bims-medebr Biomed News
on Metabolism of the developing brain
Issue of 2025–11–09
23 papers selected by
Regina F. Fernández, Johns Hopkins University



  1. Neurobiol Dis. 2025 Nov 05. pii: S0969-9961(25)00396-1. [Epub ahead of print] 107179
      Multiple sclerosis (MS) is an autoimmune disorder characterized by neuroinflammation and progressive demyelination, resulting in irreversible neuronal damage and disability. Although current immunomodulatory treatments slow disease progression, they can't effectively promote myelin regeneration. Recent research has emphasized the critical role of glial cells-microglia, astrocytes, and oligodendrocytes-in myelin repair, with fatty acid (FA) metabolism emerging as a central regulator of this process. Fatty acids are essential not only for maintaining myelin structure but also for the metabolic reprogramming of glial cells during remyelination. Microglial activation, influenced by FA signaling, can result in either pro-inflammatory or reparative phenotypes, which in turn affect remyelination efficiency. Similarly, astrocytes contribute to remyelination through cholesterol synthesis and FA oxidation; however, their reactive states can either promote or inhibit myelin repair, depending on the metabolic context. Oligodendrocyte precursor cells, crucial for myelin regeneration, are also regulated by fatty acids, impacting their differentiation and survival. Disruptions in FA metabolism or imbalanced glial activation can impair remyelination, underscoring the need for therapies targeting these metabolic pathways. This review examines the complex relationship between fatty acid metabolism and glial cell function, emphasizing the potential of targeting lipid signaling pathways to enhance remyelination in MS. Targeting fatty acid metabolism represents a promising yet still experimental therapeutic approach for MS and related demyelinating diseases. By modulating glial metabolism and immune responses, this strategy has the potential to decelerate disease progression and restore neural function, though further validation is required to translate these mechanisms into clinical applications.
    Keywords:  Astrocyte; Fatty acids; Metabolism; Microglia; Multiple sclerosis; Oligodendrocyte; Remyelination
    DOI:  https://doi.org/10.1016/j.nbd.2025.107179
  2. J Intern Med. 2025 Nov 06.
      Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline. Although amyloid-β and tau pathologies remain central to our understanding of AD, growing evidence suggests that disrupted lipid metabolism and impaired bioenergetics are closely linked to these hallmark features. Genetic, lipidomic and functional studies point to alterations in cholesterol, phospholipids and polyunsaturated fatty acids, which can influence mitochondrial function, organelle communication and glial responses. These processes are further modulated by apolipoprotein E (APOE) genotype, sex differences and systemic metabolic states such as obesity and diabetes, contributing to neuroinflammation and cognitive decline. Although findings are sometimes conflicting, an emerging theme is that lipid and energy metabolisms are central to how genetic and environmental risk factors shape AD pathogenesis. This integrated perspective highlights lipid and bioenergetic pathways as promising therapeutic targets, where metabolic modulators, lipid-directed interventions and lifestyle strategies may complement amyloid-based therapies and offer opportunities for precision approaches, particularly in women and APOE ε4 carriers.
    Keywords:  Alzheimer's disease; lipid metabolism; mitochondria; systemic metabolism
    DOI:  https://doi.org/10.1111/joim.70036
  3. NMR Biomed. 2025 Dec;38(12): e70169
      Deuterium metabolic imaging (DMI) allows non-invasive dynamic in vivo assessment of transport, uptake and metabolism of deuterated molecules. To date, DMI experiments in humans have involved ingestion of glucose-d2 ([6,6'-2H₂]glucose), where labelling of the sixth carbon facilitates 2H-label transfer to pyruvate, then to lactate (Lac) via lactate dehydrogenase, or to glutamate and glutamine (Glx) via the tricarboxylic acid cycle. There are advantages to using glucose-d7 ([1,2,3,4,5,6,6'-2H₇]glucose) for DMI as this should yield larger signals from glucose and downstream metabolites, including deuterated water (HDO). Here, we evaluated DMI at 7 T following glucose-d7 ingestion for monitoring glucose metabolism in the human brain. Results were compared to measurements using the same protocol but with oral glucose-d2. Fifteen healthy volunteers participated in the study, which involved initial measurements at natural abundance, followed by 90 min of acquisition after ingestion of 0.75 g/kg glucose-d7 (7 participants) or glucose-d2 (8 participants). A visual stimulus was applied for 10 participants. Larger 2H signals were measured following glucose-d7 ingestion, and whole-brain signal ratios at times of 100 to 120 min after glucose-d7 or glucose-d2 ingestion for HDO, Glx and lactate (with potential contamination from lipid signals) were 1.8 ± 0.3, 1.7 ± 0.3 and 1.6 ± 0.3, respectively. At natural abundance, the SNR of the HDO signal in the CSI data was 14 ± 1. For both isotopologues, the glucose signal peaked ~80 min after ingestion, while Glx, lactate + lipid and HDO signals increased throughout the measurement period. Estimated cerebral concentrations of HDO were larger for glucose-d7, but similar concentrations were found for glucose, Glx and lactate. No significant difference in signal or concentration between visually stimulated and unstimulated participants was found. These findings suggest that glucose-d7 with DMI can facilitate non-invasive in vivo assessment of metabolism in the human brain, with wide applications in experimental medicine and disease.
