University of Durham

Pleco Therapeutics is proud to announce the publication of a research paper, "Synthesis of Metal-Binding Amino Acids," in Organic & Biomolecular Chemistry. Authored by PhD-student Katherine Deck and Associate Professor Will Brittain from Durham University, UK. The paper outlines recently developed strategies for the synthesis of metal binding non-proteinogenic amino acids, which an essential part of ongoing efforts to explore novel therapies. Pleco’s support is mentioned under Acknowledgements, for which we thank the authors. This work is part of our ongoing collaborations with academic centres around the world, including Durham University, where our focus is on investigating basic mechanisms of chemoresistance. These developments align with Pleco Therapeutics' mission to enhance chemotherapy efficacy and overcome treatment resistance in cancer. We extend our congratulations to Katherine Deck and Will Brittain for their contribution. Click here for article

Biogen and Eisai’s Alzheimer’s disease (AD) drug has been approved by the Medicines and Healthcare products Regulatory Agency (MHRA) to treat patients with early stages of the neurodegenerative disease, but has not been recommended by the National Institute of Health and Care Excellence (NICE) for use on the NHS in England and Wales. Leqembi (lecanemab) has been authorised by the MHRA to treat mild cognitive impairment and mild dementia due to AD in adults who have one or no copies of the apolipoprotein E4 gene. However, in a blow to patients, NICE has stated in draft guidance that the drug’s benefits are “too small to justify the costs”. An estimated 982,000 people in the UK are living with dementia and AD accounts for the majority of cases. Administered intravenously in a healthcare setting every two weeks, Leqembi works by binding to and reducing clumps of amyloid beta protein that form plaques in the brain. The MHRA’s decision makes Leqembi the first medicine to be licensed in the UK that has been shown to slow progression of the disease and was supported by results from the late-stage Clarity AD trial, in which Leqembi reduced clinical decline by 27% compared with placebo at 18 months. Eisai, which serves as the lead for the drug’s development and regulatory submissions globally, also recently presented positive three-year data from an open-label extension of the study. Despite the improvements observed, an independent NICE committee said: “The costs of providing the treatment, including fortnightly infusions in hospital and intensive monitoring for side effects, combined with the relatively small benefits it provides to patients means it cannot be considered good value for the taxpayer.” Alzheimer’s Research UK’s chief executive, Hilary Evans-Newton, described the news as “bittersweet”. “It’s a remarkable achievement that science is now delivering licensed treatments that can slow down the devastating effects of Alzheimer’s, rather than just alleviating its symptoms. However, it’s clear our health system isn’t ready to embrace this new wave of Alzheimer’s drugs,” she said. Professor Andy Whiting, emeritus professor at Durham University and chief executive officer and co-founder of Nevrargenics, a Durham spinout company developing drugs for neurodegenerative diseases including Alzheimer’s, said in response to today’s news: “While the MHRA approval of [Leqembi] is obviously a step forward for the pharma industry, the NICE rejection reinforces the need for the biotech and pharma community to focus on better balancing of cost versus effectiveness in drug development. “[Leqembi] only targets the symptoms – the plaques – rather than the cause of those plaques. For a new drug to provide value, the impact needs to be higher, which requires our industry to develop bolder drugs for neurodegeneration that target the cause of the disease, not just the symptoms.” NICE’s independent committee will consider responses from a public consultation at a second meeting later this year before producing its final recommendations.

THURSDAY, July 18, 2024 -- Alix Popham played in two rugby World Cups and won a Six Nations Grand Slam before retiring in 2011 as a professional in the rough-and-tumble game. By 2020, he had already been diagnosed with early onset dementia and probable chronic traumatic encephalopathy (CTE), a disabling brain disease long linked to repeated head trauma. Emboldened to activism by his experience, Popham helped found Head for Change , which advocates for better ways of preventing brain damage among rugby players. “This is more evidence that big changes need to happen to protect current rugby players. World Rugby need to get their heads out of the sand and in turn protect the game," Popham said in a news release from Durham University. Similar to what's been observed in other contact sports such as football and boxing, rugby can leave players with neurological damage long after they've retired. Now, a new study out of Durham suggests that certain blood biomarkers could predict those players at highest risk for CTE and other neurological issues. That might allow for earlier interventions that could minimize the damage, researchers said. Prior research has already demonstrated that retired professional rugby players have a much higher odds for depression, anxiety and irritability compared to amateur rugby players or athletes involved in non-contact sports. In the new study, Durham researchers add to what's known about specific components of blood suggestive of neural damage from concussions and other head injuries. The study involved 56 male professional athletes, all of who gave researchers blood samples about seven years after retiring from their sport. Thirty of the athletes were retired rugby players who had each suffered five or more concussions during their careers. Their blood samples were compared to those of 26 retired rugby players with no history of concussions, as well as retired athletes from non-contact sports. Compared to athletes without high numbers of head injuries, higher levels of certain "serum exosomes" were observed in the blood of retired male rugby players who'd had multiple concussions during their playing careers. As well, levels of two blood proteins -- serum t-tau and tau-p181 -- were found to be elevated among the retired male rugby players compared to healthy controls. Those proteins are thought to play roles in the development of both Alzheimer's disease and a movement disorder known as motor neurone disease (MND), the Durham team noted. Finally, the data also showed that retired rugby players tended to have lower blood levels of a "retinoid transport protein" called RBP-4, which is crucial to healthy brain function and development. That supports the notion that medications focused on retinoids might prove to be an effective treatment for brain damage, the researchers said. “The long-term effects of concussions on rugby players, football players, boxers as well as retired military personnel is a major concern, because of the link to neurodegenerative diseases," said study senior author Paul Chazot , of Durham University’s department of biosciences. “This study gives us the beginnings of a biomarker toolbox to periodically monitor the brain health of retired contact sportspeople, particularly those with a history of concussion during their career," he said in a university news release. Chazot said certain interventions are already being looked at, to help "minimize the development of future neurodegenerative disease" in at-risk athletes. The research is part of the UK Rugby Health Project, first set up in 2016. The study was published July 17 in the International Journal of Molecular Sciences . Whatever your topic of interest, subscribe to our newsletters to get the best of Drugs.com in your inbox.