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Why Choose the Brain for Lipidomics Analysis?
The brain is one of the most lipid-rich organs in the human body, with lipids accounting for more than 50% of its dry weight. These biomolecules are not only fundamental to the structural integrity of neural membranes and myelin sheaths, but also function as signaling mediators, energy substrates, and modulators of neuroinflammation and synaptic plasticity.
Unlike peripheral tissues, the brain features a uniquely complex and dynamic lipidome shaped by regional specialization, blood-brain barrier regulation, and neuro-glial interactions. This makes the brain an exceptionally informative sample type for lipidomics studies aiming to:
- Capture CNS-specific lipid signatures that are not reflected in plasma or other biofluids
- Reveal spatially resolved lipid alterations associated with region-dependent pathology
- Study lipid-mediated neural processes, including neurotransmission, axonal repair, and neuroinflammatory resolution
- Identify early molecular perturbations in neurodegenerative or neurodevelopmental disorders
Using brain tissue as the analytical starting point enables researchers to directly profile the lipid pathways underpinning central nervous system physiology and pathology, providing greater mechanistic insight than surrogate matrices.
When Is Brain Lipidomics Recommended?
Brain lipidomics is a high-value analytical approach when your research or clinical questions involve the central nervous system.
| Application Area | Purpose of Brain Lipidomics |
|---|
| Neurodegenerative Disease Research | Detect disease-stage-specific changes in sphingolipids, ceramides, gangliosides |
| Neuroinflammation and Immunometabolism | Quantify lipid mediators like prostaglandins, resolvins, and endocannabinoids |
| Brain Energy Metabolism Studies | Assess shifts in acylcarnitines, glycerolipids, and fatty acids |
| Developmental and Pediatric Neuroscience | Track lipid remodeling during brain maturation, synaptogenesis, and myelination |
| Ischemia, TBI, or Stroke Models | Map region-specific lipid degradation, oxidation, and recovery trajectories |
| Psychiatric and Behavioral Studies | Link lipid dysregulation to neurotransmitter imbalances or cognitive phenotypes |
| Neuropharmacology and Toxicology | Evaluate lipid-based biomarkers of neurotoxicity, neuroprotection, or drug efficacy |
By targeting brain-derived lipid profiles, researchers can achieve unparalleled resolution in understanding CNS-specific biochemical changes that are often masked or diluted in systemic samples like blood or urine.
Brain Lipidomics Analysis Service in Creative Proteomics
Targeted Lipid Quantification
Absolute quantification of defined lipid panels, including ceramides, eicosanoids, sphingomyelins, and neuroactive lipid mediators.
Untargeted Brain Lipidomics
Comprehensive profiling of brain lipids using high-resolution LC-MS/MS to discover novel lipid species and pathway alterations.
Lipid Transport & Metabolism Profiling
Quantitative analysis of lipids involved in transport, storage, and metabolic fluxes—such as acylcarnitines, monoacylglycerols, and sterol derivatives—to support studies on brain energy dynamics and lipid trafficking.
Neuro-Lipid Mediator Profiling
Focused analysis of bioactive lipids involved in neuroinflammation, synaptic function, and endocannabinoid signaling.
Subcellular Lipidomics
Profiling of lipids within isolated synaptosomes, mitochondria, or nuclear fractions to support organelle-specific studies.
Microbiome–Brain Lipidomics Integration
Multi-omics service integrating lipidomics with gut microbiome sequencing to explore the gut-brain axis.
Spatial Lipidomics (Optional)
Mass spectrometry imaging or laser capture microdissection (LCM)-based lipidomics preserving anatomical localization.
Custom Lipidomics Development
Tailored method development for rare lipid species, unique brain models, or specific analytical challenges.
What Makes Our Brain Lipidomics Unique?
- Region-resolved analysis: We accommodate dissection of brain subregions for spatial lipid comparison.
- Flexible method selection: Choice of untargeted (discovery) or targeted (quantitative) workflows.
- Subcellular fractionation service: Optional mitochondrial or synaptic vesicle isolation.
- Multi-omics capability: Seamless integration with transcriptomics, proteomics, or microbiomics.
