Duan et al. systematically delineate the spatiotemporal dynamics and key regulators of pyroptosis during MASLD progression. Hepatocyte-specific Plagl2 deletion alleviates MASH by suppressing MYD88-mediated inflammasome activation and restoring metabolic homeostasis. Pyroptosis-driven IL-1β release promotes macrophage differentiation into a phagocytosis-enhanced, JAK/STAT-activated, NASH-associated phenotype.
Those who have never endured the relentless ringing of tinnitus can only dream of the torment. In fact, a bad dream may be the closest some get to experiencing anything like it.
The subjective sound, which can also be a hissing, buzzing, or clicking, is heard by no one else, and it may be present constantly, or may come and go.
Neuroscientists at the University of Oxford now suspect that sleep and tinnitus are closely intertwined in the brain.
A new study led by researchers from VIB and KU Leuven shows that immune cells called microglia can actively promote the formation of plaques in Alzheimer’s disease, challenging the long-standing view that these cells serve only as defenders against plaque buildup. The findings were recently published in the Proceedings of the National Academy of Sciences.
“Most studies suggest that microglia are there to clean up the brain and remove the amyloid plaques. What we discovered is that actually they’re part of the problem. They generate plaques,” says Prof. Joost Schymkowitz, co-senior author of the study at the VIB-KU Leuven Center for Neuroscience. “It was thought that plaques aggregate by themselves. And it seems that the microglia, by trying to deal with the problem, amplify it.”
Alzheimer’s disease affects nearly 55 million people worldwide and is characterized by the accumulation of toxic protein aggregates in the brain known as amyloid plaques. These plaques are associated with neuronal death and progressive dementia. The brain’s microglia have been hailed as protectors against plaque accumulation in the disease, being the focus of several therapies. Nonetheless, the study shows how microglia are active producers of amyloid plaques in the earlier stages of the disease, reconsidering the therapeutic paradigm for Alzheimer’s.
Scientists have successfully reconstructed videos purely from the brain activity of mice, showing what the mice were seeing, in a new study led by University College London (UCL) researchers. The findings, published in eLife, could help shed light on the intricate workings of how the brain processes visual information and open new avenues for exploring how different species perceive the world.
Over recent years, there has been a growing interest in understanding exactly how the human brain interprets signals from the eye. Images and movies have been played to people in fMRI machines and researchers around the world have tried to decode the brain’s representations of visual information on a pixel level.
Triggering receptor expressed on myeloid cells 2 (TREM2) is a cell surface transmembrane receptor from the TREM receptor family, predominantly expressed on the microglia in the central nervous system (CNS). TREM2-initiated signaling plays a crucial role in regulating neuroinflammation and neurodegeneration, particularly in the context of neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), through the activation of downstream signaling pathways and transcriptional regulation of relevant genes. In this review, we aim to provide a concise review of the role and mechanistic implications of TREM2 in neurodegeneration and neuroinflammation, with a specific focus on AD and PD. We will discuss the most recent preclinical studies to highlight current advancements in the field. This review is intended to support both basic researchers and clinicians by enhancing their understanding of microglial function in the pathophysiology of AD and PD, as well as its role in neuroinflammation and neurodegeneration. Ultimately, we hope this contribution will pave the way for new discoveries and the development of potential therapeutic interventions.
© 2026. The Author(s).
Antibody titers elicited by the current inactivated influenza vaccine were modest against #Influenza A(H3N2) subclade K compared to responses against prior H1N1 and H3N2 strains.
Lower baseline and postvaccination titers to subclade K suggest partial immune evasion, raising implications for continued transmission and the selection of upcoming influenza vaccine strains.
This cohort study examines antibody responses to influenza A(H3N2) subclade K and other strains before and after vaccination against influenza.
The identification of patients with acute myeloid leukemia (AML) who may have resistant disease when treated with standard induction chemotherapy is still challenging: Murphy and colleagues present the first prospective, multicenter study aiming to evaluate the prognostic value of the leukemic stem cell 17-gene (LSC17) score in patients with newly diagnosed AML.
Acute myeloid leukemia (AML) patients exhibit diverse molecular and cytogenetic changes with heterogeneous outcomes. The functionally-derived LSC17 gene expression score has demonstrated strong prognostic significance in retrospective analyses of adult and pediatric AML cohorts, where above-median scores are associated with worse outcomes compared to below-median scores in intensively-treated patients. Here we used a laboratory-developed clinically-validated NanoString-based LSC17 assay to test the prognostic value of the LSC17 score in a prospective multicenter study of 276 newly-diagnosed AML patients. Each patient’s score was classified as high or low by comparison to a previously-established reference score. In the entire cohort, a high LSC17 score was associated with poor risk features, including advanced age and unfavorable genetic mutations. In the subset of 190 patients treated intensively, a high LSC17 score was associated with lower remission rates (63% vs. 94% after induction; P0.0001), presence of measurable residual disease (46% vs. 10%; P0.0001), and shorter overall survival (OS, 606 days vs. not reached; P=0.0004; hazard ratio
Acute myeloid leukemia (AML) is a heterogeneous malignancy with multiple subtypes and variable clinical outcomes driven by disease characteristics as well as the clinical status of the patient.1 2,3 While genomic classification has further rationalized risk stratification in AML, many challenges remain.4 The accurate assessment of survival outcomes in AML subtypes driven by various combinations of driver mutations and cytogenetic abnormalities presents a challenge to the treating physician.5
AML is sustained by a rare subpopulation of leukemia stem cells (LSC) believed to drive therapy resistance and relapse.6,7 The LSC17 gene expression score was developed based on functionally-defined LSC populations across the spectrum of AML subtypes.8 In multiple independent retrospective cohorts, the LSC17 score has been found to robustly discriminate between patients with significantly different outcomes.9–12 Higher-than-median LSC17 scores were associated with poor treatment response and survival outcomes in both uni-and multi-variable survival analyses, independent of commonly used prognostic factors including cytogenetic and molecular risk groups.