium. 'This is a true barrier to care,' Jaar wrote. 'Clinicians are worried about the potential complications associated with hyperkalemia, such as arrhythmias and even death.' Jaar noted that the FIDELITY analysis has several strengths, including its large sample size of patients with varying stages of CKD and degrees of proteinuria, and a risk score model that incorporated readily available clinical variables. He added that it reports a stepwise increase in hyperkalemia risk across risk score tertiles in both placebo and finerenone groups, even though all patients were already on a maximally tolerated RAAS blockade agent. However, he questioned the study's generalizability, given that it excluded patients if their serum potassium was > 4.8 mmol/L. 'This risk model in predicting hyperkalemia needs to be validated in other populations where diet may be different,' Jaar wrote. 'Also, this needs to be validated in at-risk populations during real-life experience and not only in patients enrolled in clinical trials, who are typically highly motivated and selected.' Future Applications Rajiv Agarwal, MD, MS, professor emeritus of medicine at Indiana University and a lead researcher in the finerenone clinical studies, echoed the need for further validation of this tool. Although not involved with the development of the risk model, Agarwal was an author on key publications from the FIGARO-DKD, FIDELIO-DKD, and FIDELITY studies. Agarwal suggested that this model's approach could be applied to other therapies, including aldosterone synthase inhibitors in a similar population with CKD. He also noted the importance of incorporating validated risk models for hyperkalemia into electronic medical records or apps, particularly in countries with limited access to care, like China and India. This would allow more nuanced approaches for following up patients taking drugs with established hyperkalemia risk. 'If the patient cannot come after a month, can I make a clinical judgment and say, 'Okay, if you came back after 3 months, your risk of hyperkalemia is low enough that I'm willing to take that risk,'' he said. 'Or if the risk of hyperkalemia is high, you can tell the patient who can't come back in 30 days, 'I don't think I want to prescribe this drug for you'.' The work on the risk model was supported by Bayer, which also funded the FIDELIO-DKD and FIGARO-DKD studies and pooled analysis. The study's authors included Bayer employees. Other financial relationships of the authors included research support, consulting and other fees from companies including: Abbott Vascular, Amgen, Astellas, AstraZeneca, Bayer, BioVentrix, Boehringer Ingelheim, Brahms, Brainstorm Medical, Cardiac Dimensions, Cardior, Cereno Scientific, CSL Vifor, CVRx, Edwards, Eli Lilly, G3 Pharmaceuticals, Gilead, GSK, Impulse Dynamics, Janssen, KBP Biosciences, Mundipharma, Novartis, Novo Nordisk, Occlutech, PhaseBio, Proton Intel, Respicardia, Sanofi, Sarfez, scPharmaceuticals, Servier, SQ Innovation, Tricida, Vectorious, Vifor International, and V-Wave. Agarwal had received support from Bayer. He also had received consulting fees and other support from Boehringer Ingelheim, Novartis, Akebia, Intercept Pharma, Alnylam, and Vertex. Jaar reported no relevant financial disclosures.