| Biomarker | 3Hz Spike-Wave Complexes (EEG) | Full name | Electroencephalographic 3Hz Spike-Wave Complexes | Molecular Type | Electrophysiological Pattern |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Diagnosis |
| Disease(or Constitution) | Epilepsy | Disease Subtypes | Absence Epilepsy | ||
| Organ | Brain | Test Sample / Technology Platform | Scalp (Video EEG Monitoring) | ||
| Pathobiological Mechanisms | Abnormal synchronous discharge of the thalamocortical circuit, leading to transient loss of consciousness and cognitive interruption. | ||||
| Clinical Availability Status | Clinically available | ||||
| Notes and Dynamics | The gold standard diagnostic indicator for absence epilepsy; AI-assisted EEG analysis can improve the recognition accuracy to over 95%. | ||||
| Biomarker | P2X7R | Full name | P2X Purinoceptor 7 | Molecular Type | Protein |
| 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 | Serum/Brain Region Tissue (ELISA, PET Imaging) | ||
| Pathobiological Mechanisms | Activates the NLRP3 inflammasome, promotes IL-1β release, mediates anti-epileptic drug (ASM) efflux, leading to treatment resistance. | ||||
| Clinical Availability Status | Research validation stage | ||||
| Notes and Dynamics | The specific antagonist JNJ-47965567 has entered clinical phase II, which can reverse drug resistance in some patients. | ||||
| Biomarker | BRAF V600E Mut | Full name | B-Raf Proto-Oncogene V600E Mutation | Molecular Type | Gene Mutation |
| 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 (NGS, ARMS-PCR) | ||
| Pathobiological Mechanisms | Activates the MAPK/mTOR pathway, simultaneously inducing neuronal epileptogenesis and glial tumor proliferation. | ||||
| Clinical Availability Status | Under clinical validation | ||||
| Notes and Dynamics | Highly prevalent in pediatric low-grade brain tumors (e.g., ganglioglioma); BRAF inhibitors can simultaneously inhibit tumor growth and seizures. | ||||
| Biomarker | miR-27a/miR-141-3p | Full name | microRNA-27a / microRNA-141-3p | Molecular Type | Nucleic acid (miRNA, EV source) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Susceptibility to diagnose, |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Type 2 diabetes | ||
| Organ | Systemic | Test Sample / Technology Platform | Plasma/serum (qRT - PCR) | ||
| Pathobiological Mechanisms | By regulating the insulin signaling pathway, it exacerbates insulin resistance | ||||
| Clinical Availability Status | At the clinical validation stage, has not yet been incorporated into clinical guidelines, the lack of standardized testing method | ||||
| Notes and Dynamics | EV carry miRNAs are potential biomarkers of insulin resistance | ||||
| Biomarker | ZnT8 Ab | Full name | ZnT8 antibody (zinc transporter 8 antibody) | Molecular Type | Antibodies (protein) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, susceptibility |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Type 1 Diabetes | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (Immunoassay) | ||
| Pathobiological Mechanisms | Autoimmune antibodies attack islet β-cell zinc transporters and participate in β-cell dysfunction | ||||
| Clinical Availability Status | Clinical as auxiliary indexes in T1DM parting, combining with other autoantibodies, the detection alone lack of specificity | ||||
| Notes and Dynamics | Sustainability in LADA is higher than adult onset of type 1 diabetes, no clear specific clinical features | ||||
| Biomarker | IA-2 Ab | Full name | Islet antigen-2 antibody (tyrosine phosphatase antibody) | Molecular Type | Antibodies (protein) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, prognosis, |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Type 1 diabetes mellitus | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (Immunoassay) | ||
| Pathobiological Mechanisms | Autoimmune antibodies targeting islet beta cells, accelerate the beta cell damage | ||||
| Clinical Availability Status | Clinical with joint detection in order to enhance T1DM GAD65 antibody specificity, detection application less alone | ||||
| Notes and Dynamics | Combined detection with GAD65 antibody can improve the diagnostic specificity of T1DM | ||||
