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The Nobel Prize Winning Optogenetics Research that Revealed Neuron Mysteries

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From left: Peter Hegemann (Photo: Humboldt University of Berlin/Philipp Plum), Karl Deisseroth (Photo: Christopher Michel/ Wikimedia Commons, CC BY-SA 4.0), Georg Nagel (Photo: Robert Ememrich/University of Würzburg).

Karl Deisseroth, Peter Hegemann and Georg Nagel have been awarded the 2026 Nobel Prize in Physiology or Medicine for their discoveries behind optogenetics, a method that makes it possible to switch nerve cells in the brain on and off using light. The technique has given researchers new tools to understand how specific nerve cells contribute to memories, emotions and behaviour.

Which nerve cells make us feel fear or anxiety? Which ones drive us to move, eat or seek social contact?

The brain consists of billions of nerve cells that are constantly sending electrical signals to one another. For a long time, researchers could observe which nerve cells were active during specific brain processes and behaviours, but they could not determine whether they actually caused the behaviour. Optogenetics changed that.

“There was no way to test what would happen to a behaviour if I activated a particular type of nerve cell or if I stopped the activity of that type of nerve cell? Optogenetics made exactly that possible: to switch the activity of specific nerve cells on or off and observe how the behaviour changed,” says Konstantinos Meletis, professor at the Department of Neuroscience, Karolinska Institutet, who has collaborated with Karl Deisseroth.

The researchers could therefore move from correlation to causality: from observing that a nerve cell is active when a certain behaviour occurs to testing whether the activity in the nerve cell actually causes the behaviour.

“It is so incredibly fundamental, so crucial to brain research. You can divide the history of neuroscience into a ‘before’ and an ‘after’ this discovery. Optogenetics has completely transformed what is possible to do,” says Konstantinos Meletis.

From algae to nerve cells

The story behind this year’s Nobel Prize began in the early 1990s, when the German researcher Peter Hegemann became interested in how the single-celled alga chlamydomonas can detect and swim towards light.

Together with fellow Nobel laureate, George Nagel, also from Germany, he succeeded in identifying a light-sensitive type of protein in the alga during the 2000s. The protein was named channelrhodopsin.

They discovered that when blue light struck the protein, a channel in the cell membrane opened. Electrically charged particles, known as ions, could then flow into the cell and generate an electrical signal. A key finding was that the the same protein and mechanism could also function in other types of cells.

From there came the next major idea.

The American researcher Karl Deisseroth realised that the protein channelrhodopsin could be used to control nerve cells.

The researchers introduced the gene coding for the protein channelrhodopsin into nerve cells grown in a laboratory, leading to formation of the light-sensitive protein on the surface of the nerve cells. When the nerve cells were exposed to blue light, the ion channels opened and the nerve cells began to generate and transmit electrical signals, just as nerve cells naturally do in the brain.

In effect, they had created a light-controlled switch for nerve cells.

Two years later, Karl Deisseroth and his colleagues were able to use the technique to control nerve cells in the brains of living mice.

Since then, optogenetics has become a central tool in neuroscience. By controlling specific nerve cells, researchers can investigate how different brain circuits influence movement, memory, emotions and behaviour.

The technique is also being explored as a potential foundation for future treatments.

“The technology is already being used in attempts to restore vision in people who are blind. The hope is that it will also become a tool for treating neurological disorders such as Parkinson’s disease and Alzheimer’s disease, as well as psychiatric disorders such as depression, anxiety and PTSD,” says Konstantinos Meletis.

A collaboration that spread across the globe

Around 2008, Konstantinos Meletis was a postdoctoral researcher at MIT in the United States alongside Marie Carlén, now a professor at the Department of Neuroscience, Karolinska Institutet. There, they collaborated with Karl Deisseroth’s laboratory at Stanford University. This marked the beginning of a long-standing scientific collaboration. Deisseroth was invited to Karolinska Institutet on several occasions and held an affiliated research position between 2013 and 2019.

“Karl is an absolutely exceptional scientist and human being. In addition to being incredibly intelligent, he is remarkably generous. This has contributed to the breakthrough in optogenetics,” says Marie Carlén, and continues:

“As soon as he set up his lab and carried out the first optogenetics studies in the mid-2000s, he began sharing these tools with others. Since then, they have spread to thousands of laboratories around the world. I would say that is quite unique. It has enabled laboratories everywhere to continue expanding our knowledge of the brain.”

For Konstantinos Meletis, this year’s Nobel Prize is a reminder of the value of basic research and the importance of investing in work whose future significance is not yet known.

