| Biomarker | TSPO | Full name | 18kDa Transporter Protein | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Monitoring |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Temporal Lobe Epilepsy (TLE) | ||
| Organ | Brain | Test Sample / Technology Platform | Brain (PET Imaging) | ||
| Pathobiological Mechanisms | A specific marker of activated microglia, reflecting the degree of neuroinflammation. | ||||
| Clinical Availability Status | Research validation stage | ||||
| Notes and Dynamics | TSPO PET uptake in the hippocampus of TLE patients is positively correlated with seizure frequency, which can assess disease activity. | ||||
| Biomarker | Abnormal Gut Microbiota (e.g., Decreased Bifidobacterium) | Full name | Abnormal Gut Microbiota Abundance (e.g., Decreased Bifidobacterium) | Molecular Type | Microbial Community |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Risk Stratification, Monitoring |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Gut Microbiota-Associated Epilepsy | ||
| Organ | Brain | Test Sample / Technology Platform | Feces (16S rRNA Sequencing, Metagenomic Sequencing) | ||
| Pathobiological Mechanisms | Imbalance of gut microbiota metabolites (e.g., short-chain fatty acids) regulates neuroinflammation and excitability through the gut-brain axis. | ||||
| Clinical Availability Status | Research stage | ||||
| Notes and Dynamics | Probiotic intervention can improve seizure frequency in some patients; Bifidobacterium preparations have entered clinical phase I. | ||||
| Biomarker | PEDs (EEG) | Full name | Electroencephalographic Periodic Discharges | Molecular Type | Electrophysiological Pattern |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Prognosis |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Status Epilepticus (SE) | ||
| Organ | Brain | Test Sample / Technology Platform | Scalp/Intracranial (Video EEG Monitoring) | ||
| Pathobiological Mechanisms | Abnormal discharge pattern after extensive intracerebral neuronal injury, indicating severe brain dysfunction. | ||||
| Clinical Availability Status | Clinically available | ||||
| Notes and Dynamics | When the frequency of PEDs > 2Hz, the risk of poor prognosis in SE patients is increased by 3.5 times. | ||||
| Biomarker | AMPA R Ab | Full name | AMPA Receptor Antibody | Molecular Type | Autoantibody |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Etiology |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Autoimmune Epilepsy | ||
| Organ | Brain | Test Sample / Technology Platform | Serum/Cerebrospinal Fluid (ELISA, Cell-based Assay) | ||
| Pathobiological Mechanisms | Binds to AMPA receptors, enhances excitatory neurotransmission, inducing refractory epilepsy and encephalitis. | ||||
| Clinical Availability Status | Research validation stage | ||||
| Notes and Dynamics | Often accompanied by acute encephalitis; immunotherapy (e.g., rituximab) can improve epilepsy control. | ||||
| Biomarker | Ki-67 | Full name | Ki-67 Protein | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis, Risk Stratification |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Brain Tumor-Associated Epilepsy (BTRE) | ||
| Organ | Brain | Test Sample / Technology Platform | Tumor Tissue (Immunohistochemistry) | ||
| Pathobiological Mechanisms | Reflects tumor proliferation activity; higher expression indicates more significant intracerebral microenvironment disorder and increased epilepsy onset risk. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | In WHO grade II glioma patients with Ki-67 index > 5%, the postoperative epilepsy recurrence risk is increased by 2 times. | ||||
| Biomarker | HFOs (80-500Hz, EEG) | Full name | Electroencephalographic High-Frequency Oscillations (80-500Hz) | Molecular Type | Electrophysiological Pattern |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Risk Stratification |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Childhood Epilepsy | ||
| Organ | Brain | Test Sample / Technology Platform | Intracranial/Scalp (Long-term EEG Monitoring) | ||
| Pathobiological Mechanisms | Epileptogenic focus-specific electrical activity, reflecting abnormal neuronal synchronization, can localize the epileptogenic focus. | ||||
| Clinical Availability Status | Research stage | ||||
| Notes and Dynamics | Intraoperative monitoring of HFOs can improve the accuracy of epileptogenic focus resection and reduce postoperative recurrence rate. | ||||
| Biomarker | MGMT Promoter Meth | Full name | O6-Methylguanine-DNA Methyltransferase Promoter Methylation | Molecular Type | DNA Methylation |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prediction, Pharmacodynamics/Response |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Drug-Refractory Epilepsy | ||
| Organ | Brain | Test Sample / Technology Platform | Tumor Tissue (MSP, Pyrosequencing) | ||
| Pathobiological Mechanisms | Methylation silences the MGMT gene, reduces DNA repair, and enhances the efficacy of temozolomide on epilepsy-related brain tumors. | ||||
| Clinical Availability Status | Research validation stage | ||||
| Notes and Dynamics | The epilepsy control rate of chemotherapy combined with ASM treatment is increased by 40% in methylation-positive patients. | ||||
| Biomarker | SLC7A11 (xCT) | Full name | Solute Carrier Family 7 Member 11 (xCT) | Molecular Type | Transporter |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Prediction |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Brain Tumor-Associated Epilepsy (BTRE) | ||
| Organ | Brain | Test Sample / Technology Platform | Tumor Tissue (Immunohistochemistry, qPCR) | ||
| Pathobiological Mechanisms | Mediates cystine-glutamate exchange, excessively releases glutamate into the extracellular space, activates excitatory neurons, inducing epilepsy. | ||||
| Clinical Availability Status | Research validation stage | ||||
| Notes and Dynamics | The incidence of epilepsy in glioma patients with high SLC7A11 expression reaches 75%; the specific inhibitor sulfasalazine can reduce seizures. | ||||
