bims-micgli Biomed News
on Microglia
Issue of 2026–01–11
23 papers selected by
Matheus Garcia Fragas, Universidade de São Paulo



  1. Nat Commun. 2026 Jan 09. 17(1): 338
      Disrupted lipid homeostasis and neuroinflammation often co-exist in neurodegenerative disorders, including Alzheimer's disease (AD). However, the intrinsic connection and causal relationship between these deficits remain elusive. Our previous studies show that the loss of sulfatide (ST), a class of myelin-enriched lipids, causes AD-like neuroinflammatory responses, cognitive impairment, bladder enlargement, and lipid dyshomeostasis. To better understand the relationship between neuroinflammation and lipid disruption induced by ST deficiency, we established a ST-deficient mouse model with a constitutive Trem2 knockout. Our study demonstrates that TREM2 regulates ST deficiency-induced neuroinflammation and astrocyte activation at the transcriptomic level but does not affect stage 1 disease-associated microglia or astrogliosis at the protein level. Additionally, ST loss-induced lipidome disruption, free water retention, and cognitive impairment persist in the absence of TREM2. Further, these phenotypes are more severe in females compared to males. Collectively, these results emphasize the essential role of TREM2 in mediating lipid loss-associated microglia-mediated neuroinflammation, but not astrogliosis or myelin lipid disruption. Moreover, we demonstrated that attenuating TREM2-mediated neuroinflammation has a limited impact on brain ST loss-induced lipidome alteration or AD-like central and peripheral disorders. Our findings suggest that preserving the lipidome and astrocyte balance may be crucial in decelerating the progression of AD.
    DOI:  https://doi.org/10.1038/s41467-025-66222-9
  2. Stem Cell Reports. 2026 Jan 08. pii: S2213-6711(25)00383-2. [Epub ahead of print] 102779
      Altered microglial lipid metabolism is heavily implicated in Alzheimer's disease (AD) and aging. Recently, protocols were developed to generate human induced pluripotent stem cell-derived microglia-like cells (iMGL) to study microglial function in vitro, including embryoid body-based methods and induced transcription factor (iTF)-dependent approaches. Here, we performed comparative lipidomics on iMGL from these methods and report major differences in multiple lipid classes, including triglycerides (TGs), a storage form of fatty acids implicated in microglial reactivity. TGs are strongly increased in iTF microglia due to the absence of a media supplement (B-27). Supplementing iTF microglia with B-27, or its component L-carnitine, reduces TGs and promotes a homeostatic state. B-27 also renders iTF microglia metabolically responsive to immune stimuli. Overall, our data show that iMGL differentiation methods have a major impact on microglial lipidomes and warrant attention when studying AD and neuroinflammatory processes involving lipids.
    Keywords:  iPSC; lipid droplet; lipid metabolism; lipidomics; microglia; neuroinflammation; triglycerides
    DOI:  https://doi.org/10.1016/j.stemcr.2025.102779
  3. Alzheimers Dement. 2026 Jan;22(1): e71063
    Alzheimer's Disease Neuroimaging Initiative (ADNI)
       INTRODUCTION: In Alzheimer's disease (AD), females have higher prevalence and faster progression, but sex-specific molecular findings in AD are limited.
    METHODS: We comprehensively examined 6162 proteins in cerebrospinal fluid (CSF) from 2496 participants to identify sex-specific proteomic alteration by CSF amyloid beta (Aβ)42 and phosphorylated tau (p-tau) levels.
    RESULTS: We identified and replicated 68 male-specific and 116 female-specific proteins associated with Aβ42 and/or p-tau levels. Apolipoprotein E ε4 carrier status modified sex-specific alterations of multiple proteins including S100A9 and NEFL for Aβ42 and MAPK9 and MAPKAPK2 for p-tau. Male-specific proteins, enriched in microglia, were involved in activating innate immune response. The male network exhibited direct connections among 30 proteins and highlighted MAPKAPK2 as a hub. Female-specific proteins, enriched in endothelial cells, were involved in regulating protein metabolic process. The female network exhibited direct connections among 43 proteins and highlighted CSNK2A2 and PRKCA as hubs.
    DISCUSSION: Our findings provide insights into mechanistic understanding of sex differences in AD risk.