“We must be willing to trust the unexpected, to trust major discoveries that arise from things we did not anticipate. Optogenetics did not emerge because someone decided we needed a method to cure a specific disease. It developed frompeople who were deeply committed to a fundamental scientific question. Only later could its potential be recognised,” he says.

He points to Hegemann’s and Nagel’s early research on light-sensitive proteins in algae as an example. At the time, it was far from obvious how important the discovery would become for neuroscience.

“What funding body would choose to support research on algae in order to discover this protein? And yet, 20 years later, it has transformed the entire field of neuroscience. That is what makes it so inspiring.”

Facts about the 2026 Nobel Laureates

Karl Deisseroth

Born in 1971. Received his PhD in 1998 and his medical degree in 2000 from Stanford University,USA. Professor of Biomedical Engineering and of Psychiatry and Behavioural Sciences at the Howard Hughes Medical Institute and Stanford University.

Peter Hegemann

Born in 1954. Received his PhD in 1984 at the Max Planck Institute for Biochemistry in Martinsried, Germany, where the prize-winning discoveries were made. Professor of Neuroscience at Humboldt University in Berlin, Germany.

Georg Nagel

Born in 1953. Received his PhD in 1988 at the University of Frankfurt in Germany. Professor of Molecular Plant Physiology at the University of Würzburg, Germany. The prize-winning discoveries were made at the Max Planck Institute of Biophysics in Frankfurt, Germany.

Text: Anna Björklund

Source: The Nobel Foundation via Karolinska Institutet

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False Mechanism in Cancer Trial Drug Raise Concerns for Clinical Research

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Cancer drug entered clinical trials based on a false mechanism, exposing risks and costs of testing drugs without knowing their true target.

Photo by National Cancer Institute on Unsplash

A cancer drug currently being tested in patients may have entered clinical trials based on an incorrect understanding of how it works, according to a new study led by the University of Sydney in collaboration with Goethe University, Oxford University and the Institute of Cancer Research, London. 

Published in Nature Chemical Biology, the study found the experimental drug zavondemstat and a closely related research compound, QC6352 – developed to treat cancers such as colorectal, pancreatic and prostate cancer – do not primarily target KDM4, a family of proteins which can help cancer cells grow and spread when it becomes overactive. Instead, both compounds largely work by blocking DHODH, an enzyme cancer cells rely on to produce the molecules needed for rapid growth.

Lead author Professor Lenka Munoz from the University of Sydney School of Medical Sciences and Charles Perkins Centre said: “We can think of DHODH as a machine producing bricks needed to build new DNA. If you switch off the machine, the cell starts running out of bricks and can no longer efficiently copy its DNA and keep dividing.”

These findings could affect the interpretation of previous studies around the world that used the research compound (QC6352) to investigate the biology of the cancer protein and may have implications for the ongoing clinical development of the zavondemstat drug. 

The discovery emerged from research investigating whether zavondemstat and QC6352 could be repurposed for glioblastoma, the most common and aggressive form of brain cancer. 

“We tested these compounds to investigate whether they could potentially be repurposed for glioblastoma treatment,” Professor Munoz said.

“When we tested other KDM4 inhibitors, we found they did not reproduce the anti-cancer effects observed with QC6352. 

“If blocking KDM4 was driving those effects, we would have expected the other inhibitors to behave similarly. Instead, the results suggested QC6352 was acting through a different mechanism.”

“Our study shows this is not just a historical problem but one still happening today. Greater rigour is needed to ensure we understand exactly how potential treatments work before they move into clinical testing.”

Professor Lenka Munoz
Charles Perkins Centre

Using patient-derived glioblastoma stem cells, tumour models and a series of genetic, mechanistic and molecular experiments, the researchers traced the compounds’ response to DHODH rather than KDM4.

“Researchers around the world have used QC6352 as a leading tool to study KDM4 biology, while the related drug zavondemstat progressed into clinical trials based on the same understanding,” Professor Munoz said.

“Our study found much of the anti-cancer activity of these compounds is driven by blocking DHODH rather than KDM4.”

Study highlights broader issue facing cancer drug development

Professor Munoz said the findings highlight a broader challenge in cancer drug development.

“Getting a drug’s mechanism wrong can lead to poorly designed clinical trials, inappropriate patient selection and years of research focused on the wrong biological target,” she said.

“There are well-known examples of cancer drugs advancing through large clinical trials before researchers realised they were not working through the mechanism originally proposed. 

“Our study shows this is not just a historical problem but one still happening today. Greater rigour is needed to ensure we understand exactly how potential treatments work before they move into clinical testing.