    Keywords:  DMI; deuterated glucose; glucose metabolism; glycolysis; lactate
    DOI:  https://doi.org/10.1002/nbm.70169
  4. Nat Commun. 2025 Nov 07. 16(1): 9846
      Placental dysfunction is linked to neurodevelopmental disorders, with males showing greater vulnerability to perinatal inflammation-mediated brain injuries. Using our transgenic mouse model, Akr1c14cyp19aKO (plKO), we investigate how reduced placental allopregnanolone (ALLO), an anti-inflammatory neurosteroid, contributes to sex-specific brain injury. plKO mice display sex-divergent cerebellar myelination and male-specific autism-like behaviors. Here we show that placental ALLO insufficiency triggers sex-divergent neuroinflammatory responses and microglial dysfunction. Sex-divergent differential expression of inflammatory genes and distinct inflammatory cytokine/chemokine patterns are seen in the placenta and the brain. Prostaglandin E2 (PGE2)-EP4 signaling is identified as a key regulator and, consistent with male plKO cerebellar hypermyelination, male microglial myelin phagocytosis is impaired by SIRPα-CD47 signaling changes. Postnatal manipulation of these critical pathways can normalize cerebellar myelin content and rescue abnormal behavior in male plKO mice. Sex-divergent microglial dysfunction and prostaglandin signaling drive male-biased neurodevelopmental impairments in our model, suggesting new therapeutic targets to improve brain development following placental dysfunction.
    DOI:  https://doi.org/10.1038/s41467-025-64814-z
  5. J Lipid Res. 2025 Nov 03. pii: S0022-2275(25)00196-8. [Epub ahead of print] 100933
      Astrocytes comprise approximately 40% of CNS cells and have pivotal roles in brain functions. Under steady-state conditions, astrocytes maintain homeostasis in the CNS through the uptake or release of neurotransmitters. However, in neurodegenerative conditions, astrocytes are activated by inflammatory cytokines, such as interleukin-1alpha (IL-1α) and TNF-α, which are released from activated microglia. Activated astrocytes release several inflammatory cytokines and neurotoxic substances, resulting in neuronal injury. Sphingolipids are a series of bioactive lipids involved in several biological processes, such as apoptosis, inflammatory response, cell cycle, and immune response. SM is a sphingolipid that is a major component of the cellular membrane and is also involved in inflammatory responses. We report that SM promotes IL-1α/TNF-α-induced expressions of representative astrocyte mRNAs and astrocyte activation through the NF-κB pathway. In contrast, reduction of SM by knockdown of sphingomyelin synthase 1 (SMS1) and/or SMS2 suppresses astrocyte activation. Furthermore, removal of SM by the blockade of ceramide transfer protein suppresses astrocyte activation via the induction of histone deacetylase (HDAC) 1 and HDAC3; subsequently, the levels of acetylated p65 (Lys 310) are reduced, leading to the suppression of the NF-κB pathway. Our findings further the understanding of the regulation of astrocyte activation by sphingolipids.
    Keywords:  NF-κB signaling; abnormal astrocyte activation; histone deacetylase; neurodegenerative diseases; p65 acetylation; sphingomyelin
    DOI:  https://doi.org/10.1016/j.jlr.2025.100933
  6. J Neurochem. 2025 Nov;169(11): e70283
      AMP-activated protein kinase (AMPK) is a central regulator of cellular energy balance, and its activation presents a therapeutic strategy for various metabolic diseases and neuronal disorders. Yet its effects on brain function remain unclear. This review evaluates evidence from animal and human studies examining AMPK activation through pharmacological agents (synthetic or natural compounds) and exercise. The effects of AMPK activation on synaptic and cognitive function seem highly context-dependent. Peripheral or acute AMPK activation often improves cognition, whereas chronic or central nervous system (CNS) activation can impair synaptic plasticity and memory. Collectively, current studies underscore the need for rigorous research distinguishing peripheral versus central AMPK activation, clarifying isoform-specific signaling, and examining effects in healthy human populations.
    Keywords:   AMPK ; AMPK activator; Alzheimer's disease; cognition; memory; synaptic plasticity
    DOI:  https://doi.org/10.1111/jnc.70283
  7. Chin Med J (Engl). 2025 Nov 03.
       BACKGROUND: Sevoflurane impairs neurogenesis and cognitive function in the developing brain; however, the underlying mechanisms remain unclear. This study aimed to investigate the role of fatty acid β-oxidation (FAO) in neural stem/progenitor cells (NSPCs) as a potential factor in sevoflurane-induced neurogenesis inhibition and cognitive deficits.