| Biomarker | GAD65 Ab | Full name | GAD65 antibody | Molecular Type | Antibodies (proteins) |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Susceptibility to diagnose, |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Type 1 diabetes/LADA | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum (ELISA, electrochemical luminescence method) | ||
| Pathobiological Mechanisms | Autoimmune antibodies against pancreatic beta cells, leading to insulin secretion defects | ||||
| Clinical Availability Status | Clinical routine classification diagnosis for T1DM and LADA, high-risk groups preferred antibody screening index | ||||
| Notes and Dynamics | Key core autoantibodies in type 1 diabetes, LADA diagnosis markers, used in high-risk population screening | ||||
| Biomarker | C-peptide | Full name | C-peptide | Molecular Type | protein |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, Monitoring |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Distinguish between type 1/2 diabetes | ||
| Organ | Pancreas | Test Sample / Technology Platform | Serum/plasma (immunoassay) | ||
| Pathobiological Mechanisms | Proinsulin fission product, more stable than insulin secretion, reflect the endogenous insulin secretion | ||||
| Clinical Availability Status | Guidelines recommend classification key indicators, clinical routine for 1/2 type identification, quantifiable islet beta cell function, is normal function of islet transplantation monitoring project | ||||
| Notes and Dynamics | It is used for the classification of diabetes mellitus and the evaluation of islet β cell function, and the key indicators of islet transplantation monitoring | ||||
| Biomarker | 2hPG | Full name | Blood glucose 2 hours after a meal | Molecular Type | Metabolites |
| Molecular Formula | C₆H₁₂O₆ | Molecular Weight | 180.16 | Core Functional Dimensions | Diagnosis, Screening |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Diabetes Mellitus | ||
| Organ | Pancreas/Blood | Test Sample / Technology Platform | Plasma/serum (glucose oxidase method) | ||
| Pathobiological Mechanisms | To evaluate the ability of insulin secretion to control blood glucose after eating | ||||
| Clinical Availability Status | It is clinically used to confirm the cut-off value of fasting blood glucose, and it is more sensitive to early screening of insulin resistance related diabetes | ||||
| Notes and Dynamics | The sensitivity of early screening for diabetes is better than that of fasting blood glucose | ||||
| Biomarker | FPG | Full name | Fasting plasma glucose | Molecular Type | Metabolites |
| Molecular Formula | C₆H₁₂O₆ | Molecular Weight | 180.16 | Core Functional Dimensions | Diagnosis, Screening |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Diabetes Mellitus | ||
| Organ | Pancreas/Blood | Test Sample / Technology Platform | Plasma/serum (glucose oxidase method) | ||
| Pathobiological Mechanisms | Clinical routine initial screening tools, widely used in physical examination and outpatient screening, need to be combined with multiple tests to exclude short-term interference factors such as diet and stress | ||||
| Clinical Availability Status | It directly reflects the current blood glucose status and assesses glucose metabolism homeostasis | ||||
| Notes and Dynamics | It is simple and fast, and is affected by short-term factors such as diet and stress | ||||
| Biomarker | HbA1c | Full name | Glycated hemoglobin | Molecular Type | protein |
| Molecular Formula | Macromolecule | Molecular Weight | / | Core Functional Dimensions | Diagnosis, monitoring |
| Disease(or Constitution) | Diabetes Mellitus | Disease Subtypes | Diabetes Mellitus | ||
| Organ | Pancreas/Blood | Test Sample / Technology Platform | Whole blood (HPLC, immunoassay) | ||
| Pathobiological Mechanisms | It reflects the average blood sugar level over the past 2 to 3 months, formed by the combination of blood sugar and hemoglobin | ||||
| Clinical Availability Status | The core indicators recommended by international guidelines (ADA and WHO) are routinely carried out in clinical practice with a high degree of standardization, and can be directly used for diabetes diagnosis and long-term blood glucose control evaluation | ||||
| Notes and Dynamics | The core indicators of diabetes management can predict the risk of complications | ||||