“Establishing a drug’s true mechanism early can protect patients, prevent wasted research effort and help ensure what limited funding we have is directed towards genuinely promising treatments.”

The findings also point to DHODH inhibition as a potential new avenue for glioblastoma treatment. Several drugs targeting DHODH are already being investigated for other cancers, raising the possibility they could eventually be tested in patients with brain cancer.       

Beyond identifying the drug’s true target, the researchers developed new compounds that inhibit KDM4 without affecting DHODH, which could help scientists study the role of KDM4 more accurately in future cancer research. 

Source: University of Sydney

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HPV-vaccinated Women had a Lower Risk of Preterm Birth

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Source: Pixabay CC0

The benefits of the HPV vaccine may extend beyond protection against cancer. In a study published in The BMJ, researchers at Karolinska Institutet found that women who had been vaccinated against HPV were less likely to experience several pregnancy and childbirth complications, particularly preterm birth.

HPV (human papillomavirus) is the leading cause of cervical cancer. HPV infection and treatment of cervical cell changes have also been associated with an increased risk of certain pregnancy complications. A new study has investigated the link between the HPV vaccine and complications such as preterm birth, premature rupture of membranes, babies being small for their gestational age, stillbirth, and neonatal mortality.

The study is based on Swedish registers and covers 624 713 pregnancies among first-time mothers aged 16 to 35 between 2006 and 2023. Of these women, 92 620 had received the quadrivalent HPV vaccine prior to becoming pregnant, providing protection against four common types of HPV.

Stronger link when vaccinated at a younger age

Women who had been vaccinated before pregnancy consistently had a lower risk of the studied complications, particularly preterm birth. Compared with unvaccinated women, they were around five per cent less likely to give birth prematurely and around 15 per cent less likely to give birth very prematurely.

“We also observed that the associations were stronger among women who had been vaccinated before the age of 17,” says Zhongsong Zhang, doctoral student at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet. “This is consistent with previous findings that the HPV vaccine provides the best protection against HPV-related disease when administered at a younger age.” 

A large register-based study

Although the researchers took into account several factors that could have influenced the results, as this was an observational study, it was not possible to conclude that the lower risk was caused by HPV vaccination. Nevertheless, the study covered a large number of women from the Swedish population over a long period of time. 

“Even a relatively small reduction in the risk of preterm birth can be significant at a population level, given that HPV vaccination is administered to millions of young people worldwide,” says Jiayao Lei, assistant professor at the same department at Karolinska Institutet. “Our results suggest that the benefits of HPV vaccination may extend beyond cancer prevention to include the reduction of complications that can arise during pregnancy and childbirth.” 

The study was carried out in collaboration with researchers at the University of Gothenburg, Sahlgrenska University Hospital and the Norwegian Institute of Public Health. Funding for the research came from the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Cancer Society, Karolinska Institutet and ALF grants, among others. See the scientific article for information on any conflicts of interest.

Source: Karolinska Institutet

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Inside The Box with Dr Andy Gray | How Should Medicines Shortages be Managed in South Africa?

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#InsideTheBox is a column by Dr Andy Gray, a pharmaceutical sciences expert at the University of KwaZulu-Natal and Co-Director of the WHO Collaborating Centre on Pharmaceutical Policy and Evidence Based Practice. (Photo: Supplied)

By Dr Andy Gray for Spotlight

Imagine you have been taking a medicine for years. Then one day you are told at the pharmacy that supplies have run out. In his latest Spotlight column, Dr Andy Gray zooms in on how governments can monitor and plan for such shortages.

The draft text of the United Nations High-Level Declaration on Pandemic Prevention, Preparedness and Response, which failed to get consensus support at the General Assembly on 25 September 2026, contained this paragraph:

“Deeply concerned by the inequities at national and international levels that hindered timely and equitable access to health products, including vaccines, diagnostics and therapeutics to address coronavirus disease (COVID-19), and recognizing the need to address serious shortcomings at the national, regional and global levels in prevention, preparedness, response and health system recovery for public health emergencies of international concern, including pandemic emergencies;”

However, it is not only during pandemics or public health emergencies that shortages of medicines and vaccines are experienced and have to be actively managed. In fact, in recent decades the issue has become so serious that several high-income countries have taken legal and regulatory steps to address it.

Global access to medicine shortage data

South African health and medicines law does not clearly define what is meant by a “medicines shortage”. By contrast, the US Federal Food, Drug, and Cosmetic Act simply defines it as a period of time when the demand or projected demand for a medicine exceeds its supply.