    METHODS: NSPCs, NE-4C cells, and postnatal day 7 (PND 7) rats were exposed to sevoflurane. Cell viability was measured using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. Neurogenesis was assessed by immunohistochemistry. Apoptosis was detected via terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Cognitive function was tested with the Morris water maze. Lipid metabolism profiles were analyzed through lipidomics. Message RNA (mRNA) expression levels of key FAO enzymes and the major carnitine transporter were quantified by real-time reverse transcription polymerase chain reaction (RT-qPCR). Protein expression of carnitine palmitoyltransferase 1a (CPT1a) and nuclear peroxisome proliferator-activated receptor α (PPARα) was examined by Western blotting. CPT1a enzymatic activity was determined using a biochemical assay. FAO activity was measured with the FAOBlue assay.
    RESULTS: Sevoflurane exposure impaired neurogenesis and cognitive function. In NSPCs, sevoflurane exposure induced extensive alterations in lipid metabolism intermediates, inhibited the mRNA expression of acyl-CoA oxidase 1 (ACOX1), acyl-CoA oxidase 3 (ACOX3), hydroxyacyl-CoA dehydrogenase beta subunit (HADHB), CPT1a, carnitine palmitoyltransferase 2 (CPT2), acyl-CoA dehydrogenase short-chain (ACADS), and solute carrier family 22 member 5 (SLC22A5), suppressed FAO activity, reduced CPT1a expression and activity, and decreased PPARα levels in the nucleus. Enhancing FAO activity in NSPCs ameliorated the negative effects of sevoflurane on neurogenesis. Overexpression of CPT1a rescued the sevoflurane-induced inhibition of FAO activity and neurogenesis in NE-4C cells. Pretreatment with palmitoylethanolamide (PEA), a PPAPα agonist, increased both the nuclear content of PPARα protein and the expression of CPT1a in NSPCs and rat hippocampus after sevoflurane exposure. Furthermore, pretreatment with PEA or the CPT1a substrate carnitine rescued sevoflurane-induced damage to FAO activity in NSPCs, neurogenesis, and cognitive function.
    CONCLUSION: Sevoflurane impairs neurogenesis and cognitive function by suppressing FAO in NSPCs of the developing brain. Boosting FAO activity in NSPCs could be a potential strategy to prevent sevoflurane-induced cognitive deficits.
    Keywords:  Cognitive function; Fatty acid β-oxidation; Neural stem/progenitor cells; Neurogenesis; Sevoflurane
    DOI:  https://doi.org/10.1097/CM9.0000000000003864
  8. Arch Pediatr. 2025 Nov 05. pii: S0929-693X(25)00182-4. [Epub ahead of print]
       BACKGROUND: Leigh syndrome or subacute necrotizing encephalomyelopathy was first recognized as a neuropathological entity in 1951. It is a progressive neurological disease characterized by neuroradiological lesions, particularly in the brainstem and basal ganglia. Leigh's syndrome is a pan-ethnic disorder with onset usually in infancy or early childhood. Over the last six decades, this complex neurodegenerative disorder has been shown to comprise >100 separate monogenic disorders associated with enormous clinical and biochemical heterogeneity. This article reviews clinical, radiological, biochemical and genetic aspects of the disorder.
    OBJECTIVES: this overview provides a better understanding of this rare mitochondrial disease by identifying its clinical, radiological and genetic manifestations in order to improve early diagnosis, patient follow-up and genetic counseling.
    METHODOLOGY: systematic literature review RESULTS: Leigh syndromes present with childhood developmental regression, a loss of previously achieved developmental milestones. Numerous non-neurological manifestations of Leigh syndrome have been reported, many of which are related to the underlying genetic defects. These include cardiomyopathy, renal tubulopathy, gastrointestinal and endocrine dysfunction, and liver disease. Known genetic causes, including defects in 16 mitochondrial DNA (mtDNA) genes and nearly 100 nuclear genes, are categorized into disorders of subunits and assembly factors of the five oxidative phosphorylation enzymes, disorders of pyruvate metabolism and vitamin and cofactor transport and metabolism, disorders of mtDNA maintenance, and defects in mitochondrial gene expression, protein quality control, lipid remodeling, dynamics and toxicity. An approach to diagnosis is presented, together with known treatable causes and an overview of current supportive management options and emerging therapies on the horizon CONCLUSION: Management of mitochondrial diseases must be multidisciplinary, and in collaboration with a center of reference (CRMR) or a center of competence (CCMR) with expertise in mitochondrial diseases.
    Keywords:  Central nervous system; Genetic; Itochondrial DNA; Leigh syndrome; Metabolic disease; Mitochondrial disease; Neurodegeneration; Neuroimaging; Nuclear DNA; OXPHOS; Treatment
    DOI:  https://doi.org/10.1016/j.arcped.2025.04.007
  9. Front Physiol. 2025 ;16 1695681
       Background: Neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, etc., are a group of complex and heterogeneous disorders characterized by progressive synaptic loss and pathological protein alterations. Mitochondria are the main source of energy produced by neurons and support the high energy consumption of the nervous system. Mitochondrial quality control, involving processes like mitophagy and mitochondrial biogenesis, is crucial for mitochondrial homeostasis, and mitochondrial dysfunction is closely related to neurodegenerative diseases pathogenesis, making targeting mitochondrial quality control a potential therapeutic strategy. Natural products offer benefits such as cost-effectiveness, fewer side effects, and other positive qualities, making them suitable choices as supplements or alternatives to traditional drugs for treating neurodegenerative diseases.