    HIGHLIGHTS: Our proteomic study of 6162 proteins (targeted by 7006 aptamers) in cerebrospinal fluid (CSF) from 2496 participants identified and replicated 68 male-specific and 116 female-specific proteins associated with cerebrospinal fluid amyloid beta 42 and/or phosphorylated tau levels. Male-specific proteins, enriched in microglia, were involved in activation of innate immune response. The male network highlighted MAPKAPK2 involved in chronic neuronal neuroinflammation as a hub. Female-specific proteins, enriched in endothelial cells, were involved in regulation of protein metabolic process and response to external stimuli. The female network highlighted PRKCA regulating synaptic plasticity and CSNK2A2 protein involved in neuroplasticity as hubs.
    Keywords:  Alzheimer's disease, amyloid beta 42, cerebrospinal fluid, females, males, phosphorylated tau; proteomics, sex specific
    DOI:  https://doi.org/10.1002/alz.71063
  4. Immunity. 2026 Jan 07. pii: S1074-7613(25)00525-4. [Epub ahead of print]
      Single-cell transcriptomic studies have identified distinct microglial subpopulations with shared and divergent gene signatures across development, aging, and disease. Whether these microglial subsets represent ontogenically separate lineages of cells or are manifestations of plastic changes in microglial states downstream of some converging signals is unknown. Furthermore, despite the well-established role of enhancer landscapes underlying the identity of microglia, the extent to which histone modifications and DNA methylation regulate microglial state switches at enhancers has not been defined. Here, using genetic fate mapping, we demonstrated the common embryonic origin of proliferative-region-associated microglia enriched in developing white matter and tracked their dynamic transitions into disease-associated microglia and white matter-associated microglia in disease and aging contexts, respectively. This study links spatiotemporally discrete microglial states through their transcriptomic and epigenomic plasticity, while revealing state-specific enhancer histone modifications and transcription regulators that govern state transitions in health and disease.
    Keywords:  Alzheimer’s disease; DNA methylation; development; disease-associated microglia; enhancers; histone modifications; microglia; plasticity; proliferative-region-associated microglia; white matter
    DOI:  https://doi.org/10.1016/j.immuni.2025.11.023
  5. Int J Mol Sci. 2025 Dec 27. pii: 296. [Epub ahead of print]27(1):
      Neuroinflammation, a key contributor to neurodegenerative diseases, results from excessive microglial activation. Microglia that respond to pathogenic molecules switch to the M1 type and secrete various immune cytokines, which can cause neuronal damage. Therefore, our study focused on molecules that can enhance the neuroprotective role of microglia and reduce neuronal damage. The adipocyte enhancer-binding protein 1 (AEBP1) gene is known for its role in regulating immune responses in macrophages. However, its role in neuroinflammation has not been fully explored. Therefore, we investigated the role of AEBP1 in microglial cells activated by lipopolysaccharide (LPS). First, we confirmed that AEBP1 is expressed in LPS-activated microglia and demonstrated that downregulation of AEBP1 using shRNA in activated microglia reduced the immune response via the nuclear factor-kappa-B (NFκB) pathway. These results promote a shift toward neuroprotective M2 microglia, thereby reducing neuronal damage. Next, we confirmed that the expression of AEBP1 was elevated in the brains of Alzheimer's disease (AD) mice. Additionally, animal experiments to assess the therapeutic effects of AEBP1 showed that microglia gathered around amyloid beta (Aβ) and reduced its size. Taken together, our results provide the first evidence that AEBP1 can reduce inflammatory activity in microglia, suggesting its potential as a target molecule for immunotherapy.
    Keywords:  adipocyte enhancer-binding protein 1; microglia; neuroinflammation; neuronal damage
    DOI:  https://doi.org/10.3390/ijms27010296
  6. Glia. 2026 Mar;74(3): e70136
      Astrocytes are central to lipid metabolism in the central nervous system. Due to their morphological and functional characteristics, astrocytes can uptake fatty acids (FAs) from the bloodstream and extracellular space and store them in lipid droplets (LD). LD are dynamic organelles, whose accumulation in astrocytes has been shown to occur upon exposure to various stress stimuli. Different hypotheses proposed to explain motor neuron degeneration in amyotrophic lateral sclerosis (ALS) implicate mitochondrial dysfunction and oxidative stress. Mitochondrial dysfunction in astrocytes is associated with elevation of cytoplasmic lipids and lipid-binding proteins. We observed increased LD in the spinal cord of symptomatic ALS mice, as well as in human transdifferentiated astrocytes obtained from ALS patients. Using a co-culture model, we examined the effect of FA overload and its impact on astrocyte-motor neuron interaction. LD accumulation was tightly coupled with an NF-κB-driven proinflammatory response in nontransgenic astrocytes, correlating with motor neuron toxicity. These results provide additional evidence to the notion that altered energy balance may contribute to neuronal death in ALS. Furthermore, pharmacological inhibition of lactate dehydrogenase (LDH) reversed LD accumulation in mouse and human astrocytes expressing ALS-linked mutations. Genetic ablation of LDHA similarly reduced LD accumulation in response to FA treatment. Collectively, our data underscore the role of lipid metabolism in astrocyte-neuron interactions in ALS models and suggest that LD accumulation, rather than serving solely as a protective mechanism, reflects a metabolic stress state linked to a detrimental phenotypic transformation in astrocytes.