Detected Lipid Classes, Metabolites, and Pathways in Brain Lipidomics
- Glycerophospholipids
- Sphingolipids
- Glycerolipids
- Fatty Acyls
- Sterol Lipids
- Endocannabinoids
| Lipid Subclass | Representative Species | Related Metabolites | Key Pathways |
|---|
| Phosphatidylcholine (PC) | PC 16:0/18:1, PC 18:0/20:4 | Lyso-PC, Choline | Glycerophospholipid metabolism, membrane fluidity |
| Phosphatidylethanolamine (PE) | PE 18:1/18:2, PE 16:0/22:6 | Lyso-PE, Ethanolamine | Membrane remodeling, autophagy |
| Phosphatidylserine (PS) | PS 18:0/18:1 | Serine | Apoptosis signaling |
| Phosphatidylinositol (PI) | PI 18:0/20:4 | Inositol | PI cycle, intracellular signaling |
| Phosphatidic Acid (PA) | PA 16:0/18:1 | G3P | Lipid biosynthesis |
| Cardiolipin (CL) | CL 72:8, CL 70:6 | PG, G3P | Mitochondrial function, apoptosis |
| Plasmalogens (PlsEtn/PlsCho) | PlsEtn 16:0/22:6, PlsCho 18:0/20:4 | Aldehyde derivatives | Antioxidant defense, neural membrane structure |
| Lipid Subclass | Representative Species | Related Metabolites | Key Pathways |
|---|
| Ceramides (Cer) | Cer d18:1/24:0, Cer d18:1/16:0 | Sphingosine | Apoptosis, insulin resistance |
| Sphingomyelins (SM) | SM d18:1/16:0, SM d18:1/24:1 | Choline | Myelin sheath structure, cell signaling |
| Hexosylceramides (HexCer) | GluCer, GalCer | Glucose, Galactose | Glycosphingolipid metabolism |
| Lactosylceramides (LacCer) | LacCer d18:1/24:1 | UDP-Gal, Glucose | Inflammatory signaling |
| Sphingosine-1-Phosphate (S1P) | — | S1P | Immune modulation, vascular tone |
| Sulfatides | ST 18:1/24:0 | GalCer-SO3 | Myelin compaction, oligodendrocyte function |
| GM Gangliosides (GM1, GM2, etc.) | GM1 18:1/24:1, GM3 18:0/20:0 | NANA (sialic acid), UDP-sugars | Neurodevelopment, synaptic plasticity |
| Lipid Subclass | Representative Species | Related Metabolites | Key Pathways |
|---|
| Triacylglycerols (TAG) | TG 16:0/18:1/18:2, TG 18:1/18:1/18:1 | Glycerol, Free fatty acids | Lipogenesis, energy storage |
| Diacylglycerols (DAG) | DG 18:1/18:2, DG 16:0/18:1 | Glycerol, DAG | Lipid signaling, PKC activation |
| Monoacylglycerols (MG) | MG 18:1, MG 16:0 | Glycerol | Lipolysis, endocannabinoid metabolism |
| Alkylacylglycerols (Ether lipids) | AG 16:0/20:4 | Ether-linked FAs | Neuronal membrane integrity, oxidative protection |
| Lipid/Metabolite | Representative Species | Related Metabolites | Key Pathways |
|---|
| Free Fatty Acids (FFA) | Palmitate (16:0), Oleate (18:1), Arachidonate (20:4) | Acetyl-CoA | β-oxidation, fatty acid synthesis |
| Acylcarnitines | C2, C4, C16, C18:1, C18:2 | L-carnitine, CoA | Mitochondrial transport, energy homeostasis |
| Oxidized Fatty Acids | HODEs, HETEs, EETs, EpOMEs | LOX/CYP-derived species | Neuroinflammation, oxidative stress response |
| Lipid Subclass | Representative Species | Related Metabolites | Key Pathways |
|---|
| Cholesterol | Free cholesterol | Lanosterol, Desmosterol | Steroid biosynthesis, synapse formation |
| Cholesteryl Esters (CE) | CE 18:1, CE 20:4 | Cholesterol | Lipoprotein metabolism, storage |
| Oxysterols | 7-Ketocholesterol, 24S-Hydroxycholesterol | Bile acids, ROS derivatives | Oxidative signaling, bile acid synthesis |
| Neurosteroids | Pregnenolone, Allopregnanolone | Progesterone | GABAergic modulation, neuroprotection |
| Lipid Subclass | Representative Species | Related Metabolites | Key Pathways |
|---|
| Endocannabinoids | Anandamide (AEA), 2-AG | Ethanolamine, Glycerol | ECS signaling, mood regulation |
| Prostaglandins | PGD2, PGE2, PGF2α | Arachidonic acid | Inflammatory response, fever, pain |
| Specialized Pro-resolving Mediators (SPMs) | Resolvin D1, Protectin D1, Maresin 1 | DHA, EPA | Inflammation resolution, tissue repair |
| Leukotrienes | LTB4, LTC4 | 5-HPETE | Immune cell activation |
Why Choose Our Brain Lipidomics Services?