    Methods: A thorough search was conducted on many databases including Web of Science, PubMed, EMBASE, and MEDLINE to investigate the role of mitochondria in neurodegenerative diseases and the therapeutic effects of natural products.
    Results: By searching the relevant studies on neurodegenerative diseases and mitochondria in recent years, we observed a rise in the number of studies examining the functional characteristics and biological events of mitochondrial quality control systems in neurodegenerative diseases pathogenesis and the potential for natural products regulating mitochondrial quality control to improve neurodegenerative diseases.
    Conclusion: This review summarizes the functional characteristics and biological events of mitochondrial quality control systems in neurodegenerative diseases pathogenesis, and comprehensively analyzes the pharmacological mechanisms by which natural products regulate mitochondrial quality control to improve neurodegenerative diseases, aiming to provide a scientific basis for further research and new clinical drug development.
    Keywords:  mitochondrial quality control; molecular mechanisms; natural products; neurodegenerative diseases; toxicology and adverse effects
    DOI:  https://doi.org/10.3389/fphys.2025.1695681
  10. Mol Cell Biochem. 2025 Nov 03.
      Traumatic brain injury (TBI) disrupts normal brain function through inflammatory cascades that may persist for months or years. This review aimed to gather the evidence regarding kynurenine pathway (KP) dysregulation following TBI and to examine how altered KP metabolites correlate with clinical outcomes. We systematically identified relevant human studies in PubMed and Lilacs databases using descriptors linked to TBI and KP metabolites. We included original research in English, Portuguese, or Spanish with no publication date restriction. We extracted data on participant characteristics, TBI severity, metabolite levels, and clinical endpoints. We appraised risk of bias using standardized checklists for cohort and cross‑sectional designs. Twelve studies met inclusion criteria. TBI increases circulating levels of quinolinic acid (QUIN), with higher QUIN linked to mortality in severe TBI and worse mood or cognitive sequelae in mild TBI. Kynurenine and kynurenic acid changes varied across cohorts, reflecting the complexity of post-injury inflammatory processes. TBI can disrupt KP metabolism and increased levels of QUIN are associated with poor neurological outcomes. Future research should define the dynamics of KP metabolite production over time and assess whether targeted interventions can lessen neurotoxic load. Post‑injury neuroinflammation remains a critical focus for potential therapeutic intervention strategies.
    Keywords:  Cognition; Inflammation; Kynurenine Pathway; Quinolinic Acid; Traumatic Brain Injury; Tryptophan
    DOI:  https://doi.org/10.1007/s11010-025-05429-2
  11. Dis Model Mech. 2025 Nov 05. pii: dmm.052184. [Epub ahead of print]
      PLA2G6-associated neurodegeneration (PLAN) is a group of rare genetic disorders characterised by progressive neurodegeneration resulting from mutations in the PLA2G6 gene, encoding a calcium-independent phospholipase enzyme. Here, we explored the effects of decanoic acid (DA), a medium-chain fatty acid, in fruit-fly Drosophila melanogaster models of PLAN and showed that DA treatment significantly extends the lifespan, reduces bang sensitivity, and improves resistance to heat shock stress. Transcriptional analysis showed that DA affects genes in key signalling pathways, including Insulin/Insulin-like Growth Factor, mTOR, heat shock response, Sirtuin, autophagy, and mitochondrial function. Additionally, DA treatment alters the metabolite profiles in PLAN model flies, with the most pronounced changes observed in gut tissue. Pathway analysis of these metabolomic shifts highlighted potential therapeutic effects of DA in several pathways, including ATP-binding cassette (ABC) transporters, purine metabolism, cAMP signalling, and neuroactive ligand-receptor interactions. These findings suggest that DA may be a promising therapeutic agent for PLAN, offering insights into the mechanisms of the disease and paving the way for future research on medium-chain fatty acids as potential treatments for neurodegenerative diseases.