    Keywords:  LDH; NF‐κB; astrocytes; inflammation; lipid droplets
    DOI:  https://doi.org/10.1002/glia.70136
  7. Mol Neurobiol. 2026 Jan 03. 63(1): 337
      Microglia, the resident immune cells of the central nervous system (CNS), play critical roles in maintaining brain homeostasis and responding to neurological insults. Recent advances have fundamentally reshaped our understanding of how microglial mitochondrial metabolism influences neuroinflammation and disease progression. Single-cell transcriptomics has revealed unexpected metabolic heterogeneity, identifying distinct phenotypes such as disease-associated microglia (DAM) and lipid-laden microglia (LLM) that represent not merely activated states but terminal endpoints of metabolic paralysis. These discoveries converge on a unified pathogenic mechanism: mitochondrial quality control failure leads to mitochondrial DNA release, which activates the cGAS-STING pathway to create an "epigenetic lock" that drives sustained neuroinflammation. Interestingly, we highlight that the loss of metabolic flexibility-rather than glycolysis per se-is the true driver of pathology, explaining why the same metabolic shift can be protective during acute injury but pathological when sustained chronically. We critically examine conflicting evidence across Alzheimer's disease, Parkinson's disease, multiple sclerosis, and ischemic stroke, including the puzzling dual roles of glycolysis, controversies surrounding the experimental autoimmune encephalomyelitis (EAE) model in multiple sclerosis research, and the paradoxical worsening of stroke outcomes following microglial depletion. By synthesizing these mechanistic insights with lessons from failed clinical trials, we identify critical translational gaps-including the lack of longitudinal human data and validated biomarkers-and propose a precision medicine framework focused on restoring mitochondrial dynamics and metabolic flexibility in neurological diseases.
    Keywords:   Metabolic reprogramming; Mitochondrial metabolism; Neuroinflammation; Microglia
    DOI:  https://doi.org/10.1007/s12035-025-05640-8
  8. Glia. 2026 Mar;74(3): e70120
      Cortical demyelination is a critical contributor to progressive disease in multiple sclerosis (MS). The barriers to cortical remyelination following demyelination are not fully understood, and there are no remyelinating treatments for MS. We previously took advantage of the spatial and temporal resolution of longitudinal in vivo imaging to study cortical oligodendrocyte regeneration following cuprizone-induced demyelination and found that oligodendrocyte regeneration was impaired. In this study, we investigated whether cortical reactive microglia disrupt oligodendrocyte regeneration. To do so, we used a combination of in situ RNA and immunofluorescence labeling to characterize cortical microglia reactive states following cuprizone-mediated demyelination. We then depleted cortical microglia by administering a Csf1r inhibitor during the recovery period from cuprizone and quantified oligodendrocyte recovery. We found that following cortical demyelination, deep cortical microglia change morphology, downregulate homeostatic markers (P2RY12, TMEM119), and upregulate a marker (CD68) associated with activated macrophages. These reactive changes persisted through early recovery post-cuprizone but resolved by late recovery. Depleting cortical microglia post-cuprizone restored the baseline density of deep cortical ASPA+ oligodendrocytes at early and late recovery. There were also more deep cortical BCAS1+ differentiating oligodendrocytes at early recovery when microglia were depleted, suggesting that transient deep cortical reactive microglia impair oligodendrocyte differentiation following demyelinating injury. Together, we found that cortical microglia adopt spatially restricted reactive functions after demyelination and deep cortical reactive microglia transiently reduce differentiating oligodendrocytes. A potential therapeutic strategy for progressive MS could involve targeting transiently reactive microglia at the right time and place in cortical lesions to promote oligodendrocyte regeneration.
