bims-nimamd Biomed News
on Neuroimmunity and neuroinflammation in ageing and metabolic disease
Issue of 2026–10–11
nineteen papers selected by
Fawaz Alzaïd, Sorbonne Université
  1. Ultraprocessed foods evoke distinct metabolic and neural responses.
  2. Inhibiting fructose metabolism to treat fatty liver.
  3. Disadvantaged Neighborhoods Associated With Poorer Brain Health.
  4. Longitudinal multiomics reveals personalized aging trajectories.
  5. A guide to B cell metabolism.
  6. Flexible discovery of disease-associated tissue structures.
  7. Revealed: how this common gut microbe protects against heart disease.
  8. RNA architecture regulates DNA replication.
  9. Metabolic advantages of a high-protein, low-carbohydrate diet in in patients with metabolically unhealthy obesity.
  10. Correlating metabolites, lipids, and N-glycans in murine kidney microstructures via integrative mass spectrometry imaging.
  11. Longer lipids mark aging and constrain lifespan.
  12. Population Living With HIV Projected to Age in Coming Years.
  13. Trifluoroacetate mediated reduction of atherosclerosis in mice.
  14. FDA Authorizes First Continuous Ketone Monitor for Diabetes.
  15. Lipid elongation as a hallmark of aging.
  16. Before the immunological Big Bang.
  17. The Gα-interacting protein RGS4 in dorsal root ganglia maintains molecular and behavioral maladaptations in murine pain models.
  18. CGM-derived disposition index estimates beta cell function in individuals with islet autoimmunity who do not require insulin treatment; changes in the disposition index precede changes identified by CGM metrics 1 year later.
  19. Whole Grain Intake Tied to Lower Cardiovascular Disease Risk Factors.
  1. Nat Metab. 2026 Oct 05.
    Ultraprocessed foods evoke distinct metabolic and neural responses.
      
    DOI:  https://doi.org/10.1038/s42255-026-01618-5
  2. Nat Metab. 2026 Oct 07.
    Inhibiting fructose metabolism to treat fatty liver.
    Richard J Johnson, Miguel A Lanaspa, Dean R Tolan.
      
    DOI:  https://doi.org/10.1038/s42255-026-01627-4
  3. JAMA. 2026 Oct 09.
    Disadvantaged Neighborhoods Associated With Poorer Brain Health.
    Samantha Anderer.
      
    DOI:  https://doi.org/10.1001/jama.2026.20018
  4. Nat Aging. 2026 Oct 06.
    Longitudinal multiomics reveals personalized aging trajectories.
    Hannah Walters.
      
    DOI:  https://doi.org/10.1038/s43587-026-01248-2
  5. Nat Rev Immunol. 2026 Oct 07.
    A guide to B cell metabolism.
    Yavuz F Yazicioglu, Glenn R Bantug, Christoph Hess, Alexander J Clarke.
      The metabolism of immune cells must adapt dynamically to support their diverse functions. B cells, which are the key cellular mediators of humoral immunity, undergo extensive metabolic changes throughout their development and function, starting from their commitment to the B cell lineage in the bone marrow. In the periphery, further rounds of metabolic adaptation in B cells are driven by temporally regulated changes in signalling cues, energetic demands and nutrient availability within specialized tissue niches. Although they have historically been less well studied than other immune cell types, emerging evidence shows that B cells deploy mechanistically distinct metabolic strategies that are tightly linked to their effector identity. Recognizing B cell metabolism as its own biological entity is, therefore, crucial to the study of humoral immune responses. In this Review, we examine the metabolic pathways that regulate B cell homeostasis, their integration with cell signalling networks, and their adaptation to the metabolic environment across spatial and temporal scales. We further discuss how aberrations in these pathways can contribute to B cell-driven malignancies, autoimmunity, inborn errors of immunity, and B cell-tropic infections. We position B cell metabolism as a rapidly expanding frontier within immunometabolism in both health and disease.
    DOI:  https://doi.org/10.1038/s41577-026-01355-6
  6. Nat Methods. 2026 Oct 06.
    Flexible discovery of disease-associated tissue structures.
      