    Keywords:  Decanoic acid; Drosophila; Medium-chain fatty acid; Neurodegenerative disease; PLAN
    DOI:  https://doi.org/10.1242/dmm.052184
  12. Orphanet J Rare Dis. 2025 Nov 06. 20(1): 565
      Gaucher disease (GD) is a rare lysosomal disorder of sphingolipid catabolism, characterised by a block in the degradation of glucosylceramide (GlcCer) to ceramide. The resulting effect is lysosomal accumulation of GlcCer and its deacylated derivative, glucosylsphingosine. Secondary alterations in the sphingolipid metabolic pathway have been reported, including elevated concentrations of ceramide, lactosylceramide (dihexosylceramide (DHC)), and gangliosides, however, there are notable inconsistencies across different cell and tissue types and their relevance to GD pathology is not well-understood. Sphingolipids are crucial for the regulation of intra- and extracellular functions and different cell types have different requirements. For example, neurons have a high demand for complex sphingolipids due to their extensive membrane remodelling networks necessary for their communication role. We therefore performed literature searches of PubMed, Scopus, and Web of Science databases to coalesce reports of sphingolipids in different animal and cell models of GD, as well as human cells and tissues from 1965 to 2024, totalling 54 studies. We found that DHC, trihexosylceramide, and simple gangliosides, GM3, GM2, GM1, GD3, and GD2, were elevated in most reports (79%), complex GT gangliosides were largely decreased (75%), and GD1a, GD1b, and GQ1b were inconsistently reported to be both increased and decreased in individual studies. Similarly, ceramide was highly discrepant between various cell and tissue types: spleen ceramide was elevated in two of three reports, brain ceramide was largely unchanged (82%), and ceramide concentrations in the skin were not consistent by any variable, including assay technique or GD sub-variant. Some of these discrepancies may be explained by biological variability and differences in methods used to measure sphingolipids, mass spectrometry being the most common, but it is clear that there are sphingolipid alterations in GD, which likely contribute to tissue-specific pathology. Evidence that sphingolipid metabolic regulation is variable across cells and tissues highlight the importance of characterising individual sphingolipid profiles on a model-to-model basis as a driving force behind cell pathology.
    Keywords:  Altered sphingolipid regulation; Ceramide; Gangliosides; Gaucher disease; Hepatosplenomegaly; Lactosylceramide; Neurological disease; Skin abnormalities; Sphingolipid de novo synthesis; Sphingolipids
    DOI:  https://doi.org/10.1186/s13023-025-04015-5
  13. J Biol Chem. 2025 Nov 05. pii: S0021-9258(25)02763-2. [Epub ahead of print] 110911
      The organic cation transporters (OCT) 1 on the basolateral membrane of enterocytes and hepatocytes, and OCT2 on the basolateral membrane of proximal tubular cells are essential in regulating systemic micronutrient levels, while also safeguarding tissues by preventing the buildup of potentially harmful endogenous metabolites, drugs, and xenobiotics. In the present work, we integrated in vivo comparative metabolomics and lipidomics analyses of serum from wild type (WT) and Oct1/2-/- mice with in vitro uptake measurements in HEK293 cells overexpressing OCT1 or OCT2, to identify and characterize novel endogenous substrates of OCT1/2. Among the significant metabolite changes, ethanolamine in the serum of Oct1/2-/- mice was approximately 70% lower than in WT mice. The ethanolamine influx Kt mediated by OCT1/2 ranged from 7.6 ± 3.7 mmol/L (mouse Oct2) to 13.4 ± 8.1 mmol/L (mouse Oct1). OCT1/2 did not transport ethanolamine at physiologically relevant extracellular concentrations (10-100 μmol/L), suggesting that OCTs do not play a role in the hepatic/renal uptake of ethanolamine. Conversely, the release of ethanolamine by cells pre-exposed to ethanolamine at the extracellular concentration of 50 μmol/L was significantly greater in the presence of OCT1/2. Finally, the serum of the Oct1/2-/- mice was characterized by a stark elevation across phosphatidylethanolamine (PE) and lysoPE species, but not in phosphatidylcholine and diacylglycerol species. Taken together, our in vitro and in vivo data indicate that mouse Oct1 and Oct2 are essential for facilitating the exit step of free ethanolamine vectorial transport and indirectly control systemic phosphatidylethanolamine level.
    Keywords:  Drug transport; lipid metabolism; lipid synthesis; membrane transport; metabolomics
    DOI:  https://doi.org/10.1016/j.jbc.2025.110911
  14. J Cereb Blood Flow Metab. 2025 Nov 03. 271678X251387474
      Ceramide is a major constituent of membrane microdomains and controls cell signaling. Previous studies showed that ceramide exacerbates cerebral ischemia/reperfusion injury and that inhibition of acid sphingomyelinase (ASM), which converts sphingomyelin to ceramide, promotes microvascular remodeling via induction of extracellular vesicles (EVs) release. ASM inhibitors have so far not translated into clinical stroke therapies. Of note, ceramide levels can also be lowered by inhibition of serine palmitoyltransferase (SPT), which is the rate-limiting enzyme of ceramide de novo synthesis. To evaluate this pathway as a potential therapeutic target for stroke, we exposed cerebral microvascular endothelial cells to the SPT inhibitor myriocin or induced SPT knockdown by siRNA. Deactivation of de novo ceramide synthesis increased endothelial tube formation, migration, VEGF secretion, and EV release. These EVs did not induce angiogenesis in tube formation assays. Using light sheet microscopy, we demonstrate that myriocin-mediated SPT inhibition increases the length and branch density of thin microvessels (<4 µm diameter), which are drivers of angiogenesis, in the previously ischemic brain tissue of mice exposed to middle cerebral artery occlusion. These data highlight the importance of ceramide de novo synthesis for post-ischemic microvascular remodeling and angiogenesis, while its mode of action differs from ASM inhibitors.