- > 1,000 lipid species detected per sample: Comprehensive coverage across phospholipids, sphingolipids, glycerolipids, sterols, and fatty acids.
- Low detection limits: down to femtomole levels: Enables detection of low-abundance regulatory lipids critical to brain function and pathology.
- Quantification CV < 10%: High technical reproducibility supported by stable isotopic internal standards and rigorous QC.
- Pathway resolution across 30+ brain-relevant lipid pathways: Including sphingolipid metabolism, eicosanoid synthesis, myelin biosynthesis, and more.
- Dual-mode ionization (ESI+ / ESI−): Captures a broader lipidomic spectrum from zwitterionic phospholipids to negatively charged gangliosides.
- High-resolution MS (up to 240,000 FWHM): Accurate mass detection reduces false positives and improves structural resolution in complex brain matrices.
Workflow of Brain Lipidomics
MS-based analytical strategy for brain lipidomics research (Yoon, Jong Hyuk, et al., 2022).
What Platforms are Used for Brain Lipidomics Analysis?
UHPLC–Q Exactive Plus (Thermo Fisher Scientific): High-resolution Orbitrap platform ideal for untargeted lipid profiling with accurate mass detection and in-depth MS/MS fragmentation.
Agilent 6495C Triple Quadrupole LC-MS/MS: Ultra-sensitive triple quadrupole system with femtogram-level detection, ideal for targeted quantification of specific lipid species in brain tissue or cerebrospinal fluid.
TSQ Altis Triple Quadrupole (Thermo Fisher Scientific): A robust and precise platform for high-throughput, targeted lipid quantification with broad dynamic range and excellent inter-assay consistency.
Thermo Fisher Q Exactive (Orbitrap LC-MS/MS) (Figure from Thermo Fisher)
Agilent 6495C + 1260 HPLC (Figure from Agilent)
TSQ Altis Triple Quadrupole (Figure from Thermo Fisher)
Brain Lipidomics Analysis Service: Results and Data Analysis
Lipid Identification & Quantification
- High-resolution MS analysis using Orbitrap and triple quadrupole systems
- Lipid annotation based on MS/MS fragmentation, retention time, and exact mass
- Database matching: LIPID MAPS, HMDB, LipidBlast, in-house libraries
- Quantification:
- Absolute or relative concentrations
- Isotopic internal standards
- CV < 10% for technical reproducibility
Statistical & Pathway Analysis
Differential analysis:
- Fold change, p-value, FDR
- Volcano plots, heatmaps
Multivariate analysis:
- PCA, PLS-DA for sample classification
Pathway enrichment:
- KEGG, Reactome, LipidMaps integration
- Visualization of lipid-related metabolic disruptions
Deliverables
Comprehensive data report including:
- List of identified/quantified lipid species
- Lipid class distribution and trend charts
- Annotated pathway maps
- Correlation or network diagrams (if applicable)
Expert summary with key findings and suggested next steps
Explore our Lipidomics Solutions brochure to learn more about our comprehensive lipidomics analysis platform.