    Keywords:  cortex; cuprizone; microglia; oligodendrocytes; remyelination
    DOI:  https://doi.org/10.1002/glia.70120
  9. Nat Commun. 2026 Jan 08. 17(1): 300
      Wide variation of responses to identical stimuli presented to genetically inbred mice suggests the hypothesis that stochastic non-genetic variation, such as in chromatin state or enhancer activity during neurodevelopment, can mediate such phenotypic differences. However, this hypothesis is largely untested since capturing pre-existing molecular states requires non-destructive, longitudinal recording. Therefore, we tested the potential of Calling Cards (CC) to record transient neuronal enhancer activity during postnatal development in mice, and thereby associate such non-genetic variation with a subsequent phenotypic presentation - degree of seizure response to the pro-convulsant pentylenetetrazol. We show that recorded differences in enhancer activity at 243 loci predict a severe vs. mild response, and that these are enriched near genes associated with human epilepsy. We also validated pharmacologically a seizure-modifying role for two previously unassociated genes, Htr1f and Let7c. This proof-of-principle supports using CC broadly to discover predisposition loci for other neuropsychiatric traits and behaviors. Finally, as human disease is also influenced by non-genetic factors, similar epigenetic predispositions are possible in humans.
    DOI:  https://doi.org/10.1038/s41467-025-65346-2
  10. J Neuroinflammation. 2026 Jan 02.
       BACKGROUND: Cognitive dysfunction associated with type 1 diabetes (T1D) is closely linked to the accumulation of amyloid-beta (Aβ) oligomers. However, the role of microglia and their underlying molecular mechanisms in this process remain unclear. Triggering receptor expressed on myeloid cells 2 (TREM2), a microglial receptor critical for clearing neurotoxic Aβ and maintaining metabolic homeostasis, is dysfunctional in Alzheimer's disease. Here, we investigated TREM2-mediated microglial dysfunction in diabetic neurodegeneration.
    PURPOSE: To investigate the role of TREM2-mediated microglial dysfunction in Aβ clearance and cognitive impairment in T1D.
    BASIC PROCEDURES: A total of 204 male C57BL/6J mice, aged 6-8 weeks, were used in this study. We performed single-nucleus RNA sequencing (snRNA-seq) on 59,356 cells from the prefrontal cortex and hippocampus. Aβ pathology was evaluated by western blot, immunofluorescence and ELISA. TREM2 knockout mice and the murine microglial cell line BV2 were used to study the role of TREM2 in cognitive function and Aβ clearance.
    MAIN FINDINGS: T1D mice exhibited progressive memory deficits and prefrontal Aβ oligomer accumulation (36-50 kDa), with region-specific microglial activation. SnRNA-seq identified ten microglial subpopulations, with Trem2-enriched clusters (M1/M2/M3/M5) showing impaired phagocytosis and metabolic dysregulation. TREM2 knockout exacerbated cognitive deficits and Aβ accumulation in T1D mice. Mechanistically, TREM2 regulated microglial migration, phagocytosis of Aβ oligomers, and mitochondrial integrity under high-glucose conditions, potentially via the mTOR signaling pathway.
    PRINCIPLE CONCLUSIONS: These findings establish TREM2 as a critical regulator of microglial Aβ clearance in T1D, operating mitochondrial and phagocytic programs via mTOR and highlighting its therapeutic potential for diabetic neurodegeneration.
    Keywords:  Amyloid-beta; Microglia; TREM2; Type 1 diabetes
    DOI:  https://doi.org/10.1186/s12974-025-03611-3
  11. J Alzheimers Dis. 2026 Jan 05. 13872877251410206
      Single-cell RNA-sequencing has identified that Alzheimer's disease (AD) pathology in humans is associated with activation of disease-associated microglia (DAM). Microglial signatures of human AD have not been consistently identified in AD mouse models. Since the inflammatory response of rats is more like humans, we profiled microglial transcriptomes in aging TgF344-AD rats, which overexpress two human AD risk genes. Classic DAM gene activation (ApoE, Trem2, Gpnmb), and upregulation (MHC class-II) and downregulation (Ifngr1 and Fkbp5) of human AD microglial genes were identified in aging TgF344-AD rats. Thus, the TgF344-AD rat better recapitulates the microglial gene signature observed in human AD.