    Keywords:  Ischemic stroke; endothelial migration; endothelial tube formation; exosomes; light sheet microscopy; microvascular remodeling
    DOI:  https://doi.org/10.1177/0271678X251387474
  15. Cell Death Dis. 2025 Nov 03. 16(1): 788
      Ischemic stroke, a leading cause of global disability and mortality, remains inadequately treated beyond reperfusion, with persistent translational failures in neuroprotection. We posit metabolic reprogramming in ischemic stroke (MRIS) as the unifying pathophysiological driver, where acute compensatory glycolysis collides with enzymatic lipid peroxidation to ignite neuroinflammation and early deficits. This metabolic crisis transcends neuron-centric models, integrating single-cell heterogeneity with bidirectional brain-peripheral crosstalk: hepatic ketogenesis releases neuroprotective β-hydroxybutyrate; adipose lipolysis fuels inflammatory storms; and gut dysbiosis disrupts barrier integrity, amplifying neuroinflammation. MRIS progresses through temporally stratified phases. An acute glycolytic-excitotoxic crisis and nicotinamide adenine dinucleotide (NAD+) depletion trigger neuroimmune dysfunction. Subacute lipid peroxidation cascades trigger ferroptosis and microglial polarization, whereas chronic-phase recovery of executive networks is scaffolded by sirtuin-mediated mitochondrial biogenesis and the interplay between adenosine monophosphate-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR). Spatial metabolomics and single-cell omics decode cell-type-specific vulnerabilities, revealing astrocytic lipid droplets, microglial succinate accumulation, and neuron-glia lactate shuttles as targetable nodes. Chronobiology further dictates therapeutic windows: lactate dehydrogenase A (LDHA) inhibition mitigates hyperacute acidosis, while NAD+ salvage pathways optimize chronic mitochondrial plasticity. We propose that metabolic reprogramming is a central amplifier of both ischemic injury and recovery, linking cerebral vascular occlusion to systemic organ dysfunction. By reframing stroke within a vascular-metabolic continuum, MRIS shifts the paradigm from a neuron-centric view to one of systemic bioenergetic failure, accounting for past translational gaps and opening pathways for precision therapies, from pentose phosphate pathway modulation to nanoparticle-based metabolite delivery and microbiome interventions. In this framework, metabolic plasticity becomes not just a consequence but a therapeutic target, transforming stroke from an untreatable vascular event to a modifiable metabolic disorder.
    DOI:  https://doi.org/10.1038/s41419-025-08114-w
  16. Nat Metab. 2025 Nov 04.
      Neurodegenerative disorders alter mitochondrial functions, including the production of reactive oxygen species (ROS). Mitochondrial complex III (CIII) generates ROS implicated in redox signalling, but its triggers, temporal dynamics, targets and disease relevance are not clear. Here, using site-selective suppressors and genetic manipulations together with live mitochondrial ROS imaging and multiomic profiling, we show that CIII is a dominant source of ROS production in astrocytes exposed to neuropathology-related stimuli. Astrocytic CIII ROS production is dependent on nuclear factor-κB and the mitochondrial sodium-calcium exchanger (NCLX) and causes oxidation of select cysteines within immune- and metabolism-associated proteins linked to neurological disease. CIII ROS amplify metabolomic and pathology-associated transcriptional changes in astrocytes, with STAT3 activity as a major mediator, and facilitate neuronal toxicity. Therapeutic suppression of CIII ROS in mice decreases dementia-linked tauopathy and neuroimmune cascades and extends lifespan. Our findings establish CIII ROS as an important immunometabolic signal transducer and tractable therapeutic target in neurodegenerative disease.
    DOI:  https://doi.org/10.1038/s42255-025-01390-y
  17. J Neuroinflammation. 2025 Nov 07. 22(1): 263
       BACKGROUND: As primary immune sentinels of the central nervous system (CNS), microglia respond rapidly to acute brain injury and engage in dynamic crosstalk with infiltrating peripheral immune cells. This interplay critically shapes the neuroinflammatory microenvironment-a key determinant of secondary brain injury (SBI) following intracerebral hemorrhage (ICH). Fatty acid-binding protein 4 (FABP4), an adipokine associated with metabolic disorders, is recognized as a pivotal modulator of inflammatory responses; however, its role in ICH-induced SBI remains undefined.
    OBJECTIVES: To investigate the pathogenic functions of FABP4 in microglia after ICH, elucidate its molecular mechanisms, and develop targeted therapeutic strategies.
    METHODS: Blood and brain tissue samples from ICH patients were analyzed to evaluate the relationships between FABP4 expression and prognosis. Behavioral tests, Nissl staining, and Golgi-Cox staining were used to quantify neuronal damage. Immunofluorescence and flow cytometry were used to assess microglial activation and immune cell infiltration. Transcriptomic, proteomic, co-immunoprecipitation, western blotting, and ChIP‒qPCR analyses were used to examine the FABP4 regulatory network. Brain-targeted nanoparticles were engineered to deliver FABP4-specific siRNA.
