Adenosine-Astrocyte Metabolic Reset
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From Analysis:
Sleep disruption as cause and consequence of neurodegeneration
Sleep disruption as cause and consequence of neurodegeneration
Hypotheses from Same Analysis (6)
These hypotheses emerged from the same multi-agent debate that produced this hypothesis.
Description
Molecular Mechanism and Rationale
The molecular underpinnings of adenosine A2A receptor (ADORA2A) modulation in astrocytic metabolism represent a sophisticated interplay of cellular signaling, metabolic regulation, and neuroenergetic optimization. At the core of this hypothesis lies a complex molecular mechanism that integrates multiple cellular processes through a nuanced receptor-mediated signaling cascade.
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✓ Supporting Evidence 14
Species richness of marine mammals and birds is highest in cold, temperate seas-a conspicuous exception to the general latitudinal gradient of decreasing diversity from the tropics to the poles. We compiled a comprehensive dataset for 998 species of sharks, fish, reptiles, mammals, and birds to identify and quantify inverse latitudinal gradients in diversity, and derived a theory to explain these patterns. We found that richness, phylogenetic diversity, and abundance of marine predators diverge systematically with thermoregulatory strategy and water temperature, reflecting metabolic differences between endotherms and ectotherms that drive trophic and competitive interactions. Spatial patterns of foraging support theoretical predictions, with total prey consumption by mammals increasing by a factor of 80 from the equator to the poles after controlling for productivity.
Hair cells of the inner ear are essential for hearing and balance. As a consequence, pathogenic variants in genes specifically expressed in hair cells often cause hereditary deafness. Hair cells are few in number and not easily isolated from the adjacent supporting cells, so the biochemistry and molecular biology of hair cells can be difficult to study. To study gene expression in hair cells, we developed a protocol for hair cell isolation by FACS. With nearly pure hair cells and surrounding cells, from cochlea and utricle and from E16 to P7, we performed a comprehensive cell type-specific RNA-Seq study of gene expression during mouse inner ear development. Expression profiling revealed new hair cell genes with distinct expression patterns: some are specific for vestibular hair cells, others for cochlear hair cells, and some are expressed just before or after maturation of mechanosensitivity. We found that many of the known hereditary deafness genes are much more highly expressed in ha
Differences between individual human genomes, or between human and cancer genomes, range in scale from single nucleotide variants (SNVs) through intermediate and large-scale duplications, deletions, and rearrangements of genomic segments. The latter class, called structural variants (SVs), have received considerable attention in the past several years as they are a previously under appreciated source of variation in human genomes. Much of this recent attention is the result of the availability of higher-resolution technologies for measuring these variants, including both microarray-based techniques, and more recently, high-throughput DNA sequencing. We describe the genomic technologies and computational techniques currently used to measure SVs, focusing on applications in human and cancer genomics.
Sepsis expands a CD39(+) plasmablast population that promotes immunosuppression via adenosine-mediated inhibit… MEDIUM▼
Sepsis results in elevated adenosine in circulation. Extracellular adenosine triggers immunosuppressive signaling via the A2a receptor (A2aR). Sepsis survivors develop persistent immunosuppression with increased risk of recurrent infections. We utilized the cecal ligation and puncture (CLP) model of sepsis and subsequent infection to assess the role of adenosine in post-sepsis immune suppression. A2aR-deficient mice showed improved resistance to post-sepsis infections. Sepsis expanded a subset of CD39hi B cells and elevated extracellular adenosine, which was absent in mice lacking CD39-expressing B cells. Sepsis-surviving B cell-deficient mice were more resistant to secondary infections. Mechanistically, metabolic reprogramming of septic B cells increased production of ATP, which was converted into adenosine by CD39 on plasmablasts. Adenosine signaling via A2aR impaired macrophage bactericidal activity and enhanced interleukin-10 production. Septic individuals exhibited expanded CD39hi
Endothelial adenosine receptor 2A loss alleviates diabetic vascular calcification by blocking CREB1-SNAI1-driv… MEDIUM▼
