Using Transcriptome AI for Disease Characterization and Treatment Options

Understanding Fibromyalgia?

Fibromyalgia is a complex condition characterized by chronic widespread pain, fatigue, and other symptoms. It is considered a disorder of the central nervous system that affects the way the brain processes pain signals. Fibromyalgia is a relatively common condition in the United States. According to estimates from the Centers for Disease Control and Prevention (CDC), approximately 4 million adults, or about 2% of the adult population, are diagnosed with fibromyalgia. However, it’s worth noting that due to the varied and sometimes overlapping symptoms of the condition, it can be challenging to accurately diagnose and track its prevalence. Additionally, fibromyalgia is more common in women than men, with women accounting for about 80-90% of diagnosed cases.

How Can Transcriptome AI Analysis be Beneficial for Addressing Fibromyalgia?

Transcriptome AI analysis can contribute to the development of personalized treatment strategies for fibromyalgia patients. By analyzing individual gene expression profiles, we can gain insights into the unique molecular characteristics of each patient’s condition. This information can assist in tailoring treatment plans and selecting therapies that are effective for each individual.

Rheumatoid Arthritis
Systemic Lupus Erythematosus
Fibromyalgia
Multiple Sclerosis
Crohn’s Disease
Myasthenia Gravis
Obesity Metabolic Syndrome
Polymyalgia Rheumatica
Polymyositis
Hashimoto’s Thyroiditis
Behcet’s Disease
Sjogren’s Syndrome
Dermatomyositis
Systemic Sclerosis
IBS
Chronic Fatigue Syndrome (CFS)
IgG4-Related Disease
Celiac Disease
Ankylosing Spondylitis
Graves’ Disease
Psoriatic Arthritis
Autoimmune Hepatitis
Guillain-Barre Syndrome
Mast Cell Activation Syndrome
Hypothyroidism Small Fiber Neuropathy
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
Amyloidosis, Lichen Planus
Pernicious Anemia
Antiphospholipid Syndrome
Vitiligo
Fibrosing Alveolitis
Chronic Inflammatory Arthropathy
Type 1 Diabetes
Uveitis
Alopecia Areata
Chronic Lyme Disease
Interstitial Cystitis
Pemphigus
Autoimmune Inner Ear Disease (AIED)
Polyarteritis Nodosa
Autoimmune thrombocytopenic purpura (ITP)
Wegener’s Granulomatosis
Goodpasture’s Syndrome
Temporal Arteritis
Ehlers-Danlos Syndrome
CREST Syndrome
Churg Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis)
Vasculitis
Primary Biliary Cholangitis (PBC)
Primary Sclerosing Cholangitis (PSC)
POTS (Postural Orthostatic Tachycardia Syndrome)
Polychondritis
Autoimmune Pancreatitis.

Fibromyalgia Pipeline

BIOMARKERS • PATHWAYS • DISEASE RELATED TREATMENT

Rheumatoid Arthritis, Systemic Lupus Erythematosus, Fibromyalgia, Multiple Sclerosis, Crohn’s Disease, Myasthenia Gravis, Obesity Metabolic Syndrome, Polymyalgia Rheumatica, Polymyositis, Hashimoto’s Thyroiditis, Behcet’s Disease, Sjogren’s Syndrome, Dermatomyositis, Systemic Sclerosis, IBS, Chronic Fatigue Syndrome (CFS), IgG4-Related Disease, Celiac Disease, Ankylosing Spondylitis, Graves’ Disease, Psoriatic Arthritis, Autoimmune Hepatitis, Guillain-Barre Syndrome, Mast Cell Activation Syndrome, Hypothyroidism, Small Fiber Neuropathy, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Amyloidosis, Lichen Planus, Pernicious Anemia, Antiphospholipid Syndrome, Vitiligo, Fibrosing Alveolitis, Chronic Inflammatory Arthropathy, Type 1 Diabetes, Uveitis, Alopecia Areata, Chronic Lyme Disease, Interstitial Cystitis, Pemphigus, Autoimmune Inner Ear Disease (AIED), Polyarteritis Nodosa, Autoimmune thrombocytopenic purpura (ITP), Wegener’s Granulomatosis, Goodpasture’s Syndrome, Temporal Arteritis, Ehlers-Danlos Syndrome, CREST Syndrome, Churg Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis), Vasculitis, Primary Biliary Cholangitis (PBC), Primary Sclerosing Cholangitis (PSC), POTS (Postural Orthostatic Tachycardia Syndrome), Polychondritis, Autoimmune Pancreatitis.

