Kami Alexander Pekayvaz, a clinician scientist and research group leader at the Medical Clinic and Polyclinic I of LMU University Hospital, will investigate a newly identified role for neutrophils in thrombosis. Thrombosis remains a leading global cause of morbidity and mortality, and inflammation is recognized as a central driver of its development. In thromboinflammation, proinflammatory neutrophils and the coagulation system can mutually amplify one another and potentially produce thrombotic occlusions of blood vessels.

Pekayvaz has discovered that neutrophils can also infiltrate existing thrombi and promote their resolution, a process described as immunothrombolysis. His ERC project, I-CLEAR, will examine how neutrophils change their role during thrombosis and switch from driving thromboinflammation to promoting resolution, as well as the biological mechanisms and switches underlying that transition. Pekayvaz said this work could open new paths for reducing bleeding risks through targeted activation of the body’s own thrombus-resolution mechanisms, but that possibility remains an aim of the planned research rather than a demonstrated treatment.

Steffen Tiedt, a researcher and attending physician at LMU University Hospital’s Institute for Stroke and Dementia Research, will use the SURPASS grant to investigate the biology of acute stroke. Patients with acute stroke lose millions of neurons every hour, yet effective treatments remain limited. In only a subset of patients can an occluded blood vessel be reopened in time, while a major reason for the lack of additional therapies is the limited understanding of biological processes unfolding during a stroke.

SURPASS will analyze blood samples collected from patients throughout the critical first 48 hours after stroke with high temporal resolution and molecular depth. The researchers seek biomarkers that reflect the progression of brain injury, distinguish biologically different forms of stroke and help predict recovery. They also plan to integrate the molecular data with brain imaging and detailed clinical information to develop a molecular classification of acute stroke.

The SURPASS project will subsequently validate its most promising biomarkers in clinical studies. Its longer-term aim is to develop ultrasensitive point-of-care tests for routine clinical use that allow continuous monitoring of brain damage. Tiedt said making the biological evolution of stroke measurable could change how acute stroke is understood, diagnosed and treated, but the award supports a staged research program: biomarker discovery comes first, followed by clinical validation and development of tests.

The announcement does not report that the proposed classification system, biomarkers or diagnostic tests are already available or clinically established. Economist Arthur Seibold will use the PENSIONREF grant to study the foundations of effective pension reform, including its impact, design and political economy. Pension systems account for a large share of government expenditure across Europe.

As societies age and the number of contributors continues to fall, the source notes an urgent need for political action. Seibold’s research will analyze administrative data to reveal causal relationships between reforms and economic consequences, including effects on employment, productivity and innovation. It will also address distributional concerns and examine the circumstances under which populations support reforms through Europe-wide surveys.

His aim is to contribute to the political feasibility of pension reform by identifying factors that influence public acceptance. “Pension reforms are as necessary as they are unpopular,” Seibold said, adding that it is important to show what shapes whether populations accept them. The grant funds research into these questions; it does not itself prescribe or evaluate a specific reform package.

Postdoctoral researcher Mireia Marimon Tarter will use the BASIS project to ask whether infants possess a form of inner speech before they begin to talk. Infants produce little spoken language during their first year, but they already recognize many familiar words. BASIS, short for Babies’ Silent Speech, will study children between six and 24 months to examine their articulatory readiness for speech, the silent production of familiar words and the internal processing of multi-word utterances.

Marimon Tarter’s method registers synchrony between brain activity and the auditory signal of speech through pupillary responses, with the aim of rendering infants’ inner speech measurable for the first time. She said the results could provide new insights into the earliest stages of language acquisition and inform fundamental debates about theories of language development and human cognition. The planned work is experimental and is intended to determine whether and how silent speech occurs, not to prescribe early language training.

Psychologist Jonas Dora will address an apparent contradiction in addiction science through the CODED project. For decades, addiction research has often operated on the assumption that people drink alcohol to regulate negative emotions. That account faces an empirical paradox: laboratory studies show that stress and negative emotions can increase alcohol consumption, while naturalistic studies of daily life indicate that people are less likely to drink on days marked by high stress and negative emotions.