    DOI:  https://doi.org/10.1038/s41592-026-03242-3
  7. Nature. 2026 Oct 07.
    Revealed: how this common gut microbe protects against heart disease.
    Max Kozlov.
      
    Keywords:  Cardiovascular biology; Diseases; Microbiome; Therapeutics
    DOI:  https://doi.org/10.1038/d41586-026-03189-7
  8. Nat Cell Biol. 2026 Oct 09.
    RNA architecture regulates DNA replication.
    Sabrya Carim.
      
    DOI:  https://doi.org/10.1038/s41556-026-02093-6
  9. Cell Metab. 2026 Oct 06. pii: S1550-4131(26)00368-2. [Epub ahead of print]38(10): 1941-1942
    Metabolic advantages of a high-protein, low-carbohydrate diet in in patients with metabolically unhealthy obesity.
    Nicola Guess.
      Whether dietary macronutrient content has metabolic benefits beyond weight loss is unknown. In this issue, a carefully controlled trial demonstrates that a higher-protein, lower-carbohydrate dietary pattern improves hepatic glucose and lipid metabolism in people with prediabetes and steatosis compared to a lower-protein, high-carbohydrate diet, even though all groups lost 10% of body weight.
    DOI:  https://doi.org/10.1016/j.cmet.2026.08.016
  10. Nat Commun. 2026 09 04. pii: 10544. [Epub ahead of print]17(1):
    Correlating metabolites, lipids, and N-glycans in murine kidney microstructures via integrative mass spectrometry imaging.
    Nina Ogrinc, Rick Ursem, Hans Dalebout, Jesper Kers, Martin Giera, Manfred Wuhrer, Noortje de Haan.
      Understanding how metabolites, lipids and glycans interact within tissues at the same cellular layer is key to uncovering their roles in health and disease. Herein, we present an integrative multi-omic mass spectrometry imaging (MSI) approach correlating metabolites, lipids and N-glycans, including their linkage-specific sialic acid information, in a single renal tissue section. Our protocol enables the sequential detection of hundreds of metabolites and lipids species alongside diverse glycosylation traits in small cell clusters across the kidney. Importantly, our pixel-to-pixel co-registration and clustering correlates glycans (recorded in positive mode MS), metabolites, and lipids (both in negative mode MS) across kidney microstructures. This analysis reveals strong association between taurine, TCA metabolites, sulfatides, and polyunsaturated phospholipids, and specific sialic acid linkages on N-glycans in the thick ascending limb and collecting ducts. The robust strategy maximizes molecular insights from scarcely available samples and offers a powerful tool for exploring tissue complexity in both normal and disease states.
    DOI:  https://doi.org/10.1038/s41467-026-77127-6
  11. Nat Aging. 2026 Oct 06.
    Longer lipids mark aging and constrain lifespan.
    Weisha Li, Bauke V Schomakers, Maria M Trętowicz, Laura Hartshorne, Jonathan Sulc, Helgi I Ingólfsson, Tugba N Ozturk, Rob Ofman, Luc Legon, Kasandra Ippel, Michel van Weeghel, Martin A T Vervaart, Eric J M Wever, Simone W Denis, Signe Mosegaard, Adriana S Passadouro, Arwen W Gao, Hans R Waterham, Joris Hoeks, Patrick Schrauwen, Gajja S Salomons, Evan G Wiliams, Paul M L Janssen, Vincent A J Warnaar, Linda Partridge, Johan Auwerx, Sebastian Grönke, Mirre J P Simons, Jolanda van der Velden, Frédéric M Vaz, Riekelt H Houtkooper, Georges E Janssens.
      Aging drives molecular changes that impair cellular and tissue function. Lipids are central to membrane structure, signaling and energy storage, yet their remodeling during aging remains unclear. Here, using cross-species, multi-tissue lipidomics, we identify elongation of lipid acyl chains as a conserved hallmark of aging across mice, Caenorhabditis elegans, Drosophila and humans. Similar lengthening occurs during the progression of human heart disease, whereas dietary restriction shortens cardiac lipids in mice. Integrated analyses reveal that aging is characterized by a shift toward longer lipids accompanied by depletion of shorter species, indicating ratiometric remodeling. Following this, we identify the lipid remodeler Plb1 as a regulator of this process, with expression correlating with lifespan in mice and genetic analyses supporting a causal role in human frailty. In C. elegans, Plb1 knockdown reverses lipid elongation and extends lifespan in a lipid-length-dependent manner. Together, these findings establish lipid chain length remodeling as a conserved, actionable hallmark of aging.
    DOI:  https://doi.org/10.1038/s43587-026-01223-x
  12. JAMA. 2026 Oct 09.
    Population Living With HIV Projected to Age in Coming Years.
    Samantha Anderer.
      