Strategy

CATEGORIZE TREATMENR • PRECISE TREATMENT OPTIONS • TREATMENT MONITORING • ADVERSE SIDE EFFECTS PREDICTION

• Simple Blood Draw of less than 4 ml
• Via F420 Draw Station Centers
• Fibromyalgia Testing Kit Distribution (F420 Kit)
• Immune cells circulating in blood are early responders to various biological triggers
• mRNA in the immune cells provide a unique map of gene and biological activity
• Full Tanscriptome analysis of mRNA by NGS Sequencing reveals the status of the immune system and the host-response
• Al-Based algorithm of Transcriptome profiling – Analysis – Bioinformatics
• Report within 7 business days or less

• Transcriptome profiling – analysis interpretation to help Categorize the Illness, help find the best Precise Treatment Options, Treatment Monitoring, and Predict Adverse Side Effects.
• Subscription, one time testing, or 4 times testing every 3 months plan or per request any time (recommended), 6 times or more based on case circumstances.
• No Physician order is required.
• Consultation with our Ayass Research Institute Team is available in person or via Teleconference.

18,000 Transcriptome Gene Tested

Expression Patterns and Molecular Pathways involved in Fibromyalgia

1. Neurotransmitter Signaling Pathways:
– Serotonin signaling pathway
– Dopamine signaling pathway
– Norepinephrine signaling pathway
– Glutamate signaling pathway
– GABA signaling pathway
2. Ion Channel Function:
– Voltage-gated sodium channels
– Voltage-gated potassium channels
– Calcium channels
– TRP (transient receptor potential) channels
3. Neuronal Receptors and Signaling Pathways:
– Opioid receptor signaling pathway
– Cannabinoid receptor signaling pathway
– G-protein-coupled receptor signaling pathways
– MAPK (mitogen-activated protein kinase) signaling pathway
– CREB (cAMP response element-binding protein) signaling pathway
4. Neuropeptides and Neuromodulators:
– Substance P signaling pathway
– Calcitonin gene-related peptide (CGRP) signaling pathway
– Endogenous opioid signaling pathway
– Neurokinin signaling pathway