    RESULTS: Clinical analyses revealed microglia-specific FABP4 upregulation in ICH patients, correlating with poor neurological outcomes. Microglial Fabp4 knockout in mice attenuated neuronal loss, ameliorated cerebral edema, and enhanced functional recovery after ICH. Mechanistically, FABP4 promoted lipid droplet accumulation and inhibited the ubiquitin-proteasome-mediated degradation of S100A9 in microglia, synergistically amplifying neuroinflammation. Moreover, the activity of FABP4 in microglia facilitated neutrophil transendothelial migration into the brain parenchyma, exacerbating injury via the release of neutrophil extracellular traps (NETs). Finally, pharmacological FABP4 inhibition using brain-targeted nanoparticles conferred significant neuroprotective effects in ICH models.
    CONCLUSION: This study establishes that FABP4 acts as a novel orchestrator of post-ICH neuroinflammation through dual enzymatic and nonenzymatic pathways. We also demonstrate a targeted nanotherapeutic strategy to suppress FABP4 and improve neurological outcomes.
    Keywords:  FABP4; Intracerebral hemorrhage; Lipid droplet; Microglia; Neutrophil; S100A9
    DOI:  https://doi.org/10.1186/s12974-025-03573-6
  18. J Clin Invest. 2025 Nov 06. pii: e179985. [Epub ahead of print]
      Demyelination associated microglia (DMAM) orchestrate the regenerative response to demyelination by clearing myelin debris and promoting oligodendrocyte maturation. Peroxisomal metabolism has emerged as a candidate regulator of DMAMs, though the cell-intrinsic contribution in microglia remains undefined. Here we elucidate the role of peroxisome integrity in DMAMs using cuprizone mediated demyelination coupled with conditional knockout of peroxisome biogenesis factor 5 (PEX5) in microglia. Absent demyelination, PEX5 conditional knockout (PEX5cKO) had minimal impact on homeostatic microglia. However, during cuprizone-induced demyelination, the emergence of DMAMs unmasked a critical requirement for peroxisome integrity. At peak demyelination, PEX5cKO DMAMs exhibited increased lipid droplet burden and reduced lipophagy suggestive of impaired lipid catabolism. Although lipid droplet burden declined during the remyelination phase, PEX5cKO DMAMs accumulated intralysosomal crystals and curvilinear profiles, which features were largely absent in controls. Aberrant lipid processing was accompanied by elevated lysosomal damage markers and downregulation of the lipid exporter gene Apoe, consistent with defective lipid clearance. Furthermore, the disruptions in PEX5cKO DMAMs were associated with defective myelin debris clearance and impaired remyelination. Together, these findings delineate a stage-specific role for peroxisomes in coordinating lipid processing pathways essential to DMAM function and necessary for enabling a pro-remyelinating environment.
    Keywords:  Cell biology; Demyelinating disorders; Inflammation; Macrophages; Neuroscience
    DOI:  https://doi.org/10.1172/JCI179985
  19. Eur J Nucl Med Mol Imaging. 2025 Nov 03.
       BACKGROUND: While 18F-fluorodeoxyglucose (18F-FDG) PET supports increased neuronal activity in tinnitus, synaptic density abnormalities via synaptic vesicle protein 2 A (SV2A) imaging remain unexplored. This study used 18F-SynVesT-1 PET to evaluate SV2A changes in tinnitus patients and compared them to 18F-FDG patterns.
    METHODS: 28 tinnitus patients (acute/chronic) and 24 healthy controls underwent MRI and static PET with both 18F-SynVesT-1 and 18F-FDG. Standardized uptake values (SUV/SUVr) were calculated, followed by brain network analysis and EEG microstate assessment. Correlations with clinical features were examined.
    FINDINGS: Lesions in the brain of chronic tinnitus patients had increased 18F-SynVesT-1 uptake compared with controls, corresponding to high metabolism detected by 18F-FDG PET. The patients revealed increased SV2A uptake of 14 brain areas, whereas the left inferior frontal gyrus showed decreased SV2A uptake. However, acute tinnitus patient results revealed a decreased synaptic density in five brain areas as compared to that of HCs. 18F-SynVesT-1 uptake had a more broaden pattern of induction than 18F-FDG in tinnitus lesions (P < 0.05). SUVR of these two imaging agents were positively correlated in insula lobe. Tinnitus Handicap Inventory (THI) scores negatively correlated with synaptic density in limbic regions. Brain network anaylsis showed that network connectivity was enhanced in tinnitus, highest acutely. Microstate analysis of EEG showed conserved microstate alternation.
    INTERPRETATIONS: This first direct evidence demonstrates chronic tinnitus involves synaptic density elevation, while acute phase shows reduction, indicating bidirectional synaptic remodeling. 18F-SynVesT-1 outperforms 18F-FDG in detecting tinnitus-linked synaptic reorganization, with abnormality extent correlating to symptom severity, suggesting novel therapeutic targets for synaptic modulation.
