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TREM2 in neurodegeneration and diseases

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).

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An Overview of the Pathogenesis, Transmission, Diagnosis, and Management of Endemic Human Coronaviruses: A Reflection on the Past and Present Episodes and Possible Future Outbreaks

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.

Real-world validation study of the LSC17 score for risk prediction in patients with newly diagnosed acute myeloid leukemia

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


=2.16; 95% confidence interval [CI]: 1.39−3.35) and relapse-free survival (RFS, 541 days vs. not reached; P=0.001; HR=1.99; 95% CI: 1.29−3.08). In multivariable analysis considering age, white blood cell count and European LeukemiaNet 2022 risk groups, the LSC17 score remained an independent predictor of RFS and OS. Allogeneic stem cell transplantation improved OS for patients with a high but not a low LSC17 score. This study establishes the real-world value of the LSC17 score as a robust tool for risk assessment in AML and paves the way for its incorporation into routine clinical practice.

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.

New strategy to fight chronic kidney inflammation

Mayo Clinic researchers have identified a drug-and-supplement combination therapy that is capable of reducing the harmful effects of senescent cells – also known as “zombie cells” – in diabetic kidney disease.

In eBioMedicine, a publication of The Lancet, the team reported that the combination of the cancer drug dasatanib and a naturally occurring substance known as quercetin decreased inflammation and boosted protective factors in the kidney.

Diabetic kidney disease affects more than 12 million people in the U.S. and is the leading cause of kidney failure. While newer treatments can delay loss of kidney function, there is currently no cure.

Alzheimer’s Disease: From Molecular Mechanisms to Promising Therapeutic Strategies

Brain vasculature in ischemic stroke.

Ischemic stroke induces dynamic cellular structural changes in the neurovascular unit, leading to disrupted structural integrity of the blood–brain barrier, neuronal degeneration, and responsive angiogenesis coordinated by endothelial cells, reactive astrocytes, and pericytes.

After ischemic stroke, the neurovascular coupling function of the neurovascular unit is also disrupted, manifested by the metabolic dysregulation of glucose, lipid/fatty acid, and amino acids.

Neurovascular unit dynamic structural remodeling and metabolic dysfunction following ischemic stroke show cellular states and spatiotemporal heterogeneities, revealing new perspectives on ischemic stroke pathogenesis and future therapeutic strategies.

Multidimensional approach aiming to repair neurovascular unit structural disorganization and restore metabolic homeostasis with cellular and spatiotemporal precision is the optimal therapeutic strategy for ischemic stroke. sciencenewshighlights ScienceMission https://sciencemission.com/neurovascular-unit-in-ischemia


The neurovascular unit (NVU) is a multicellular system functioning to maintain healthy brain homeostasis and regulate the exchange of essential elements between the blood and the brain. Recent studies have shown that, in response to ischemic stroke (IS), the NVU undergoes dynamic structural remodeling and metabolic dysfunction, revealing new features of IS pathogenesis. Recent breakthroughs in single-cell multiomics provide emerging evidence regarding the spatiotemporal heterogeneity of NVU responses to IS. To date, clinical treatments for IS-induced brain injury remain very limited. These new studies have advanced our knowledge of the dynamic cellular and molecular changes of the NVU after IS, paving the way for new therapeutic strategies.

Physicists Finally Realize Long-Predicted 2D Topological Crystal in the Lab

Researchers in Finland have experimentally realized a long-predicted class of quantum material: a two-dimensional topological crystalline insulator. Physicists at the University of Jyväskylä and Aalto University (Finland) have successfully created a two-dimensional topological crystalline insulat

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