1. Pro-inflammatory Cytokine Signaling Pathways:
– Nuclear factor-kappa B (NF-κB) signaling pathway
– Interleukin-6 (IL-6) signaling pathway
– Tumor necrosis factor-alpha (TNF-α) signaling pathway
2. Chemokine Signaling Pathways:
– C-C chemokine receptor signaling pathway
– C-X-C chemokine receptor signaling pathway
3. Toll-like Receptor (TLR) Signaling Pathways:
– TLR4 signaling pathway
– TLR7/8 signaling pathway
4. Interferon Signaling Pathways:
– Type I interferon signaling pathway
– Interferon-gamma (IFN-γ) signaling pathway
5. Complement System Pathway
6. MAPK Signaling Pathway:
– Extracellular signal-regulated kinase (ERK) pathway
– p38 MAPK pathway
– c-Jun N-terminal kinase (JNK) pathway
7. Phosphoinositide 3-kinase (PI3K)/Akt Signaling Pathway
8. Nuclear Factor Erythroid 2-related Factor 2 (Nrf2) Pathway
9. Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) Signaling Pathway
10. Nuclear Factor-kappa B (NF-κB) Signaling Pathway:
– NF-κB transcription factor complex activation
– NF-κB target gene expression regulation
11. JAK-STAT Pathway:
– Janus Kinase (JAK) family of protein kinases activation
– Signal Transducer and Activator of Transcription (STAT) proteins phosphorylation and activation
– STAT-mediated gene transcription
12. Interleukin Signaling Pathways:
– Signal transduction pathways activated by interleukins such as IL-1, IL-4, and IL-17
– IL receptor binding, leading to downstream signaling events
13. Transforming Growth Factor-beta (TGF-β) Signaling Pathway:
– TGF-β receptor activation and subsequent signaling events
– Regulation of cell differentiation, proliferation, and immune responses
14. Nuclear Factor-E2-Related Factor 2 (Nrf2) Pathway:
– Activation of Nrf2 transcription factor
– Nrf2-mediated antioxidant response and cellular defense against oxidative stress
15. Reactive Oxygen Species (ROS) Pathway:
– Differentially expressed genes involved in ROS generation and scavenging
– Oxidative stress-related gene expression modulation
16. HIF-1 (Hypoxia Inducible Factor-1) Signaling Pathway:
– Activation of HIF-1 transcription factor under hypoxic conditions
17. NLRP3 Inflammasome Pathway:
– Activation of the NLRP3 inflammasome, leading to the processing and release of pro-inflammatory cytokines IL-1β and IL-18.
18. Interleukin-10 (IL-10) Signaling Pathway:
– IL-10 receptor binding and downstream signaling events
– Regulation of immune responses and inflammation
19. B Cell Receptor (BCR) Signaling Pathway:
– Activation of B cells and their signaling cascade upon recognition of antigens
– Implication in antibody production and immune response modulation
20. Major Histocompatibility Complex (MHC) Class II Pathway:
– Genes involved in MHC class II antigen presentation and immune cell activation
– Regulation of adaptive immune responses
21. NFAT (Nuclear Factor of Activated T cells) Signaling Pathway:
– Activation of NFAT transcription factors and subsequent gene expression changes
– Contribution to immune cell activation and inflammation
22. ERK/MAPK (Extracellular Signal-Regulated Kinase/Mitogen-Activated Protein Kinase) Cascade:
– Activation of MAPK signaling pathway components, including ERK1/2
– Regulation of gene expression involved in immune responses and inflammation
23. TGF-β/BMP (Transforming Growth Factor-beta/Bone Morphogenetic Protein) Signaling Pathway:
– Signaling events downstream of TGF-β and BMP receptors
– Modulation of cell growth, differentiation, and immune responses
24. Interferon Regulatory Factor (IRF) Signaling Pathway:
– Activation of IRF transcription factors and subsequent gene expression changes
– Regulation of interferon-mediated immune responses
25. Th17 (T-helper 17) Cell Differentiation Pathway:
– Differentiation of CD4+ T cells into Th17 cells
– Production of IL-17 and other pro-inflammatory cytokines
26. IL-23/IL-17 Signaling Pathway:
– Activation of IL-23 receptor and downstream signaling events
– Induction of IL-17 production and promotion of inflammatory responses
27. TLR (Toll-like Receptor) Signaling Pathway:
– Activation of TLRs by pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs)
– Induction of pro-inflammatory cytokines and immune responses
28. Apoptosis Signaling Pathway:
– Gene expression changes in apoptotic signaling components
– Dysregulation of cell death and survival mechanisms in immune cells
29. Leukocyte Trafficking Pathways:
– Genes involved in leukocyte adhesion, extravasation, and migration
– Regulation of immune cell recruitment and infiltration at sites of inflammation
30. Nucleotide-Binding Oligomerization Domain (NOD)-Like Receptor Signaling Pathway:
– Activation of NOD-like receptors and downstream signaling events
– Modulation of inflammatory responses and cytokine production
31. Autophagy Pathway:
– Regulation of autophagy-related genes involved in cellular homeostasis and clearance of damaged cellular components
– Dysregulation of autophagy in immune cells and its impact on inflammation
32. Nuclear Factor of Activated T-cell (NFAT) Signaling Pathway:
– Activation of NFAT transcription factors and subsequent modulation of gene expression
– Involvement in immune cell activation, proliferation, and cytokine production
33. Interleukin-1 (IL-1) Signaling Pathway:
– Activation of IL-1 receptors and downstream signaling events
– Implication in immune responses, inflammation, and pain modulation
34. Toll-like Receptor (TLR) Signaling Pathway:
– Activation of TLRs and subsequent induction of pro-inflammatory cytokines
– Involvement in immune cell activation, antigen presentation, and inflammatory responses
35. Myeloid Differentiation Primary Response 88 (MyD88) Signaling Pathway:
– Activation of MyD88 adaptor protein downstream of TLRs and IL-1 receptors
– Modulation of inflammatory responses and cytokine production
36. Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) Pathway:
– Activation of Nrf2 transcription factor and subsequent regulation of antioxidant and cytoprotective genes
– Implication in oxidative stress and inflammation modulation
37. Tumor Necrosis Factor (TNF) Signaling Pathway:
– Activation of TNF receptors and downstream signaling events
– Involvement in immune responses, cytokine production, and cell survival