Vascular calcification (VC), a common complication associated with diabetes mellitus (DM), substantially increases the risk of cardiovascular diseases and is associated with elevated mortality in individuals with DM. Endothelial-to-mesenchymal transition (EndMT) imparts phenotypic plasticity to vascular endothelial cells (VECs), granting them the potential for osteogenic differentiation, which is a crucial mechanism in regulating VC. Notably, adenosine-ADORA2A-mediated endothelial dysfunction plays a pivotal regulatory role in cardiovascular diseases. However, the specific role of endothelial ADORA2A in diabetic VC remains to be elucidated. In this study, we found that ADORA2A was upregulated in the endothelium of diabetic mice and cultured human aortic endothelial cells (HAECs) with high glucose treatment. Deletion of endothelial Adora2a or pharmacologic inhibition of ADORA2A with KW6002 attenuated EndMT, osteogenic differentiation, and calcium deposit in diabetic aortas of Ins2Akita/
Targeting adenosine 2A receptor signaling suppresses vascular calcification by restraining smooth muscle osteo… MEDIUM▼
Vascular calcification (VC) is a major contributor to cardiovascular morbidity and mortality, particularly in patients with chronic kidney disease (CKD). Adenosine 2 A receptor (ADORA2A) is highly expressed in vascular cells and implicated in cardiovascular disease; however, its specific role in VC pathogenesis remains unclear. Here, we investigated the role of ADORA2A using in vitro (vascular smooth muscle cells; VSMCs), ex vivo (mouse aortic rings), and in vivo (5/6th nephrectomy with high phosphate and cholecalciferol) models of VC. The ADORA2A expression was significantly upregulated in calcified human and murine aortic tissues, as well as in VSMCs, under osteogenic conditions. Genetic deletion of Adora2a (global or VSMC-specific) or pharmacological antagonism of ADORA2A markedly attenuated aortic calcification and the expression of osteogenic markers in vivo. Consistent findings were observed in in vitro and ex vivo models. Conversely, ADORA2A overexpression exacerbated the osteog
Adenosine 2A receptor-dependent activation of AMPK represses T(H)17 cell pathogenicity through epigenetic and … MEDIUM▼
Metabolic reprogramming controls protective and pathogenic T helper 17 (TH17) cell responses. When naïve T cells are differentiated into TH17 cells in vitro, the presence of the cytokine activin A promotes their maturation into a nonpathogenic state. Here, we found that nonpathogenic TH17 cells induced by activin A displayed reduced aerobic glycolysis and increased oxidative phosphorylation (OXPHOS). In response to activin A, signaling through the adenosine A2A receptor (A2AR) and AMP-activated protein kinase (AMPK) enhanced OXPHOS and reprogrammed pathogenic TH17 cells toward nonpathogenic states that did not induce central nervous system autoimmunity in a mouse model of multiple sclerosis. In pathogenic TH17 cells, the transcriptional coactivator p300/CBP-associated factor (PCAF) increased acetylation at histone 3 Lys9 (H3K9ac) of genes involved in aerobic glycolysis and TH17 pathogenic programs. In contrast, in nonpathogenic activin A-treated TH17 cells, AMPK signaling suppressed PC
Transcriptional control of pancreatic cancer immunosuppression by metabolic enzyme CD73 in a tumor-autonomous … MEDIUM▼
Cancer cell metabolism contributes to the establishment of an immunosuppressive tumor microenvironment. Aberrant expression of CD73, a critical enzyme in ATP metabolism, on the cell surface results in the extracellular accumulation of adenosine, which exhibits direct inhibitory effects on tumor-infiltrating lymphocytes. However, little is known about the influence of CD73 on negative immune regulation-associated signaling molecules and transduction pathways inside tumor cells. This study aims to demonstrate the moonlighting functions of CD73 in immunosuppression in pancreatic cancer, an ideal model characterized by complex crosstalk among cancer metabolism, immune microenvironment, and immunotherapeutic resistance. The synergistic effect of CD73-specific drugs in combination with immune checkpoint blockade is observed in multiple pancreatic cancer models. Cytometry by time-of-flight analysis shows that CD73 inhibition reduces tumor-infiltrating Tregs in pancreatic cancer. Tumor cell-au
BACKGROUND: Methamphetamine (METH) abuse often results in persistent depressive-like behaviors, while current treatments show limited efficacy. Parthenolide, a natural compound with neuroprotective and anti-inflammatory properties, has shown benefits in several CNS disorders, but its role in METH-induced depression remains unknown. PURPOSE: This study aimed to evaluate whether parthenolide alleviates METH-induced depressive-like behaviors and to identify key brain regions and molecular targets involved. METHODS: Mice were administered METH using a 15-day escalating regimen and treated with parthenolide. Behavioral tests, histopathology, Nissl staining, and c-Fos mapping were conducted to assess neural alterations. Metabolomics and network pharmacology were used to predict targets, followed by molecular docking, dynamics simulations, cellular thermal shift assay, and pharmacological modulation for validation. RESULTS: Parthenolide significantly improved METH-induced depressive-like beha