| Biomarker | S100B | Full name | S100 Calcium-Binding Protein B | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis, Monitoring |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Temporal Lobe Epilepsy (TLE) | ||
| Organ | Brain | Test Sample / Technology Platform | Serum (ELISA) | ||
| Pathobiological Mechanisms | Released after astrocyte activation, involved in neuroinflammation and blood-brain barrier disruption, reflecting the degree of brain injury. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | Serum S100B peaks within 24 hours after TLE seizures, and levels are positively correlated with the degree of hippocampal sclerosis. | ||||
| Biomarker | 8-OHdG | Full name | 8-Hydroxy-2’-deoxyguanosine | Molecular Type | Metabolites (oxidative stress markers) |
| Molecular Formula | C₁₀H₁₃N₅O₅ | Molecular Weight | 283.24 | Core Functional Dimensions | Monitoring and prognosis |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Diabetes Mellitus | ||
| Organ | Systemic/Cells | Test Sample / Technology Platform | Plasma/urine (mass spectrometry, ELISA) | ||
| Pathobiological Mechanisms | Oxidative stress leads to DNA damage products, reflecting the degree of oxidative damage in diabetes | ||||
| Clinical Availability Status | As diabetes clinical auxiliary indicators of oxidative stress status and complications of risk assessment, lack of unified reference standard | ||||
| Notes and Dynamics | Positively related to the risk of diabetic microvascular complications | ||||
| Biomarker | P-gp | Full name | P-Glycoprotein | Molecular Type | Transporter |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prediction, Pharmacodynamics/Response |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Drug-Refractory Epilepsy | ||
| Organ | Brain | Test Sample / Technology Platform | Brain Microvessels/Plasma (Immunohistochemistry, Western Blot) | ||
| Pathobiological Mechanisms | Overexpressed at the blood-brain barrier, actively pumps out ASMs, reducing intracerebral drug concentration, leading to treatment resistance. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | COX-2 inhibitors (e.g., celecoxib) can downregulate P-gp expression, reversing multidrug resistance in some patients. | ||||
| Biomarker | SV2A | Full name | Synaptic Vesicle Protein 2A | Molecular Type | Protein |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prediction, Pharmacodynamics/Response |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Brain Tumor-Associated Epilepsy (BTRE) | ||
| Organ | Brain | Test Sample / Technology Platform | Tumor Tissue (Immunohistochemistry, PET Imaging) | ||
| Pathobiological Mechanisms | A specific binding target of the anti-epileptic drug levetiracetam; expression levels directly affect drug sensitivity. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | The response rate to levetiracetam is increased by 30% in patients with high SV2A expression; PET imaging can guide individualized medication. | ||||
| Biomarker | miR-29a/b | Full name | microRNA-29a / microRNA-29b | Molecular Type | Nucleic acid (miRNA) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, risk assessment |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Gestational diabetes mellitus (GDM) | ||
| Organ | Placenta/Systemic | Test Sample / Technology Platform | Serum (qRT - PCR) | ||
| Pathobiological Mechanisms | It regulates glucose metabolism and insulin sensitivity, and its expression is abnormal during pregnancy | ||||
| Clinical Availability Status | Validation phase in clinical research, diagnosis of GDM AUC 0.944 joint detection, the accuracy is better than that of single index, but has not yet been incorporated into the clinical guidelines | ||||
| Notes and Dynamics | The diagnostic accuracy of combined detection was better than that of single index (AUC 0.944). | ||||
| Biomarker | miR-146a | Full name | MicroRNA-146a | Molecular Type | MicroRNA |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis, Monitoring |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Temporal Lobe Epilepsy (TLE) | ||
| Organ | Brain | Test Sample / Technology Platform | Plasma/Cerebrospinal Fluid (qRT-PCR) | ||
| Pathobiological Mechanisms | Regulates the TLR4/NF-κB pathway, upregulated expression exacerbates neuroinflammation, promoting epilepsy progression. | ||||
| Clinical Availability Status | Research validation stage | ||||
| Notes and Dynamics | Meta-analysis shows that CSF miR-146a levels in TLE patients are elevated by 1.8 times, correlated with disease severity. | ||||
| Biomarker | miR-128 | Full name | MicroRNA-128 | Molecular Type | MicroRNA |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Prognosis, Monitoring |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Temporal Lobe Epilepsy (TLE) | ||
| Organ | Brain | Test Sample / Technology Platform | Plasma/Cerebrospinal Fluid (qRT-PCR) | ||
| Pathobiological Mechanisms | Targets and regulates neuron excitability-related genes (e.g., SOX9), downregulated expression is associated with hippocampal sclerosis and epilepsy recurrence. | ||||
| Clinical Availability Status | Research validation stage | ||||
| Notes and Dynamics | Positively correlated with postoperative recurrence risk in TLE patients; plasma levels can be used as a non-invasive recurrence monitoring indicator. | ||||
| Biomarker | P2X7R rs208294 Polym | Full name | P2X7R Gene rs208294 Polymorphism | Molecular Type | Gene Polymorphism |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Risk Stratification |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Childhood Febrile Convulsions | ||
| Organ | Brain | Test Sample / Technology Platform | Peripheral Blood (Gene Sequencing, PCR-RFLP) | ||
| Pathobiological Mechanisms | Gain-of-function mutation enhances P2X7R-mediated inflammatory response, reducing the epileptic seizure threshold. | ||||
| Clinical Availability Status | Research stage | ||||
| Notes and Dynamics | Children carrying this mutation have a 2.8-fold higher risk of developing epilepsy from febrile convulsions than wild-type. | ||||