1. Glutamatergic Signaling Pathways:
– Regulation of the expression and function of glutamate receptors
– Dysregulation of glutamate uptake and clearance mechanisms
2. GABAergic Signaling Pathways:
– Alterations in the expression levels of GABA receptors and transporters
– Dysregulation of GABAergic neurotransmission
3. Dopaminergic Signaling Pathway:
– Changes in the expression and function of dopamine receptors
– Dysregulation of dopamine-related neurotransmission
4. Serotonergic Signaling Pathway:
– Abnormalities in the expression and function of serotonin receptors
– Dysregulation of serotonin-related neurotransmission
5. Noradrenergic Signaling Pathway:
– Alterations in the expression levels and function of noradrenaline receptors
– Dysregulation of noradrenaline-related neurotransmission
6. Neuroinflammation and Microglial Activation:
– Transcriptomic changes associated with neuroinflammatory processes
– Activation of microglia and their contribution to central sensitization
7. Neurotrophic Factors and Neurogenesis:
– Dysregulation of neurotrophic factors like brain-derived neurotrophic factor (BDNF)
– Altered gene expression related to neurogenesis and neuronal plasticity
8. Pain Modulatory Pathways:
– Changes in gene expression involved in pain modulation systems, such as endogenous opioids

1. Dysregulation of Stress Response Pathways:
– Upregulation of stress-related genes involved in hypothalamic response to stress, including corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), and urocortin.
– Dysregulated expression of genes involved in the adrenal response to stress, including enzymes responsible for cortisol synthesis.
2. Dysregulation of the Hypothalamic-Pituitary-Adrenal (HPA) Axis:
– Alterations in the expression of key regulators and components of the HPA axis, including corticotropin-releasing hormone receptors (CRHR1 and CRHR2), glucocorticoid receptors (NR3C1), and corticotropin-releasing hormone-binding protein (CRHBP).
– Dysregulated expression of genes involved in cortisol synthesis, metabolism, and transport, such as steroidogenic enzymes.
3. Inflammatory and Immune Signaling:
– Increased expression of genes involved in inflammatory signaling, including pro-inflammatory cytokines (e.g., interleukin-6, interleukin-1β) and chemokines.
– Dysregulation of immune-related genes implicated in neuro-immune interactions, such as microglial activation markers and immune cell signaling molecules.
4. Neuroendocrine Genes:
– Dysregulated expression of genes involved in neuropeptides and neurotransmitters related to pain modulation, mood regulation, and sleep regulation, such as substance P, serotonin receptors, and gamma-aminobutyric acid (GABA) receptors.
– Altered expression of genes involved in stress response and modulation of neuroendocrine signaling.
5. Epigenetic modifications, including DNA methylation and histone modifications, affecting the transcriptional activity of stress-related and HPA axis regulator genes.
– Dysregulation of genes involved in epigenetic modifications and regulation of stress response pathways.
– Epigenetic modifications, including DNA methylation and histone modifications, affecting the transcriptional activity of stress-related and HPA axis regulator genes.
– Dysregulation of genes involved in epigenetic modifications and regulation of stress response pathways.