    DOI:  https://doi.org/10.1001/jama.2026.20016
  13. Nat Commun. 2026 09 02. pii: 10459. [Epub ahead of print]17(1):
    Trifluoroacetate mediated reduction of atherosclerosis in mice.
    Wei Tang, Audrey S Black, Romana Moench, Katayoon Marzban, Juan Antonio Raygoza Garay, James J Zheng, Louis Conway, Antonio F M Pinto, Christopher G Parker, Alan Saghatelian, Luke J Leman, M Reza Ghadiri.
      Trifluoroacetate (TFA) has been assumed to be an innocuous counterion in countless synthetic bioactive peptides and a few FDA-approved therapeutics. Here we show that TFA is in fact bioactive, inducing peroxisome proliferation and causing significant metabolic effects in three strains of mice (wild-type C57BL/6 J, Ldlr-/-, and Apoe-/-) and cultured liver cells. In a high-fat diet induced Ldlr-/- mouse model of atherosclerosis, TFA reduced the levels of plasma LDL cholesterol, triglycerides, and the development of atherosclerotic lesions. These physiological effects were observed with TFA alone, or with TFA present as a counterion of a variety of short, unrelated synthetic peptide sequences. Multiple lines of mechanistic evidence supported that TFA acts by binding to peroxisome proliferator activated receptor (PPAR)-α to induce peroxisome proliferation. These findings indicate the need to assess the contribution of TFA to phenotypic effects observed in some studies using synthetic peptides and, if these effects extend to humans, suggest potential therapeutic applications as well as broader health implications of widespread environmental TFA exposure.
    DOI:  https://doi.org/10.1038/s41467-026-77341-2
  14. JAMA. 2026 Oct 09.
    FDA Authorizes First Continuous Ketone Monitor for Diabetes.
    Samantha Anderer.
      
    DOI:  https://doi.org/10.1001/jama.2026.20013
  15. Nat Aging. 2026 Oct 06.
    Lipid elongation as a hallmark of aging.
    Shanshan Pang.
      