Sepsis is characterized by profound immunometabolic dysregulation, yet the role of purine precursor synthesis in immune reprogramming remains poorly defined. Intracellular purine nucleotides, such as ATP, are generated by de novo synthesis, which assembles purinosomes to build inosine monophosphate (IMP) from small precursors, or by the salvage pathway, which recycles purine bases such as hypoxanthine. Here, we investigated how these pathways regulate macrophage activation and host responses in sepsis. Silencing the de novo purine enzyme glycinamide ribonucleotide transformylase (GART) in LPS-stimulated macrophages induced marked transcriptomic remodeling, suppressing anti-inflammatory mediators, including IL-10 and TIMP-1, while increasing TNF-α. These effects were reversed by hypoxanthine supplementation, indicating rescue through salvage. Similar findings were observed with silencing of phosphoribosyl pyrophosphate amidotransferase (PPAT) or pharmacological GART inhibition with azas
Surface d-Band Modulation via Biodirected Mineralization Enables Nanoenzymes to Inhibit Radiation-Induced T-Ce… MEDIUM▼
Immunoradiotherapy (iRT) has emerged as a promising strategy for liver hepatocellular carcinoma (LIHC) treatment to synergistically activate both localized antitumor immunity and systemic immune responses. However, radiation will aggravate LIHC hypoxia, resulting in an adenosine metabolism level elevation, which promotes the differentiation of T cells into terminally exhausted phenotypes and weakens the efficacy of immunotherapy. To overcome this challenge, we engineered a nanocatalytic probiotic-based radiation-metabolic modulator, in which Escherichia coli Nissle 1917 (EcN) was programmed to in situ synthesize gold-palladium bimetallic nanocatalysts (EcNcGP) via biodirected mineralization. Guided by lattice mismatch and interfacial strain engineering, engineered EcN orchestrates the epitaxial assembly of Au atoms on Pd nanoclusters, yielding a precisely strain-tuned heterostructure with a modulated d-band electronic structure. This architectural design optimizes oxygen intermediate a
Research demonstrates inhibition of retinal AdoRA2a activity, which aligns with the hypothesis's focus on ADOR… MEDIUM▼
Although 7-methylxanthine, a nonselective adenosine receptor (AdoRs) antagonist, suppresses myopia, the specific receptor subtype and target tissue involved remain unclear. This study aimed to investigate whether the AdoRA2a subtype plays a critical role in the regulation of myopia progression. Monocular form deprivation myopia (FDM) was induced in mice to measure retinal concentrations of adenosine and its synthetic enzymes (CD39/CD73). Retina-specific AdoRA2a knockout (AdoRA2a-CKO) mice and th
High-throughput screening for antidepressants targeting adenosine A(2A) receptors directly supports the hypoth… MEDIUM▼
The adenosine A2A receptor (A2AR) is a promising therapeutic target for depression, as evidenced by the notable antidepressant-like efficacy of its antagonists. However, conventional screening methods for A2AR ligands are hampered by low throughput and operational complexity. To address this, we developed a high-throughput screening (HTS) strategy based on the detection of calcium flow fluorescence signals in engineered HEK-ADORA2A cells. After rigorous optimization, this HTS platform was deploy
Explores caffeine's mechanisms of action involving adenosine receptors, which relates to the hypothesis's mole… MEDIUM▼
Ergogenic aids have long attracted scientific interest for their potential to enhance neuromuscular performance, with caffeine being among the most extensively studied. While traditionally attributed to peripheral actions on skeletal muscle, accumulating evidence indicates that, at physiological doses, caffeine's ergogenic effects are predominantly mediated by antagonism of central adenosine receptors. This antagonism leads to increased arousal, reduced inhibitory neuromodulation, enhanced corti
✗ Opposing Evidence 9
More than 3000 per- and polyfluoroalkyl substances (PFASs) are, or have been, on the global market, yet most research and regulation continues to focus on a limited selection of rather well-known long-chain PFASs, particularly perfluorooctanesulfonate (PFOS), perfluorooctanoic acid (PFOA) and their precursors. Continuing to overlook the vast majority of other PFASs is a major concern for society. We provide recommendations for how to proceed with research and cooperation to tackle the vast number of PFASs on the market and in the environment.