Download Brochure
Sample Requirements for Brain Lipidomics Solutions
| Sample Type | Recommended Amount | Notes |
|---|
| Brain Tissue (fresh/frozen) | ≥ 50 mg | Snap-frozen in liquid nitrogen; avoid thawing |
| Cerebrospinal Fluid (CSF) | ≥ 200 µL | Collected in sterile, lipid-free tubes |
| Serum / Plasma | ≥ 100 µL | EDTA or heparin anticoagulants preferred |
| Cultured Cells | ≥ 1 × 10⁷ cells | Washed with PBS, stored at -80°C |
| Organoids / Brain Slices | Equivalent to ≥ 50 mg tissue | Ensure sample integrity and minimal handling |
What Our Brain Lipidomics Analysis Is Used For
Neuroscience Research
Elucidates lipid signaling roles in synaptic plasticity, neurogenesis, and brain development.
Aging Research
Tracks lipid composition changes associated with brain aging and cognitive decline.
Nutritional Neuroscience
Assesses dietary lipid effects (e.g., omega-3 PUFA) on brain lipid homeostasis.
Environmental Toxicology
Evaluates neurotoxic effects of pollutants or chemicals via lipid profile alterations.
Pharmacological Mechanism Studies
Monitors brain lipid changes in response to neuroactive compound exposure.
Animal Model Validation
Characterizes lipidomic phenotypes in transgenic or chemically induced brain disorder models.
FAQs for Brain Lipidomics Analysis Service
Can I submit different types of brain samples within the same project?
Yes. We can analyze mixed sample types (e.g., tissue, CSF, plasma) in the same project, provided each sample meets the quantity and storage requirements. Please contact us in advance to optimize experimental design and extraction protocols.
How do you handle low-yield or limited samples?
For scarce samples (e.g., microdissected brain regions), we offer modified extraction protocols and sensitive quantification workflows using triple quadrupole instruments to maximize lipid recovery and detection.
Can I provide my own internal standards?
Yes. You may supply custom internal standards, and we will integrate them into the extraction and quantification process. Please provide standard concentration and chemical details for compatibility.
Do you provide assistance with study design or statistical planning?
Absolutely. Our scientific support team offers free consultation on sample grouping, statistical power estimation, and biological replicates to ensure robust, publication-ready results.
Can you help interpret results if I'm not a lipidomics specialist?
Yes. All projects include expert annotations, biological pathway mapping, and a summary written for both technical and non-technical users. We also provide follow-up meetings upon request.
What data formats do you deliver?
We provide results in Excel (.xlsx), raw data files (.raw/.mzML), statistical output files (.csv/.pdf), and image files for figures (e.g., .png, .svg). Custom formats (e.g., for MetaboAnalyst or Cytoscape) are available on request.
Is it possible to re-analyze data later with updated targets or pathways?
Yes. We archive raw and processed data securely and can reprocess or re-annotate datasets with new lipid targets, updated databases, or additional statistical models upon request.
Publication
- White matter lipid alterations during aging in the rhesus monkey brain. GeroScience, 2024. https://doi.org/10.1007/s11357-024-01353-3
- Characterization of Dnajc12 knockout mice, a model of hypodopaminergia. bioRxiv, 2024. https://doi.org/10.1101/2024.07.06.602343
- Annexin A2 modulates phospholipid membrane composition upstream of Arp2 to control angiogenic sprout initiation. The FASEB Journal, 2023. https://doi.org/10.1096/fj.202201088R
- Lipid Membrane Engineering for Biotechnology (Doctoral dissertation, Aston University). Lipid Membrane Engineering for Biotechnology, 2023. https://doi.org/10.48780/publications.aston.ac.uk.00046663
- Multi‐omics identify xanthine as a pro‐survival metabolite for nematodes with mitochondrial dysfunction. EMBO Journal, 2019. https://doi.org/10.15252/embj.201899558
- Evidence for phosphate-dependent control of symbiont cell division in the model anemone Exaiptasia diaphana. mBio, 2024. https://doi.org/10.1128/mbio.01059-24
- The olfactory receptor Olfr78 promotes differentiation of enterochromaffin cells in the mouse colon. EMBO reports, 2024. https://doi.org/10.1038/s44319-023-00013-5
- Metabolomic Studies in Girls With Central and Peripheral Precocious Puberty. Fabad Journal of Pharmaceutical Sciences, 2023. https://doi.org/10.55262/fabadeczacacilik.1344851
- Prospective randomized, double-blind, placebo-controlled study of a standardized oral pomegranate extract on the gut microbiome and short-chain fatty acids. Foods, 2023. https://doi.org/10.3390/foods13010015