Since 2012, marketing authorisation holders in the US have been under a legal obligation to report shortages to that country’s medicines regulator. These obligations were strengthened during the COVID-19 pandemic and now require manufacturers to report any interruption in their manufacturing process that is likely to lead to a meaningful disruption in supply, as well as to disclose the reasons for the interruption. Manufacturers are also required to give advanced warning of permanent discontinuation of production, and the reasons for that decision. The US Food and Drug Administration (FDA) maintains a publicly accessible database of current resolved shortages and discontinuations. In addition, the American Society of Health-System Pharmacists maintains a separate database.

Medicines shortages have also been recognised as a critical public health issue by the European Medicines Agency (EMA) and its national agencies. Since 2022, manufacturers have been required to report shortages to the European Shortages Monitoring Platform. The EMA maintains an accessible database of current and resolved shortages, as do each of the national agencies.

A similar resource is provided by the Australian Therapeutic Goods Administration (TGA).

The gap in South Africa

The South African Health Products Regulatory Authority (SAHPRA) has no equivalent reporting requirement, nor does it make any such data publicly accessible.

SAHPRA’s online register includes not only those products with current registration, but also includes those where the status is noted as “Cancelled”. Unfortunately, while the date of registration is recorded, there is no date of cancellation stated, nor any reason provided for discontinuation of the product. Health professionals and patients only find out about product discontinuations after the fact and the regulator has no advanced warning of the decision, nor is it provided with the reasons for discontinuation. There is also no accounting for how many medicines have been withdrawn from the South African market.

Section 19(2) of the Medicines and Related Substances Act allows SAHPRA to request any information from manufacturers, sellers or prescribers of medicines, but the intent is to enable response to a specific request, within a stipulated time period. This provision does not create an ongoing obligation or a permanent reporting process, so cannot be used to impose the type of reporting demanded in the US, Europe or Australia.

A valuable resource – the health department’s “hotlist”

The National Health Department’s website includes a recent innovation, in the form of a “hotlist”, defined as “a list of all essential medicines on contract with stock availability of below 90% and with total orders exceeding supplier stock on hand and total provincial stock on hand less than two months of forecasted demand”. Importantly, the list also documents “the root cause for the supply challenge and proposed remedial actions for each listed item”. The list is updated on a monthly basis and the August 2026 version lists 29 “new” items, 98 described as “longer term” and 120 resolved items. Of particular note, a separate tab lists products which were not being supplied to particular provinces because of non-payment of accounts. The reasons for shortages vary considerably, from delays in quality assurance procedures to delays in accessing critical components, whether active ingredients, excipients or packaging materials. Global supply constraints were also identified, as were local regulatory actions (or delays in obtaining regulatory approval for changes in production).

The health department’s website also provides a link to the current Master Health Product List, which includes all medicines for which a tender has been awarded. One of the columns on the spreadsheet documents the “VEN” status of the medicine. This refers to a judgment on whether a medicine is considered “vital”, “essential” or “non-essential”, in terms of the immediate health consequences of a shortage. Lack of access to a vital medicine, for which alternatives might not exist, would be expected to have immediate and serious health consequences for patients. One way to mitigate that risk would be to contract multiple suppliers of a vital medicine. Such split tenders are used for some essential medicines, notably the first-line antiretrovirals used to treat HIV, but not for all medicines listed as vital.

The private sector – adrift

Not only is there no equivalent of the “hotlist” for the private sector in South Africa, but one of the key responses used by the public sector to manage shortages is also not available. The National Department of Health Contract Management Unit’s website lists the products for which SAHPRA has granted the public sector permission, in terms of section 21 of the Medicines and Related Substances Act, to import unregistered medicines in bulk. In the private sector, similar bulk approvals are not issued, and individual applications are required for every patient seeking access to an alternative product, should there not be a registered alternative on the local market.

Health professionals in the private sector are therefore at a distinct disadvantage, lacking access to timely information about medicine shortages and also denied access to a key mechanism for responding to shortages.

In Australia, the equivalent legal provision (section 19A) enables access to unregistered, imported medicines to manage a medicine shortage considered to be of public health importance. Access is enabled for the entire health system, not only for facilities operated by the state.

The concept of “critical medicines”

European authorities have extended the concept of VEN status to create a list of “critical medicines”. In May 2026, political agreement was reached on the Critical Medicines Act, which will enable a number of important interventions to promote resilience in the pharmaceutical market. One of these interventions will require manufacturers to hold contingency stocks of critical medicines and mandate sharing of data on such stocks when reallocation is required, triggering a call for solidarity between Member States. Procurement of medicines will also be required to promote regional manufacturing in the EU.