| Biomarker | QUINA | Full name | Quinolinic Acid | Molecular Type | Amino Acid Metabolite |
| Molecular Formula | C7H6N2O4 | Molecular Weight | 178.13 g/mol | Core Functional Dimensions | Pathological Confirmation |
| Disease(or Constitution) | Depression | Disease Subtypes | Chronic Depression, Neurodegenerative Depression | ||
| Organ | Brain | Test Sample / Technology Platform | Cerebrospinal Fluid (LC-MS/MS) | ||
| Pathobiological Mechanisms | A neurotoxic metabolite of tryptophan metabolism that excessively activates NMDA receptors and induces excitotoxic injury of hippocampal neurons. | ||||
| Clinical Availability Status | Research Stage | ||||
| Notes and Dynamics | Cerebrospinal fluid QUINA levels in patients with chronic depression are 3.2 times higher than those in healthy individuals, negatively correlated with hippocampal volume reduction. | ||||
| Biomarker | Melatonin | Full name | Melatonin | Molecular Type | Hormone |
| Molecular Formula | C13H16N2O2 | Molecular Weight | 232.28 g/mol | Core Functional Dimensions | Diagnosis, Disease Monitoring |
| Disease(or Constitution) | Brain | Disease Subtypes | Saliva/Plasma (ELISA, LC-MS/MS) | ||
| Organ | Brain | Test Sample / Technology Platform | Saliva/Plasma (ELISA, LC-MS/MS) | ||
| Pathobiological Mechanisms | Circadian rhythm disturbance leads to decreased melatonin secretion, weakening its anti-inflammatory, antioxidant, and neuroprotective effects. | ||||
| Clinical Availability Status | Research Stage | ||||
| Notes and Dynamics | Nighttime melatonin <10pg/mL is positively correlated with depression-related insomnia symptoms; exogenous supplementation can improve sleep quality. | ||||
| Biomarker | miR-207 | Full name | MicroRNA-207 | Molecular Type | Non-coding RNA |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Disease Monitoring |
| Disease(or Constitution) | Depression | Disease Subtypes | Major Depressive Disorder (MDD), Responsive Depression | ||
| Organ | Brain | Test Sample / Technology Platform | Plasma Extracellular Vesicles (Quantitative Real-Time PCR qRT-PCR) | ||
| Pathobiological Mechanisms | Targets and inhibits the Tril-NF-κB pathway, reduces the release of astrocyte inflammatory factors, and alleviates neurotoxicity. | ||||
| Clinical Availability Status | Research Stage | ||||
| Notes and Dynamics | NK cell-derived miR-207 can be delivered to the brain through extracellular vesicles, improving depression-like behaviors. | ||||
| Biomarker | miR-146a | Full name | MicroRNA-146a | Molecular Type | Non-coding RNA |
| Molecular Formula | / | Molecular Weight | / | Core Functional Dimensions | Disease Monitoring, Prognosis |
| Disease(or Constitution) | Depression | Disease Subtypes | Major Depressive Disorder (MDD), Responsive Depression | ||
| Organ | Brain | Test Sample / Technology Platform | Plasma Extracellular Vesicles (Quantitative Real-Time PCR qRT-PCR) | ||
| Pathobiological Mechanisms | Downregulates the expression of pro-inflammatory factors (IL-6/TNF-α), regulates neuroinflammatory responses, and improves synaptic plasticity. | ||||
| Clinical Availability Status | Research Stage | ||||
| Notes and Dynamics | Expression is upregulated 1.8-fold after 4 weeks of antidepressant treatment, and can predict treatment response. | ||||
| Biomarker | TRP/KYN | Full name | Tryptophan/Kynurenine Ratio | Molecular Type | Amino Acid Metabolite |
| Molecular Formula | C11H12N2O2/C10H12N2O3 | Molecular Weight | 204.23/208.21 g/mol | Core Functional Dimensions | Pathological Confirmation, Etiological Confirmation |
| Disease(or Constitution) | Depression | Disease Subtypes | Inflammatory Depression, Chronic Depression | ||
| Organ | Brain | Test Sample / Technology Platform | Plasma (LC-MS, High-Performance Liquid Chromatography HPLC) | ||
| Pathobiological Mechanisms | Inflammation-induced elevation of IDO/TDO enzyme activity shifts tryptophan metabolism toward the kynurenine pathway, leading to accumulation of the neurotoxic QUINA. | ||||
| Clinical Availability Status | Research Validation Stage | ||||
| Notes and Dynamics | A ratio <20 indicates inflammation activation, associated with impaired executive function in depression patients (increased error rate in WCST). | ||||