    DOI:  https://doi.org/10.1038/s43587-026-01229-5
  16. Science. 2026 Oct 08. 394(6820): 170-171
    Before the immunological Big Bang.
    Bali Pulendran.
      The nature of the gut microbiome before vaccination influences later inflammatory reactions and fever.
    DOI:  https://doi.org/10.1126/science.ael7318
  17. Sci Signal. 2026 Oct 06. 19(958): eaed7175
    The Gα-interacting protein RGS4 in dorsal root ganglia maintains molecular and behavioral maladaptations in murine pain models.
    Randal A Serafini, Bruno Giotti, Alex Luebbers, Kerri D Pryce, Ilinca M Giosan, Madden J Tuffy, Jeffrey Zimering, Aarthi Ramakrishan, Donghoon Lee, Ekaterina Kintsurashvili, Feodora L Bertherat, Neelakshi Patne, John F Fullard, Panos Roussos, Li Shen, Mikel Garcia-Marcos, Alexander M Tsankov, Venetia Zachariou.
      Regulator of G protein signaling 4 (RGS4) is a Gα subunit-interacting protein that modulates the functional responses of various G protein-coupled receptors (GPCRs) and that is present in several components of the nociceptive circuitry. Here, we found that RGS4 in lumbar dorsal root ganglia (DRGs) is required for the maintenance of chronic pain states in mice. Rgs4 knockout in Mrgprd+ nonpeptidergic C-fibers was sufficient to attenuate sensory hypersensitivity in several acute and chronic injury models without affecting acute nociceptive responses. Single-nucleus RNA sequencing in ipsilateral lumbar DRGs from mice with prolonged peripheral nerve injury identified cell subset-specific gene expression changes in Rgs4 knockout mice after recovery from mechanical hypersensitivity, including Gabbr2, which encodes the GABAB receptor, in Mrgprd+ fibers. RGS4 competed with Gαi-interacting protein (GINIP) to modulate GABAB receptor signaling, which suppresses neuronal excitability. Analysis of genetically modified mice suggested that imbalances in the interplay between RGS4 and GINIP contribute to the maintenance of sensory hypersensitivity and chronic pain states. Overall, our study reveals critical G protein-modulatory pathways in the DRG that promote the maintenance of sensory hypersensitivity in chronic pain models.
    DOI:  https://doi.org/10.1126/scisignal.aed7175
  18. Diabetologia. 2026 Oct 07.
    CGM-derived disposition index estimates beta cell function in individuals with islet autoimmunity who do not require insulin treatment; changes in the disposition index precede changes identified by CGM metrics 1 year later.
    Hadija Marchiori, Michele Schiavon, Eileen Tichy, Michele Alguard, Marcia DeSousa, Simone Del Favero, Jason L Gaglia, Jennifer L Sherr, Chiara Dalla Man, Alfonso Galderisi.
       AIMS/HYPOTHESIS: Monitoring of beta cell function in individuals with islet autoimmunity who do not require insulin treatment (preclinical type 1 diabetes) is normally done via OGTTs, posing major challenges given the invasiveness of the test. Here, we validated a disposition index (DI) derived from continuous glucose monitoring (CGM) metrics (DICGM), which is a proxy of beta cell function, against the gold-standard OGTT DI (DIMM), in a cohort of individuals with one or more islet autoantibodies who do not require insulin treatment.
    METHODS: Participants underwent a 3 h 10-point OGTT with measurement of glucose, insulin and C-peptide while wearing a blinded CGM. The sensor was started 24 h prior to the OGTT. DICGM was computed using CGM data during the 3 h OGTT and two blood glucose calibrations, and compared with the DI from the oral minimal model (DIMM), which uses plasma glucose, insulin and C-peptide. The association between the baseline DICGM and duration of glucose levels above 7.8 mmol/l (140 mg/dl) (TA140) at 1 year was explored.
    RESULTS: Twenty-four participants (median age 16.8 years [IQR 13.5-27.7] ) were enrolled, of whom 18 completed both the OGTT (ten with pre-stage 1, seven with stage 1 and one with stage 3a type 1 diabetes) and CGM at baseline, and had repeat CGM 1 year later. The baseline DICGM was highly correlated with the DIMM (r=0.90, p<0.001). Lower baseline DICGM was associated with higher 1 year TA140 (r=-0.61, p=0.014) and higher 1 year mean sensor glucose (r=-0.62, p=0.020).
    CONCLUSIONS/INTERPRETATION: Beta cell function can be estimated using CGM during a glucose load. DICGM correlates with a 1 year clinically relevant outcome (TA140) in individuals with islet autoimmunity who do not require insulin therapy.
    Keywords:  Beta cell function; CGM; Continuous glucose monitoring; Digital biomarkers; Model identification; Preclinical T1D; Stage 1 T1D; Stage 2 T1D; Type 1 diabetes
    DOI:  https://doi.org/10.1007/s00125-026-06895-z
  19. JAMA. 2026 Oct 09.
    Whole Grain Intake Tied to Lower Cardiovascular Disease Risk Factors.
    Samantha Anderer.
      
    DOI:  https://doi.org/10.1001/jama.2026.20014
This page is being maintained by Thomas Krichel. It was last updated on 2026‒10‒13 at 17:56.