Many reasons, key gaps

There can be many reasons for medicines shortages, some related to the national market, others impacted upon by global shifts. Regulatory action by SAHPRA in response to non-compliance with good manufacturing standards has resulted in a number of disruptions in supply, notably in the small volume injectable market.

Although the second single exit price adjustment in 2026 will be welcomed by the pharmaceutical industry, other actions noted in the joint government-industry-regulator statement in August 2026 still require attention. Some immediate actions include a joint review of the pricing regulations, to improve transparency and predictability and also explore alternative reimbursement models for specific medicines. In the longer term, the industry is seeking appropriate incentives, including public sector procurement that supports local production and attracts new investment.

According to the FDA definition, a medicine such as lenacapavir is already showing signs of a shortage, with demand exceeding supply. Improved transparency, applied across both public and private sectors, is crucial if medicine shortages are to be prevented, identified and acted upon with the urgency they deserve.

 – Gray is a Senior Lecturer at the University of KwaZulu-Natal and Co-Director of the WHO Collaborating Centre on Pharmaceutical Policy and Evidence Based Practice.

Disclosure: Gray serves on three technical advisory committees at the South African Health Products Regulatory Authority.

*This column was published by Spotlight – health journalism in the public interest. Sign up to the Spotlight newsletter.

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HASA Confirms Continued Board Leadership

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Gale Shabangu, HASA Board Chairperson

The Hospital Association of South Africa (HASA) has confirmed the continuation of the majority of its previous Board of Directors following its Annual General Meeting, with Gale Shabangu from Mediclinic Southern Africa continuing as Chairperson and Mark Bishop from Lenmed continuing as Deputy Chairperson.

The continued composition of the Board provides stability and continuity as HASA builds on its work in policy engagement, sector collaboration and its contribution to South Africa’s healthcare priorities.

The Board brings together leaders from across the private hospital sector, with experience spanning healthcare operations, strategy, governance and stakeholder engagement.

HASA Chief Executive Officer, Dr Dumisani Bomela, welcomed the continuation of the Board and said:

“The continued leadership of the HASA Board provides an important foundation for the Association as we enter the next chapter of our work. We are fortunate to have a Board with significant sector experience, combined with fresh perspectives that will help us engage constructively on the opportunities and challenges facing healthcare in South Africa.”

He added: “Our focus remains on meaningful engagement and collaboration across the healthcare sector. HASA will continue to work with government, healthcare professionals and other stakeholders to support practical solutions that contribute to a stronger, more resilient and sustainable health system.”

HASA Board 2026/27

  1. Gale Shabangu (Chairperson)
  2. Mark Bishop (Deputy Chairperson)
  3. Andre Joseph
  4. Amrita Raniga
  5. Bert von Wielligh
  6. Dr Biancha Mentoor
  7. Charles Vikisi
  8. Hendrica Ngoepe
  9. Dr Melanie Stander
  10. Prathna Sookoo
  11. Vishnu Rampartab

Alternate Directors:

  1. Dr Ashley Chengadoo
  2. Chantel Heyns
  3. Mary Ann Nabbie

As HASA moves forward, the continued Board leadership will support the Association’s ongoing engagement with stakeholders across the healthcare sector and its role in contributing to national health priorities.

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Even Limited Vaping can Cause Lasting Lung Damage and Weaken Immune Defence

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Photo by Toan Nguyen on Unsplash

Just days of e-cigarette vapor exposure can injure the lungs’ most delicate tissue and leave it more vulnerable to viral infection, according to a study led by National Jewish Health researchers and published in JCI Insight.

The research team studied human lung epithelial and endothelial cells, along with precision-cut human lung tissue, all taken from the distal lung – the deep, delicate region where oxygen passes into the bloodstream. They exposed these tissues to e-cigarette vapor alone, and separately tested vapor exposure followed by infection with a respiratory virus, in preclinical models. Within 24 hours, e-cigarette vapor damaged the protective barrier of the distal lung, triggered cellular stress, impaired cells’ internal process for clearing damaged components, slowed cell growth and repair, and increased cell death.

Strikingly, signs of lung stress persisted 10 days after just a five-day exposure period ended. The team observed lasting changes in barrier function, tissue remodeling, and Th1 immunity – a branch of the immune system critical to fighting viral infections.

Prior vaping exposure also increased SARS-CoV-2 viral burden and suppressed several antiviral genes following infection.