    Keywords:  Alzheimer’s disease; gene expression; microglia; neuroinflammation; rat; scRNA-seq
    DOI:  https://doi.org/10.1177/13872877251410206
  12. Acta Neuropathol Commun. 2026 Jan 07. 14(1): 12
      We have evaluated the diagnostic potential of the seeding amplification assay (SAA) in detecting α-synuclein seeding activity in postmortem brain and cerebrospinal fluid (CSF) samples from patients with primary and co-pathology α-synucleinopathies. Moreover, we investigated potential SAA positivity in control samples which may suggest unrecognized co-pathology. A total of 15 brain and 14 CSF samples with definite dementia with Lewy bodies (DLB, n = 6), Alzheimer´s disease with amygdala Lewy body (AD/ALB, n = 3), and patients with concomitant Creutzfeldt-Jakob disease and Lewy body pathology (CJD/LBP, n = 6) comorbidity were tested for α-synuclein seeding activity using SAA assay utilizing recombinant α-synuclein (WT) with N-terminal His-tag. Control samples consisted of other neurodegenerative diseases (n = 17 for brain and n = 18 for CSF samples) and healthy corneal donors (n = 17). The analysis of seeding activity in brain samples suggested 100% sensitivity and 91.2% specificity. Five out of 34 brain control samples gave a positive SAA outcome. However, upon reevaluation, two of these samples were reclassified as Alzheimer´s disease (AD) with synucleinopathy co-pathology. The analysis of CSF also suggested 100% sensitivity and 94.4% specificity, although dilution of some samples was necessary to decrease the effect of inhibitors. We report a good performance of the SAA not only in postmortem samples from primary synucleinopathies with advanced pathology, but also in co-pathology synucleinopathies with isolated Lewy bodies in the amygdala in AD cases. Our findings highlight the importance of careful diagnostic evaluation in AD patients, where co-existing synucleinopathy may otherwise go unrecognized.
    Keywords:  Alpha-synuclein; Comorbidities; RT-QuIC; Real-time quaking-induced conversion assay; SAA; Seeding activity; Seeding amplification assay; Synucleinopathy
    DOI:  https://doi.org/10.1186/s40478-025-02195-6
  13. bioRxiv. 2025 Dec 29. pii: 2025.12.29.696915. [Epub ahead of print]
      Loss-of-function mutations in Progranulin (GRN) cause neuronal ceroid lipofuscinosis (NCL) and hereditary frontotemporal dementia, presumably through lysosomal dysfunction. The effect of progranulin deficiency on cell type-specific lysosomal composition in the mammalian brain has not been examined. We used cell type-specific LysoIP to perform tandem-mass-tag mass-spectrometry and detected distinct aberrant proteomic signatures in progranulin-deficient astrocytes, neurons, and microglia, indicating cell type-specific dysregulation of key lysosomal proteins with crucial functions in sphingolipid metabolism and lysosome organization. These proteins markedly differed from progranulin-deficient RNAseq data sets, suggesting progranulin regulates lysosomal composition through post-translational mechanisms including the sorting of nascent proteins to the lysosome. Validation experiments confirmed that Mfsd8 and Ppt1, proteins whose mutation on their own cause NCL, were essentially absent from progranulin-deficient neuronal and microglial lysosomes, respectively. Our findings suggest that progranulin may function as an essential hub protein during endolysosomal sorting and highlight the necessity of restoring stoichiometric levels of progranulin expression in the secretory pathway for the development of effective therapeutic strategies.
    DOI:  https://doi.org/10.64898/2025.12.29.696915
  14. Cell Death Dis. 2026 Jan 09. 17(1): 21
      Alzheimer's disease (AD) is a devastating neurodegenerative disease and the most prevalent type of dementia characterized by pathological deposition of amyloid-β plaques/deposits and tau tangles within the brain parenchyma. This progressive ailment is featured by irreversible cognitive impairment and memory loss, often misdiagnosed as the consequence of old age in elderlies. Pathologically, synaptic dysfunction occurs at the early stages and then progresses into neurodegeneration with neuronal cell death in later stages. In this review, we aimed to critically discuss and highlight recent advances in the pathological footprints of amyloid-β and tau in AD. Specifically, we focused our attention on the interplay and synergistic effects of amyloid-β and tau in the pathogenesis of AD. We hope that our paper will provide new insights and perspectives on these pathological features of AD and spark new ideas and directions in AD research and treatment.
    DOI:  https://doi.org/10.1038/s41419-025-08186-8
  15. Glia. 2026 Mar;74(3): e70131
      Microglia, the brain's innate immune cells, possess complex, highly motile branched processes. These act independently, enabling individual processes to carry out entirely distinct functions in parallel. Intracellular Ca2+ signaling is implicated in many of these distinct microglial functions. However, it has been difficult to quantify how such Ca2+ activity is compartmentalized in space and time to prevent unwanted cross-talk between signaling pathways. Previous studies have typically relied on manually drawn regions-of-interest (ROIs), which averages fluorescence within predefined compartments and therefore cannot resolve the fine-scale spatio-temporal propagation patterns that may be functionally relevant. To address this, we adopt an unbiased non-ROI-based analytical approach to comprehensively characterize the temporal, spatial and spatio-temporal dimensions of microglial Ca2+ activity in vivo. We find that microglial Ca2+ activity predominantly occurs in processes, tends to remain localized at its site of origin, and, when it propagates, often follows a well-defined direction (either toward or away from the soma) rather than spreading isotropically as would be expected under purely passive diffusion. The tendency of microglial Ca2+ activity to spread between intracellular regions does not correlate with peak amplitude, but appears to be limited by the branching points of the microglial processes. Finally, we show that Ca2+ activity can differ between the microglial soma and its processes in response to various pharmacological stimuli. These results suggest that Ca2+ signals are actively compartmentalized within microglia in a context dependent manner, rather than being synchronized across the entire cell.