Caffeine causes most of its biological effects via antagonizing all types of adenosine receptors (ARs): A1, A2A, A3, and A2B and, as does adenosine, exerts effects on neurons and glial cells of all brain areas. In consequence, caffeine, when acting as an AR antagonist, is doing the opposite of activation of adenosine receptors due to removal of endogenous adenosinergic tonus. Besides AR antagonism, xanthines, including caffeine, have other biological actions: they inhibit phosphodiesterases (PDEs) (e.g., PDE1, PDE4, PDE5), promote calcium release from intracellular stores, and interfere with GABA-A receptors. Caffeine, through antagonism of ARs, affects brain functions such as sleep, cognition, learning, and memory, and modifies brain dysfunctions and diseases: Alzheimer's disease, Parkinson's disease, Huntington's disease, Epilepsy, Pain/Migraine, Depression, Schizophrenia. In conclusion, targeting approaches that involve ARs will enhance the possibilities to correct brain dysfunction
Caenorhabditis elegans is an animal with few cells but a wide diversity of cell types. In this study, we characterize the molecular basis for their specification by profiling the transcriptomes of 86,024 single embryonic cells. We identify 502 terminal and preterminal cell types, mapping most single-cell transcriptomes to their exact position in C. elegans' invariant lineage. Using these annotations, we find that (i) the correlation between a cell's lineage and its transcriptome increases from middle to late gastrulation, then falls substantially as cells in the nervous system and pharynx adopt their terminal fates; (ii) multilineage priming contributes to the differentiation of sister cells at dozens of lineage branches; and (iii) most distinct lineages that produce the same anatomical cell type converge to a homogenous transcriptomic state.
Hair cells of the inner ear are essential for hearing and balance. As a consequence, pathogenic variants in genes specifically expressed in hair cells often cause hereditary deafness. Hair cells are few in number and not easily isolated from the adjacent supporting cells, so the biochemistry and molecular biology of hair cells can be difficult to study. To study gene expression in hair cells, we developed a protocol for hair cell isolation by FACS. With nearly pure hair cells and surrounding cells, from cochlea and utricle and from E16 to P7, we performed a comprehensive cell type-specific RNA-Seq study of gene expression during mouse inner ear development. Expression profiling revealed new hair cell genes with distinct expression patterns: some are specific for vestibular hair cells, others for cochlear hair cells, and some are expressed just before or after maturation of mechanosensitivity. We found that many of the known hereditary deafness genes are much more highly expressed in ha
Intestinal microbiota: A potential target for enhancing the antitumor efficacy and reducing the toxicity of im… MEDIUM▼
Accumulating evidence suggests that the intestinal microbiota is associated with the antitumor efficacy of immune checkpoint inhibitors (ICIs) and the occurrence of immune-related adverse events (irAEs) following ICI treatment. However, the mechanisms underlying these interactions remain unclear. Recent technological advances have allowed more extensive investigation into the interplay between the intestinal microbiota and the tumor immune microenvironment. Breakthroughs by two research groups revealed that Bifidobacterium enhanced the efficacy of ICIs via the stimulator of interferon genes (STING) and adenosine 2A receptor (A2AR) signaling pathways, highlighting the molecular mechanisms through which the intestinal microbiota modulates immunotherapy. In this review, we summarize recent findings related to the potential role and mechanisms of the gut microbiota in ICI therapy, available microbiota-targeting strategies, and ongoing clinical trials. Further we discuss the associated chal
Pharmacogenetics and induction/consolidation therapy toxicities in acute lymphoblastic leukemia patients treat… MEDIUM▼