“Our findings suggest that even short-term vaping exposure can initiate injury in the deepest and most delicate regions of the lung,” said senior author Irina Petrache, MD, pulmonologist and chief of the Division of Pulmonary, Critical Care and Sleep Medicine at National Jewish Health. “Importantly, some effects persisted after exposure ended and altered the immune response to a subsequent viral infection.”

The findings, which will need to be confirmed in future studies in people, point to biological mechanisms that may help explain why vaping has been linked to lung injury and greater susceptibility to respiratory infections. The researchers noted that repeated exposure could potentially contribute to chronic lung disease by sustaining cellular injury and disrupting normal repair.

Source: National Jewish Health

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Poor Antibody Validation Wastes Millions of Biological Samples, but Solutions Exist

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Two linked studies provide effective recommendations for publishers, funders, institutions, and manufacturers

Tubes of samples going into clinical waste. Image credit: Only Good Antibodies team at the University of Leicester (CC-BY 4.0)

A widespread failure to validate research antibodies before use is estimated to lead to the avoidable waste of millions of animal and human tissue samples worldwide, and an international expert panel has reached consensus on how to address the problem, according to two studies published October 6th in the open access journal PLOS Biology by Harvinder Virk of the University of Leicester, UK, and colleagues.

Antibodies are critical reagents that enable researchers to detect, quantify, and isolate specific proteins in biological samples. However, research antibodies do not always bind their intended targets, or may bind additional unintended targets. Studies have suggested that many antibodies do not bind as advertised. This lack of specificity can misdirect biomedical research across fields.

In the first study, Virk and first author Michael Biddle combined data from focus groups (12 researchers), a survey (107 researchers), and an analysis of 785 publications linked to antibodies that had failed rigorous, knockout-controlled testing. Among 760 publications where validation status could be determined, only 120 (15.8%) presented any validation evidence, despite 72.0% of surveyed researchers reporting having used at least one recommended validation method. The papers lacking antibody validation used a minimum of 8064 animal samples and 4424 human tissue samples. Extrapolating, the researchers estimate that millions of animal and human tissue samples have been consumed globally without adequate validation.

“This study provides, to our knowledge, the first systematic quantification of biological sample waste attributable to the use of poorly performing antibodies without context-specific validation,” the researchers say.

In the second study, Virk and first author Katherine Blades convened 32 international experts – including researchers, publishers, funders, antibody manufacturers and institutional leaders – for a two-round Delphi consensus exercise to rate proposed reforms for antibody validation. The panel agreed that 15 actions, including institutional training, dedicated validation budgets in grant applications, and publisher reporting requirements, were both effective and feasible for implementation by 2030; a further 15 actions were judged effective but of uncertain feasibility. Participants pointed to diffuse ownership of the problem, and market incentives that fail to reward antibody quality as key barriers.

“The findings lend themselves to a programme of targeted stakeholder consultation,” the authors say. “To support this, we have prepared separate documents for each stakeholder group – publishers, funders, institutions, and manufacturers – presenting consensus recommendations alongside implementation options derived from the panel’s qualitative feedback. These present options rather than prescriptions, recognising that the optimal approach will vary across organisations, countries, and contexts.”

Harvinder Virk (corresponding author on both papers) says, “Around ten years ago I discovered that data I had submitted in a grant application relied on an antibody that did not detect its intended target. The data included staining of bronchial biopsies from patients who had given informed consent. They would not have expected their donation to be wasted. That has driven this work ever since.”

Michael Biddle (first author, “Inadequate antibody validation places substantial numbers of animal and human tissue samples at risk of waste”) adds, “Researchers told us they validate their antibodies: 72% reported using at least one recommended method. But only 120 of the 760 papers we could assess showed any validation evidence. The other 640 studies reported at least 8,064 animal and 4424 human tissue samples used with antibodies that had failed independent testing; we describe these samples as at risk of waste. In the clearest cases – where the antibody has since been withdrawn from sale, so the work cannot be reproduced at all – scaling to the commercial antibody market gives a lower-bound global estimate of 4 to 7 million animal samples and 6 to 11 million human tissue samples.”

Katherine Blades (first author, “Actionable solutions to address antibody validation failures”) states, “What struck us was the level of agreement once researchers, funders, publishers, institutions and manufacturers were brought into the same process. The panel reached consensus on 15 actions that are both effective and achievable by 2030. Progress is held back not by disagreement about what to do, but because no single group owns the problem – so everyone waits for someone else to move first.”