Dora will combine laboratory experiments and real-world studies with computational decision-making models. The project goes beyond predicting whether a person will drink by examining how the decision is made, including the information considered, the possible role of unconscious biases and when the choice is made. Its goal is to identify mechanisms through which emotions influence alcohol decisions and to develop a unified mathematical theory explaining the discrepancy between laboratory and naturalistic findings.

Dora said resolving the mystery could have implications for understanding how addiction develops and, in the long term, could contribute to more precise and individualized approaches to preventing and treating alcohol dependency. Those potential applications remain a future prospect rather than a demonstrated outcome of CODED. Dora currently works as an Acting Assistant Professor at the University of Washington in Seattle and is expected to move to LMU’s Faculty of Psychology in 2027.

Communication scientist Sophia Volk will study when corporate science communication builds public trust in science and when it erodes that trust. Firms that invest heavily in research and development, including pharmaceutical, automotive and technology companies, play an increasingly influential role in science communication. Such activity can encourage public engagement with science and innovation, but commercial incentives may also lead companies to selectively present or exaggerate scientific evidence in their favor, a practice the source calls sciencewashing.

That behavior can fuel skepticism toward industry science and may spill over into broader mistrust of science. Volk’s COSCOM project will systematically map corporate science communication, examine the conditions associated with trust-building and erosion, and investigate interventions that can reduce risks while preserving potential benefits. Based on its findings, the project intends to develop tools and guidelines for communication and journalism professionals, members of the public, and decision-makers in politics and public administration.

Ruth Wendt will examine how adolescents communicate across different social relationships and what constant digital connectivity may mean for their well-being. Her DIGIREL project focuses on communication patterns that occur between calls, messages and face-to-face interaction, including the skills adolescents need in these settings. Wendt said conventional theoretical and methodological approaches have failed to account adequately for the complex and dynamic forms of communication between adolescents and their social contacts.

The planned research will analyze these interstitial communication patterns and address how the coexistence of digital and non-digital forms affects adolescents’ relationships and well-being.

Subject of Research: Seven ERC Starting Grants supporting LMU research across biomedicine, social science, humanities and communication studies

Article Title: Seven LMU research projects awarded ERC grants

Article References: Seven LMU research projects awarded ERC grants. Original publication (Bibliographic details unavailable.)

Image Credits: AI Generated

DOI: Not provided

Keywords: ERC Starting Grants, LMU, research funding, thrombosis, acute stroke, pension reform, infant language, alcohol use, science communication, digital media, Seven, research

The team, led by Dr. Corinne Benakis, set out to understand how signals originating in the intestine reach the immune cells that help determine stroke outcome. Their starting point was an observation in mouse models of severe stroke: bacteria capable of producing a metabolite called indole became more abundant in the gut following the injury. Indole is a small molecule with a distinctive property that makes it a plausible messenger between microbes and the body — it is produced only in the gut, by bacteria that carry a gene known as tnaA. That gene encodes an enzyme allowing these microbes to convert tryptophan, an amino acid obtained from food, into indole. In other words, a dietary building block is transformed by bacterial metabolism into a signaling molecule that can act on the host immune system.

When the researchers examined what this meant for the brain, the results were striking. In mice, the presence of indole-producing bacteria worsened brain injury after stroke. This established a causal link rather than a mere correlation: the microbial metabolite was not simply a byproduct of the disease state but an active participant in shaping how much damage the stroke inflicted. The discovery adds stroke to a growing list of conditions in which gut-derived molecules have been shown to reach beyond the digestive tract and influence distant organs, often through the immune system.

The next question was mechanistic: how does a molecule made in the gut alter events in the brain? The answer lies with a receptor called the aryl hydrocarbon receptor, or AHR, a sensor found in dendritic cells. Dendritic cells are immune sentinels that patrol the intestinal lining, sampling their surroundings and helping to coordinate immune responses throughout the body. Indole, the team found, acts on AHR in these cells, and that interaction changes their behavior in ways that matter for stroke recovery.