Drug-related toxicities represent an important clinical concern in chemotherapy, genetic variants could help tailoring treatment to patient. A pharmacogenetic multicentric study was performed on 508 pediatric acute lymphoblastic leukemia patients treated with AIEOP-BFM 2000 protocol: 28 variants were genotyped by VeraCode and Taqman technologies, deletions of GST-M1 and GST-T1 by multiplex PCR. Toxicities were derived from a central database: 251 patients (49.4%) experienced at least one gastroi
Cord blood gene expression supports that prenatal exposure to perfluoroalkyl substances causes depressed immun… MEDIUM▼
Perfluoroalkyl and polyfluoroalkyl substances (PFAS) are a class of synthetic compounds that have widespread use in consumer and industrial applications. PFAS are considered environmental pollutants that have various toxic properties, including effects on the immune system. Recent human studies indicate that prenatal exposure to PFAS leads to suppressed immune responses in early childhood. In this study, data from the Norwegian BraMat cohort was used to investigate transcriptomics profiles in ne
Hypercholesterolaemia plays a crucial role in the development of atherosclerotic diseases in general and coronary heart disease in particular. The risk of progression of the atherosclerotic process to coronary heart disease increases progressively with increasing levels of total serum cholesterol or low density lipoprotein (LDL) cholesterol at both the individual and the population level. The statins are reversible inhibitors of the microsomal enzyme HMG-CoA reductase, which converts HMG-CoA to
The integration of pharmacophore-based 3D QSAR modeling and virtual screening in safety profiling: A case stud… MEDIUM▼
Safety pharmacology screening against a wide range of unintended vital targets using in vitro assays is crucial to understand off-target interactions with drug candidates. With the increasing demand for in vitro assays, ligand- and structure-based virtual screening approaches have been evaluated for potential utilization in safety profiling. Although ligand based approaches have been actively applied in retrospective analysis or prospectively within well-defined chemical space during the early d
🧬 Theorist Proposes novel mechanisms and generates creative hypotheses ▼
Novel Therapeutic Hypotheses: Sleep-Neurodegeneration Interface
1. Circadian Glymphatic Rescue Therapy
Description: Pharmacological enhancement of aquaporin-4 polarization and melatonin signaling could restore sleep-dependent glymphatic clearance of protein aggregates. This approach would target the circadian regulation of cerebrospinal fluid flow to prevent accumulation of amyloid-β and tau proteins during critical sleep phases.Target: AQP4 (Aquaporin-4) and MTNR1A/1B (Melatonin receptors)
Supporting Evidence: Glymphatic system activity increases dramatically during sleep
🔍 Skeptic Identifies weaknesses, alternative explanations, and methodological concerns ▼
Critical Evaluation of Sleep-Neurodegeneration Therapeutic Hypotheses
1. Circadian Glymphatic Rescue Therapy
Major Weaknesses:
- Translation barrier: Most glymphatic evidence comes from rodent models with uncertain human relevance (PMID:30962395)
- AQP4 targeting specificity: No established methods for selective CNS AQP4 enhancement without systemic effects
- Oversimplified mechanism: Assumes AQP4 polarization is solely rate-limiting for clearance
- Human glymphatic function shows minimal circadian variation compared to rodents (PMID:30962395)
- AQ
🎯 Domain Expert Assesses practical feasibility, druggability, and clinical translation ▼
Practical Feasibility Assessment: Sleep-Neurodegeneration Therapeutics
1. Circadian Glymphatic Rescue Therapy
Revised Confidence: 0.45Druggability Assessment
AQP4: Extremely challenging. No selective small molecule modulators exist. Protein is a water channel with limited allosteric sites. MTNR1A/1B: Highly druggable GPCRs with established pharmacology.Chemical Matter & Existing Compounds
- Melatonin receptor agonists: Ramelteon (Rozerem®), Tasimelteon (Hetlioz®), Agomelatine (Valdoxan®)
- AQP4 modulators: None clinically viable. TGN-020 (research tool, po
⚖ Synthesizer Integrates perspectives and produces final ranked assessments ▼
Price History
| Event | Price | Change | Source | Time | |
|---|---|---|---|---|---|
| ⚖ | Recalibrated | $0.557 | ▼ 0.2% | 2026-04-12 10:15 | |