Harvinder Virk notes, “Together these papers show the problem has significant impact with ethical dimensions, and is solvable. Since completing this work, we have embedded champions for better practice in 14 UK research institutions, and the University of Leicester has made antibody validation training mandatory for its bioscience postgraduate researchers. We are working with two national funders – the NC3Rs and Cancer Research UK – on implementation solutions, and have built free tools publishers can use to protect the integrity of what they publish.”

Provided by PLOS

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Neurosurgery Samples Reveal New Drug Target for Alzheimer’s Disease

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Promising anti-inflammatory drug target can block receptors in the brain and potentially dampen down pathways to major brain conditions

Photo by Natanael Melchor on Unsplash

Inflammatory conditions in the brain, including traumatic brain injury and degenerative diseases like Alzheimer’s could be targeted with an existing drug thanks to new research that shows it can work in brain cells.

In a study published in Brain, a team led by Professor Nicholas Barnes at the University of Birmingham has identified a critical receptor that when blocked inhibits neuroinflammation. This first-of-its-kind work with human brain tissue demonstrates how interrupting this pathway could open the door to treating a wide spectrum of chronic neurological conditions. These include not only traumatic brain injury (TBI), but also neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease, and even psychiatric disorders such as depression and psychosis, these latter conditions are increasingly understood to have a neuroinflammatory component.

Using live cultures of human brain cells and slices of brain tissue obtained during neurosurgery, the researchers investigated the role of a receptor known as the P2X7 receptor, which is responsible for triggering inflammatory signalling.

This exciting discovery marks a major step toward repurposing existing therapeutics to combat neuroinflammation at its source. The identification of this receptor could have far-reaching implications for some of the most debilitating and widespread brain disorders

Professor Nicholas Barnes, Professor of Neuropharmacology

Their findings reveal that these P2X7 receptors drive the release of key proteins called cytokines involved in controlling inflammation. By blocking this receptor with a specific antagonist, the team was able to significantly reduce the inflammatory response in human brain tissue.

Professor Nicholas Barnes from the College of Medicine and Health at the University of Birmingham and corresponding author of the paper said: “This exciting discovery marks a major step toward repurposing existing therapeutics to combat neuroinflammation at its source. The identification of this receptor could have far-reaching implications for some of the most debilitating and widespread brain disorders such as Alzheimer’s Disease, Parkinson’s and Multiple Sclerosis, or inflammation-linked psychiatric conditions like schizophrenia and depression”.

Brain’s resident immune sentinels

In order to study how brain cells respond to and manage inflammation, the team developed a way of turning a type of white blood cell into microglia, replicating a normal cellular transformation that has recently been identified to occur in the brain as a natural part of human ageing. These microglia are the central coordinators of the immune system in the brain.

Using readily accessible human peripheral monocytes taken from blood samples, the researchers converted them into microglia-like cells that were used to see how microglia are likely to respond to the inflammation signals. Using the P2X7 receptor antagonist, the team were then able to interrupt the triggers that these microglia give off as they are damaged and die.

Professor Barnes said: “Studying human microglia has long been a major challenge: once removed from their native brain environment, they rapidly lose their defining characteristics, likely due to the absence of critical regulatory signals. Our approach involved the use of monocyte-derived microglia which provide a powerful, scalable, and virtually unlimited platform for studying human microglial biology with unprecedented precision.

“Having identified the response in the human monocyte-derived microglia, this provided the impetus to translate these findings with human brain obtained following neurosurgical procedures. This successful translation means the next stage for this research is the development of clinical trials in patients with neurodegenerative conditions and patients with TBI where there are no effective pharmacological treatments to reduce the neuroinflammation and arising damage.”

Source: University of Birmingham

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A Few Licks of this Candy-coated Device Measures Medication Levels in Saliva

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A few licks of the lollipop-like prototype collects enough saliva to test for paracetamol levels.

The red, peach-flavoured candy coating on Lollylab stimulates saliva production, and a sensor at the bottom analyses it for paracetamol. Adapted from ACS Sensors 2026, DOI: 10.1021/acssensors.6c00691

What if checking medication levels were as simple as enjoying a lollipop? A candy-coated device, called Lollylab, could provide the answer. In ACS Sensors, researchers describe how the lollipop’s stem transfers saliva to a sensor that measures acetaminophen levels. In an initial test, a peach-flavoured prototype reliably detected the pain reliever in six people’s saliva in less than two minutes. Participants also found it more comfortable and easier to use than traditional collection swabs.