    Keywords:   P2Y12 ; Ca2+ imaging; awake state; in vivo two‐photon imaging; microglia; neuronal activity; purinergic signaling
    DOI:  https://doi.org/10.1002/glia.70131
  16. Alzheimers Dement (Amst). 2026 Jan-Mar;18(1):18(1): e70240
       Introduction: We aimed to evaluate the potential of the microglial marker transmembrane protein 119 (TMEM119) in the cerebrospinal fluid (CSF) as a (differential) diagnostic biomarker for neurodegenerative diseases.
    Methods: Following assay validation, we used enzyme-linked immunosorbent assay to measure CSF TMEM119 in 174 patients from six diagnostic groups: Alzheimer's disease (AD, n = 35), amyotrophic lateral sclerosis (ALS, n = 33), cerebral microangiopathy (CM, n = 25), frontotemporal lobar degeneration (FTLD, n = 28), Lewy body diseases (n = 21), and non-neurodegenerative controls (n = 33).
    Results: CSF TMEM119 levels were elevated in the AD group compared to the control (p = 0.004), CM (p = 0.005), and FTLD (p = 0.023) groups. Levels were higher in both mild cognitive impairment (MCI-AD) and dementia (ADD) subgroups when compared to controls. For the discrimination of AD from controls, the area under the curve (AUC) was 0.78.
    Discussion: Our results indicate that CSF TMEM119 may have potential as a biomarker representing microglial involvement in early and later stages of AD.
    Highlights: Elevated levels of TMEM119 were observed in the CSF of patients with AD.Increased CSF TMEM119 was seen in MCI-AD patients compared to controls.Elevated levels in MCI-AD underscore early microglial involvement in AD.In the AD group, an association was found between CSF TMEM119 and CSF total tau.CSF TMEM119 may provide valuable information on neuroinflammation.
    Keywords:  Alzheimer's disease; biomarkers; cerebrospinal fluid; microglia; neuroinflammation
    DOI:  https://doi.org/10.1002/dad2.70240
  17. Neurol Neuroimmunol Neuroinflamm. 2026 Mar;13(2): e200527
      Triggering receptor expressed on myeloid cells 2 (TREM2) is a key immunomodulatory receptor broadly expressed on myeloid cells such as macrophages and microglia. It plays versatile roles in neurodegenerative diseases, tissue repair, and tumor immunity by orchestrating glucose metabolism and inflammatory responses. This review systematically summarizes the structural characteristics of TREM2, its ligand-binding mechanisms, and downstream signaling pathways-including the phosphoinositide 3-kinase/protein kinase B(PI3K/Akt), mitogen-activated protein kinase (MAPK), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and signal transducer and activator of transcription 3 (STAT3) cascades-with a particular focus on its central role in macrophage metabolic reprogramming.In neurodegenerative diseases such as Alzheimer disease, TREM2 contributes to the attenuation of neuroinflammation and slows disease progression by promoting β-amyloid (Aβ) clearance, inhibiting tau hyperphosphorylation, and modulating microglial polarization. Loss-of-function sequence variants, such as R47H, disrupt lipid metabolism, impair phagocytic activity, and destabilize immune homeostasis, thereby significantly increasing disease susceptibility. Furthermore, by enhancing glycolysis and suppressing fatty acid oxidation, TREM2 facilitates macrophage polarization toward a reparative M2 phenotype, promoting neuroregeneration and remyelination in conditions such as spinal cord injury and multiple sclerosis.Within the tumor microenvironment, TREM2 influences tumor progression and therapeutic resistance by modulating the metabolic reprogramming of tumor-associated macrophages (TAMs)-notably through activation of pyruvate kinase muscle isozyme M2 (PKM2)-dependent glycolysis-and promoting an immunosuppressive phenotype. In metabolic disorders such as diabetes and obesity, TREM2 exerts protective effects by inhibiting NLRP3 inflammasome activation and maintaining lipid homeostasis, highlighting its therapeutic potential.This review also outlines the translational prospects of TREM2 as a therapeutic target, including the development of agonists, gene regulatory strategies, and its potential use as a biomarker. Future studies should aim to elucidate the ligand-specific biased signaling and dynamic regulatory networks of TREM2 within tissue microenvironments to advance precision interventions in neuroimmunometabolic diseases.