| ⚖ | Recalibrated | $0.559 | ▼ 1.5% | 2026-04-12 05:13 | |
| ⚖ | Recalibrated | $0.567 | ▼ 0.5% | 2026-04-10 15:58 | |
| ⚖ | Recalibrated | $0.570 | ▲ 0.6% | 2026-04-10 15:53 | |
| ⚖ | Recalibrated | $0.567 | ▲ 0.5% | 2026-04-08 18:39 | |
| ⚖ | Recalibrated | $0.564 | ▲ 4.8% | 2026-04-06 04:04 | |
| ⚖ | Recalibrated | $0.538 | ▼ 2.2% | 2026-04-04 16:38 | |
| ⚖ | Recalibrated | $0.550 | ▲ 1.8% | 2026-04-04 16:02 | |
| 📄 | New Evidence | $0.540 | ▲ 0.6% | evidence_batch_update | 2026-04-04 09:08 |
| ⚖ | Recalibrated | $0.537 | ▼ 23.2% | 2026-04-03 23:46 | |
| ⚖ | Recalibrated | $0.699 | ▲ 5.1% | market_dynamics | 2026-04-03 01:06 |
| 📄 | New Evidence | $0.665 | ▲ 1.1% | evidence_batch_update | 2026-04-03 01:06 |
| ⚖ | Recalibrated | $0.658 | ▲ 16.0% | market_dynamics | 2026-04-03 01:06 |
| ⚖ | Recalibrated | $0.567 | ▲ 9.2% | 2026-04-02 21:55 | |
| ⚖ | Recalibrated | $0.519 | ▼ 10.0% | market_recalibrate | 2026-04-02 19:14 |
Clinical Trials (10) Relevance: 53%
Active
Completed
Total Enrolled
Highest Phase
📚 Cited Papers (41)
📓 Linked Notebooks (1)
Wiki Pages
KG Entities (44)
Linked Experiments (4)
Related Hypotheses
Estimated Development
🧪 Falsifiable Predictions (21)
Knowledge Subgraph (192 edges)
associated with (4)
causes (1)
co associated with (21)
generates (1)
implicated in (7)
mediates (1)
participates in (6)
promoted: Adenosine-Astrocyte Metabolic Reset (1)
regulates (1)
Mechanism Pathway for ADORA2A
Molecular pathway showing key causal relationships underlying this hypothesis
graph TD
ADORA2A["ADORA2A"] -->|regulates| adenosine_metabolism["adenosine_metabolism"]
ADORA2A_1["ADORA2A"] -->|associated with| neurodegeneration["neurodegeneration"]
ADORA2A_2["ADORA2A"] -->|promoted: Adenosin| neurodegeneration_3["neurodegeneration"]
ADORA2A_4["ADORA2A"] -->|participates in| Astrocyte_reactivity_sign["Astrocyte reactivity signaling"]
BMAL1["BMAL1"] -->|co discussed| ADORA2A_5["ADORA2A"]
HCRTR2["HCRTR2"] -->|co discussed| ADORA2A_6["ADORA2A"]
CLOCK["CLOCK"] -->|co discussed| ADORA2A_7["ADORA2A"]
BDNF["BDNF"] -->|co discussed| ADORA2A_8["ADORA2A"]
AQP4["AQP4"] -->|co discussed| ADORA2A_9["ADORA2A"]
MTNR1A["MTNR1A"] -->|co discussed| ADORA2A_10["ADORA2A"]
CX3CR1["CX3CR1"] -->|co discussed| ADORA2A_11["ADORA2A"]
HCRT["HCRT"] -->|co discussed| ADORA2A_12["ADORA2A"]
CACNA1G["CACNA1G"] -->|co discussed| ADORA2A_13["ADORA2A"]
ADORA2A_14["ADORA2A"] -->|co discussed| ADRA2A["ADRA2A"]
ADRA2A_15["ADRA2A"] -->|co discussed| ADORA2A_16["ADORA2A"]
style ADORA2A fill:#ce93d8,stroke:#333,color:#000
style adenosine_metabolism fill:#81c784,stroke:#333,color:#000
style ADORA2A_1 fill:#ce93d8,stroke:#333,color:#000
style neurodegeneration fill:#ef5350,stroke:#333,color:#000
style ADORA2A_2 fill:#ce93d8,stroke:#333,color:#000
style neurodegeneration_3 fill:#ef5350,stroke:#333,color:#000
style ADORA2A_4 fill:#ce93d8,stroke:#333,color:#000
style Astrocyte_reactivity_sign fill:#81c784,stroke:#333,color:#000
style BMAL1 fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_5 fill:#ce93d8,stroke:#333,color:#000
style HCRTR2 fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_6 fill:#ce93d8,stroke:#333,color:#000
style CLOCK fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_7 fill:#ce93d8,stroke:#333,color:#000
style BDNF fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_8 fill:#ce93d8,stroke:#333,color:#000
style AQP4 fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_9 fill:#ce93d8,stroke:#333,color:#000
style MTNR1A fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_10 fill:#ce93d8,stroke:#333,color:#000
style CX3CR1 fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_11 fill:#ce93d8,stroke:#333,color:#000
style HCRT fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_12 fill:#ce93d8,stroke:#333,color:#000
style CACNA1G fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_13 fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_14 fill:#ce93d8,stroke:#333,color:#000
style ADRA2A fill:#ce93d8,stroke:#333,color:#000
style ADRA2A_15 fill:#ce93d8,stroke:#333,color:#000
style ADORA2A_16 fill:#ce93d8,stroke:#333,color:#000
3D Protein Structure
🧬 ADORA2A — PDB 4EIY Click to expand 3D viewer
Source Analysis
Sleep disruption as cause and consequence of neurodegeneration
neurodegeneration | 2026-04-01 | completed