    Keywords:  Cortical reorganization; Positron emission tomography; SV2A; Tinnitus
    DOI:  https://doi.org/10.1007/s00259-025-07633-0
  20. Free Radic Biol Med. 2025 Oct 31. pii: S0891-5849(25)01320-6. [Epub ahead of print]
      X-linked adrenoleukodystrophy (X-ALD) is caused by pathogenic ABCD1 variants, leading to a dysfunctional peroxisomal ABCD1 transporter, crucial for β-oxidation of very long chain fatty acids (VLCFA). The clinical manifestation ranges from asymptomatic carriers to severe childhood cerebral ALD (CALD). The underlying pathophysiology remains unclear, and while elevated oxidative stress and signs of mitochondrial dysfunction have been observed in X-ALD cells and tissues, their precise roles are still uncertain. This study aims to elucidate the interplay among excess VLCFA, mitochondrial function and oxidative stress in fibroblasts derived from CALD and non-CALD patients. Therefore, we measured reactive oxygen species (ROS) using the 2',7'-dichlorofluorescein diacetate assay, mitochondrial function with the Seahorse XFe24 flux analyzer and assessed the regulation of stress homeostasis on the genetic level by qPCR of NRF2-dependent genes NQO1, AR1B10 and AKR1C1. Additional stress was induced by exposure to tert-butyl hydroperoxide (TBHP) and hexacosanoic acid (C26:0). Scanning confocal microscopy and STED super-resolution microscopy was implemented for evaluation of mitochondrial structure and peroxisomal-mitochondrial crosstalk. Our findings indicate that non-CALD cell lines exhibit an overall compromised oxidative status under basal conditions, characterized by significantly reduced oxygen consumption rates (OCR) relative to both CALD and healthy controls, along with diminished expression of NRF2-regulated genes. Notably, ROS levels in non-CALD cells are comparable to those observed in CALD cells. However, when exposed to additional stress, these non-CALD cells show greater potential of defense mechanisms and compensation compared to CALD cells. These findings significantly improve our understanding of metabolic changes in X-ALD, focusing on the ability of different X-ALD phenotypes to cope with oxidative stress. They pave the way for further investigations to understand the different phenotypes and their disease progression, to find reliant biomarkers, and to develop therapeutic approaches and preventive measures for individual patients.
    Keywords:  ABCD1; NRF2; X-linked Adrenoleukodystrophy; mitochondrial dynamics; reactive oxygen species
    DOI:  https://doi.org/10.1016/j.freeradbiomed.2025.10.289
  21. J Alzheimers Dis. 2025 Nov 05. 13872877251391771
      Alzheimer's disease (AD) is a major neurodegenerative disease in the aging global population. Exploring the underlying mechanism is helpful to develop the novel strategy. Lipid metabolism disorder is the core accelerator of the occurrence and development of AD. Lipid deposition exacerbates the aging of microglia and astrocytes, leading to neural dysfunction, and consequently, neurodegeneration. In recent years, the crosstalk of gut microbiota and lipid metabolism has gained increasing attention. The gut microbiota and its metabolic products interfere with brain lipid metabolism via the gut-brain axis. This review explores the detrimental interactions between the disorder of lipid metabolism and gut microbiota, discusses its implications in potential pathogenesis, and highlights how restoring the imbalance ameliorates AD progression.
    Keywords:  Alzheimer's disease; gut microbiota; gut-brain axis; lipid metabolism; unfriendly dialogue
    DOI:  https://doi.org/10.1177/13872877251391771
  22. Ann Med Surg (Lond). 2025 Nov;87(11): 7695-7700
       Introduction and importance: Beta-ketothiolase deficiency (BKTD) is a rare inborn error of metabolism that impairs both isoleucine catabolism and ketone body utilization. The disorder may present with acute metabolic crises, often precipitated by infections or fasting, and can lead to life-threatening complications if not promptly diagnosed and managed.
    Case presentation: We report the case of a previously healthy 2.8-year-old man who developed vomiting, diarrhea, and fever, followed by progressive loss of consciousness. Neurological examination revealed generalized muscle rigidity, limb spasticity, and asymmetrical pupils. Laboratory investigations showed severe metabolic acidosis, hyperammonemia, and acute kidney injury. Neuroimaging findings included bilateral basal ganglia involvement and cerebellar abnormalities. Metabolic workup demonstrated elevated urinary organic acids, confirming BKTD, which was subsequently validated through genetic analysis identifying an ACAT1 gene mutation.
    Clinical discussion: This case underscores the importance of considering metabolic disorders in critically ill pediatric patients presenting with acute neurological symptoms and metabolic deterioration. Early recognition of BKT deficiency is crucial, as targeted metabolic management - including dietary intervention and comprehensive supportive care - can mitigate acute crises and prevent long-term neurological sequelae.
    Conclusion: Early metabolic evaluation in children with unexplained neurological decline remains essential. Prompt diagnosis and timely initiation of appropriate management strategies significantly improve outcomes in patients with BKTD.
    Keywords:  ACAT1 gene mutation; beta-ketothiolase deficiency; inborn error of metabolism; ketone body metabolism disorder; mitochondrial acetoacetyl-CoA thiolase; neurological impairment in metabolism
    DOI:  https://doi.org/10.1097/MS9.0000000000003958