To test this directly, the researchers switched off AHR specifically in dendritic cells. The effect on the mice was protective: without the receptor, they were better shielded against brain injury after stroke. The reason, according to the study, lies in how the cells behave once the indole signal is removed. Dr. Rosa Delgado Jiménez, who shares first authorship of the paper with Alexandria Ruggles and Mujeeb Adedokun, described the change in vivid terms. Dendritic cells, she explained, have long extensions, like arms, that allow them to sense changes in their environment, including metabolites produced by gut bacteria. When AHR was switched off, the behavior of these cells changed completely: they became more potent at migrating from the intestine to the meninges, the membrane surrounding the brain.

That migration proved to be consequential. Once in the meninges, the dendritic cells promoted protective T cells, a class of immune cells capable of dampening inflammation and tissue damage, and thereby helped reduce the injury in the brain. The picture that emerges is a chain of events running from the dinner plate to the brain’s outer membranes: dietary tryptophan is converted by tnaA-carrying bacteria into indole; indole engages AHR in intestinal dendritic cells; that engagement restrains the cells from migrating and from fostering protective T cells; and the resulting immune balance tilts toward greater brain damage after a stroke. Blocking the receptor breaks the chain at its immunological link and tips the balance back toward protection.

Crucially, the researchers found evidence that this pathway may not be a peculiarity of mice. In a cohort of human patients with ischemic stroke, the ISD team observed that a higher abundance of bacterial TnaA — the gene that enables indole production — was associated with poorer functional outcome. The patient samples for this analysis were provided by collaborating teams led by Fernández-Cadenas in Barcelona and Lorenz Hirt in Lausanne. The human data, while correlational, align with the mouse experiments and suggest that the same microbial machinery could be operating in people, influencing how well patients recover from stroke in the real world.

The study also uncovered a connection to stroke risk factors themselves. Bacteria carrying the tnaA gene and capable of producing indole were more abundant in people with conditions known to raise stroke risk, including obesity and type 2 diabetes. This observation hints at a possible mechanism by which metabolic disease could prime the immune system for a worse response to brain injury, though the researchers are careful to note that much remains to be established about whether the full pathway identified in mice also operates in patients.

The complexity of the work made collaboration essential. The study drew on the Transregional Collaborative Research Centre TRR 355, a research network funded by the German Research Foundation (DFG) that focuses on regulatory T cells. Benakis emphasized that the project required expertise a small group could not have covered alone: the TRR 355 network provided financial support and access to the knowledge of group leaders within the consortium. In addition, the team worked with Michael Zimmermann at EMBL and Michael Gigl at TUM to detect tryptophan metabolites and microbial indole, measurements that are technically challenging because of the low concentrations and complex chemistry involved. It was, as Benakis put it, a real team effort.

Beyond its immediate findings, the study opens a question that could reshape how scientists think about stroke prevention: could changing the gut microbiome, or the metabolites it produces, in healthy individuals help prepare the immune system to respond differently if a stroke occurs? Most stroke research and therapy focuses on the brain itself — clot removal, neuroprotection, rehabilitation — while the systemic immune context in which the injury unfolds has received far less attention as a target. If the gut’s contribution proves as influential in humans as it appears to be in mice, interventions ranging from diet to microbial or metabolic therapies could conceivably be used to tilt the immune system toward a protective configuration before a stroke ever happens, particularly in people at elevated risk. As Delgado Jiménez observed, stroke is usually thought of as an injury restricted to the brain, but the findings show that the gut can help shape the immune response to that injury. Benakis noted that the team still needs to determine whether the mechanism identified in mice also occurs in patients, but the work opens new avenues for investigating whether the gut microbiota could eventually be targeted to improve stroke outcome, including through preventive approaches in those most vulnerable.

Subject of Research: How the gut bacterial metabolite indole influences immune responses and brain damage after stroke

Article Title: How gut bacteria can shape the brain’s response to stroke

Article References: How gut bacteria can shape the brain’s response to stroke. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: stroke, gut microbiota, indole, tryptophan, aryl hydrocarbon receptor, dendritic cells, T cells, meninges, ischemic stroke, tnaA, immune response, LMU