Taking more than the maximum recommended dose of paracetamol can cause serious side effects, such as liver damage. This is especially concerning for children who can be at risk of an unintentional overdose at low levels of the medication. Because paracetamol concentrations in saliva closely reflect those in blood, Sina Khazaee Nejad, Maral Mousavi, and colleagues thought saliva could be a simple, noninvasive way to monitor the medication’s levels. 

Mousavi says they were inspired by the saliva sampling system CandyCollect — a lollipop-like device meant to replace throat swabs — but those specimens need to be analysed elsewhere. In this work, the researchers wanted to create a miniature laboratory-on-a-lollipop, or Lollylab. “By turning a familiar object like a lollipop into both a saliva collection device and a sensor, Lollylab can collect the sample and perform the measurement directly at the point of care,” says Nejad, the first author of the paper.

Lollylab is built from two plastic pieces (each with a round end and a thinner stem) snapped together, with holes at the top for saliva to enter through. The team coated the top of the device with a red, peach-flavoured edible candy shell, which did not interfere with measurements. Saliva flows through the glass fibre paper-lined lollipop stem toward a graphene sensor at the bottom, which measures acetaminophen levels as changes in electrical current. The prototype device detected acetaminophen in both artificial and human saliva.

As proof of concept, six adults used Lollylab before and an hour after taking a standard adult dose of paracetamol (650 milligrams). The device reliably measured the drug in the participants’ saliva in less than two minutes, and they said it was easy to use and more comfortable than typical saliva swabs.

“The main takeaway is that diagnostic testing can be made much easier and more comfortable, especially for children,” says Nejad. Next, the researchers plan to validate Lollylab’s paracetamol measurements with more participants, including children, and develop it to detect other substances in saliva such as naturally occurring stress markers. “Our longer-term goal is to create a multi-assay platform capable of measuring several biomarkers, which could then be evaluated alongside acetaminophen [paracetamol] in larger clinical studies.”

Source: American Chemical Society

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Suspected Plague Incident Leaves 1 Dead, 200 under Quarantine in Siberia

On By ModernMedia
Scanning electron micrograph of Yersinia pestis, which causes bubonic plague, on proventricular spines of a Xenopsylla cheopis flea. Credit: NIAID

A 28-year old female lab technician at the Irkutsk Research Anti-Plague Institute of Siberia, Russia, died of double pneumonia (infection in both lungs) late last week.

Government officials in Russia have not confirmed that the woman died from pneumonic plague, but several media reports suggest she died after an accident involving a broken vial containing a live sample of plague, a deadly bacterial infection. Now, a rumoured 200 people are suspected to be under quarantine. 

Rospotrebnadzor, the official Russian infectious disease agency, said, “No micro-organisms associated with the employee’s professional duties were detected in samples taken from the patient.”

But over the weekend, media in Russia and elsewhere in Europe started to stoke concerns over a lab leak incident or fears that the woman worked in a bioterrorism unit. They suspected that the Russian government was covering up something that posed a serious risk to global health. 

Case does not cause ‘undue concern’

Michael Osterholm, PhD, MPH, director of the University of Minnesota’s Center for Infectious Disease Research and Policy (CIDRAP), which publishes CIDRAP News, said that if the woman did die from pneumonic plague, it would be possible to contain, and close contacts and fellow lab workers would be given prophylactic (preventive) antibiotics. 

This case does not cause undue concern.

“This case does not cause undue concern,” Osterholm said. “We would like more information, of course.”

Osterholm explained that if this incident happened in a friendly nation, people would not be so quick to jump to allegations of bioterrorism. But information from Russia, China, or North Korea often lacks transparency. Osterholm also said that, despite the attention-grabbing headlines, plague infections occur every year around the world. 

The bacterium Yersinia pestis is linked to three main types of plague. The first, bubonic plague, is the one associated with the Black Death and the Middle Ages. It’s spread through flea bites and attacks the lymph nodes. Septicaemic plague is also spread through flea bites and occurs when the bacteria enter the bloodstream.

Pneumonic plague attacks the lungs and is the deadliest of the three main plague types. It’s also the most dangerous in terms of biosecurity, because it can be transmitted from person to person via respiratory droplets. It is considered extremely contagious and has a short incubation period (time from exposure to first symptoms) of roughly 24 hours. 

From 2019 to 2025, the World Health Organization estimates there were 3800 suspected plague cases (mostly bubonic) in 10 countries, resulting in 423 deaths. The last recorded plague case in South Africa was in 1982.

The United States tracks five to seven cases of bubonic plague each year, most often in the Southwest. Though plague kills 30% to 60% of people without treatment, all three strains are very sensitive to modern antibiotics.

Source: University of Minnesota