    DOI:  https://doi.org/10.1212/NXI.0000000000200527
  18. Cell Death Dis. 2026 Jan 09. 17(1): 26
      Lipophagy is a form of selective autophagy that targets the lipid droplets for lysosomal decay and has been implicated in the onset and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Factors that augment lipophagy have been identified as targets for MASLD therapeutic development. TMEM55B is a key regulator of lysosomal positioning, which is critical for lysosome fusion with the autophagosome, but is less well studied. Here, we demonstrate that the absence of TMEM55B in murine models accelerates MASLD onset and progression to metabolic dysfunction-associated steatohepatitis (MASH). In cellular models, TMEM55B deficiency enhances incomplete lipophagy, whereby lysosome-lipid droplet interactions are increased, but lysosomal cargo is not fully degraded and/or released, leading to the development of lipid-filled lysosomes (lipolysosomes). Loss of TMEM55B also impairs mitophagy, causing an accumulation of dysfunctional mitochondria. This imbalance leads to increased lipid accumulation and oxidative stress, worsening MASLD. These findings underscore the importance of lysosomal positioning in lipid metabolism and suggest that targeting lipophagy for MASLD therapeutic development should be carefully considered to ensure promotion of the entire lipophagic flux pathway and whether it occurs in the context of mitochondrial dysfunction.
    DOI:  https://doi.org/10.1038/s41419-025-08210-x
  19. bioRxiv. 2025 Dec 22. pii: 2025.12.19.695600. [Epub ahead of print]
      Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia. It is characterized by cognitive decline and accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles. Accumulating evidence indicates that viral infection may worsen and/or increase development of established AD pathology. The COVID-19 pandemic has brought attention to the link between SARS-CoV-2 infection and neurologic conditions that vary in severity and duration, as well as the worsening of clinical symptoms in elderly people with dementia. To better understand potential mechanisms by which SARS-CoV-2 infection impacts AD neuropathology, aged 5xFAD and wildtype (WT) mice were intranasally infected with mouse-adapted SARS-CoV-2 (MA10). Intranasal infection of aged-matched (10-14 month) 5xFAD or wild type (WT) C57BL/6 mice with MA10 resulted in viral infection of the lungs that correlated with acute viral pneumonia characterized by lymphocyte inflammation and antiviral immune responses. Viral RNA was not detected within the central nervous system (CNS) of either WT or 5xFAD mice at days 7 or 21 post-infection (p.i.), nor were there signs of overt glial activation or neuroinflammation. There were no differences in either Aβ plaque volume or number within the brains of MA10-infected 5xFAD mice compared to uninfected 5xFAD mice. However, bulk RNA sequencing and spatial transcriptomics revealed evidence of altered expression of genes associated with neuronal and glial dysfunction, as well as reduced expression of genes encoding adhesion molecules in vascular endothelial cells. Collectively, these findings demonstrate that MA10 infection did not affect Aβ plaque size or numbers in 5xFAD mice, yet in both WT and 5xFAD mice, there were numerous down-stream effects on gene expression associated with resident CNS cell function.
    DOI:  https://doi.org/10.64898/2025.12.19.695600
  20. Nat Med. 2026 Jan 05.
      Blood biomarkers have emerged as accurate tools for detecting Alzheimer's disease (AD) pathology, offering a minimally invasive alternative to traditional diagnostic methods such as imaging and cerebrospinal fluid (CSF) analysis. Yet, the logistics surrounding venipuncture for blood collection, although considerably simpler than the acquisition of imaging and CSF, require precise processing and storage specific to AD biomarkers that are still guided by medical personnel. Consequently, limitations in their widescale use in research and broader clinical implementation exist. The DROP-AD project investigates the potential of dried plasma spot (DPS) and dried blood spot (DBS) analysis, derived from capillary blood, for detecting AD biomarkers, including phosphorylated tau at amino acid 217 (p-tau217), glial fibrillary acidic protein and neurofilament light. Here, 337 participants from 7 centers were included, with 304 participants providing paired capillary DPS or DBS and venous plasma samples. We observed strong correlations between DPS p-tau217 and venous plasma p-tau217 (rS = 0.74, P < 0.001). DPS p-tau217 progressively increased with increasing disease severity, and showed good accuracy in predicting CSF biomarker positivity (area under the curve = 0.864). Similarly, we demonstrated the successful detection of glial fibrillary acidic protein and neurofilament light with strong correlations between DBS and DPS, respectively, using paired venous plasma samples. Notably, the method was also effective in individuals with Down syndrome, a population at high genetic risk for AD but in whom standard blood sampling by venipuncture may be more complicated, revealing elevated biomarkers in those with dementia compared with asymptomatic individuals. The study also explored unsupervised blood collection, finding high concordance between supervised and self-collected samples. These findings underscore the potential of dried blood collection and capillary blood as a minimally invasive, scalable approach for AD biomarker testing in research settings. Yet, further refinement of collection and analytical protocols is needed to fully translate this approach to be viable and useful as a clinical tool.
    DOI:  https://doi.org/10.1038/s41591-025-04080-0
  21. bioRxiv. 2025 Dec 25. pii: 2025.12.22.696064. [Epub ahead of print]
      Diffuse midline glioma (DMG) is a near-universally lethal form of pediatric high-grade glioma, driven by neuronal activity-regulated paracrine signaling and synaptic integration of malignant cells into neural circuits. In turn, DMG increases neuronal excitability, augmenting neuron-to-glioma signaling. In the healthy brain, microglia, the resident immune cells of the central nervous system (CNS), regulate neuronal excitability and synaptic connectivity. However, the role of microglia in promoting tumor-associated hyperexcitable neural networks in glioma remains unknown. Here, we investigate the activity-regulated engulfment of neuronal synapses by microglia in both healthy and glioma-bearing mice, and further explore how glioma cells alter microglia-mediated circuit refinement, contributing to pathogenic neuronal hyperexcitability. Microglia-mediated circuit refinement in the glioma microenvironment was characterized through synaptic engulfment analysis of both excitatory and inhibitory synapses by microglia in healthy mice and patient-derived DMG xenograft models, paired with optogenetic stimulation in the neocortex. We found that glutamatergic neuronal activity in the healthy brain increased excitatory synaptic engulfment by microglia in a previously unappreciated negative feedback mechanism that may guard against hyperexcitability. In contrast, this activity-regulated increase in excitatory synaptic engulfment was abrogated in DMG-infiltrated brains. Instead, inhibitory synaptic engulfment was significantly increased in DMG in response to glutamatergic neuronal activity. Together, these dysregulated synaptic engulfment mechanisms may create imbalance in the excitatory to inhibitory (E:I) synapse ratio predicted to increase neuronal excitability. Complementary single-nuclei sequencing studies revealed concordant tumor-specific, activity-regulated changes in microglia-neuron signaling showing reduced expression of excitatory synaptic refinement gene programs in microglia, potentially mediating the aberrant synaptic engulfment observed in DMG. These findings reveal novel cancer-neuron-immune interactions in DMG and provide an opportunity to potentially modulate tumor-associated neuronal hyperexcitability by targeting aberrant microglial synaptic engulfment.
    DOI:  https://doi.org/10.64898/2025.12.22.696064
  22. Neuron. 2026 Jan 07. pii: S0896-6273(25)00930-4. [Epub ahead of print]114(1): 1-3
      In this issue of Neuron, Zhang et al.1 identified a subset of BST2-high astrocytes that emerge at the ischemic injury border and promote microglial recruitment through the C3-C3aR pathway. These findings highlight BST2 as a key modulator of astrocyte-microglia communication and a potential therapeutic target for CNS injury.
    DOI:  https://doi.org/10.1016/j.neuron.2025.12.003
  23. Trends Immunol. 2026 Jan 07. pii: S1471-4906(25)00310-2. [Epub ahead of print]
      Bidirectional crosstalk between the immune and nervous systems, via 'neuroimmune circuits', regulates homeostatic and inflammatory responses essential for health. Microglia, long-lived brain macrophages, act as key hubs integrating immune signals into coordinated brain responses by shifting into distinct functional states in response to local and systemic cues. In this review, we focus on how environmental signals shape these microglial states, how microglia influence other brain cells through both direct and indirect mechanisms, and emerging evidence of how microglia are impacted by, and respond to, peripheral changes. We highlight microglia as central players in systemic neuroimmune communication, influencing both brain and peripheral health, while outlining recent tools and key knowledge gaps to guide future research into mechanisms of neuroimmune circuit communication.
    Keywords:  immune signals; microglia; neurodegeneration; neuroimmune interactions; peripheral immune response
    DOI:  https://doi.org/10.1016/j.it.2025.12.002