1. Altered Mitochondrial Function:
– Dysregulated expression of genes involved in mitochondrial energy production, such as those encoding components of the electron transport chain (ETC) and oxidative phosphorylation (OXPHOS).
– Abnormal expression of genes involved in mitochondrial biogenesis, fission, fusion, and dynamics.
– Dysregulation of genes involved in mitochondrial antioxidant defense mechanisms.
2. Oxidative Stress:
– Upregulation of genes related to oxidative stress, including those encoding reactive oxygen species (ROS) generating enzymes and genes involved in antioxidant response pathways.
– Dysregulation of genes involved in redox homeostasis and detoxification of ROS.
3. Impaired Metabolism and ATP Production:
– Dysregulation of genes involved in glucose metabolism and mitochondrial utilization of carbohydrates and fatty acids.
– Downregulation of genes related to ATP synthesis and cellular energy availability.
4. Inflammation and Immune Activation:
– Dysregulated expression of genes involved in immune and inflammatory responses within the mitochondria.
– Increased expression of immune-related genes, such as cytokines, chemokines, and markers of inflammation, affecting mitochondrial function.
5. Disrupted Calcium Homeostasis:
– Dysregulation of genes involved in calcium signaling and handling within the mitochondria.
– Alterations in genes encoding calcium channels, transporters, and regulatory proteins.
6. Mitochondrial DNA (mtDNA) Abnormalities:
– Changes in the expression of genes involved in the maintenance and replication of mtDNA.
– Dysregulated expression of genes involved in mitochondrial genome stability and repair mechanisms.

1. Dysregulation of Neuropeptides:
– Altered expression of genes encoding neuropeptides involved in pain modulation, such as substance P, calcitonin gene-related peptide (CGRP), and neuropeptide Y (NPY).
– Dysregulated expression of genes related to the processing and degradation of neuropeptides.
2. Altered Serotonin Signaling:
– Changes in the expression levels of serotonin-related genes, including serotonin receptors (e.g., 5-HT1A and 5-HT2 receptors) and enzymes involved in serotonin synthesis and metabolism (e.g., tryptophan hydroxylase and serotonin transporter).
– Dysregulation of genes involved in serotonin signaling, impacting pain perception, mood regulation, and sleep disturbances.
3. Disrupted Dopaminergic Signaling:
– Dysregulated expression of dopamine-related genes, including dopamine receptors (e.g., D1-like and D2-like receptors) and enzymes involved in dopamine synthesis and metabolism.
– Impaired dopamine signaling affecting reward pathways, pain modulation, and mood regulation.
4. Altered GABAergic Signaling:
– Dysregulation of genes encoding GABA receptors (e.g., GABAA and GABAB receptors), enzymes involved in GABA synthesis, and GABA transporters.
– Changes in the expression of genes related to GABAergic neurotransmission, impacting inhibitory signaling and pain modulation.
5. Hormonal Dysregulation:
– Abnormal expression of genes involved in the regulation and function of hormones, such as cortisol, adrenocorticotropic hormone (ACTH), and growth hormone.
– Dysregulated genes related to hypothalamic and pituitary hormones, including thyroid-stimulating hormone (TSH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH).

1. Microglial Activation: Microglia are the resident immune cells of the central nervous system. In fibromyalgia, microglial activation has been observed in certain brain regions, indicating an immune response and neuroinflammation. The transcriptomic analysis of activated microglia can reveal changes in gene expression patterns associated with inflammation and immune responses.
2. Astrocytic Activation: Astrocytes are glial cells involved in various brain functions, including the regulation of neurotransmitter balance and synaptic plasticity. In fibromyalgia, astrocytic activation has also been reported. Transcriptomic analysis of activated astrocytes can provide insights into the gene expression changes associated with altered neurochemical balance and synaptic dysfunction.
3. Inflammatory Signaling: Glial cell activation is often associated with the release of pro-inflammatory molecules, such as cytokines and chemokines. The glial cell activation transcriptome in fibromyalgia may reveal upregulation of genes associated with inflammatory pathways, indicating an immune response within the central nervous system.
4. Interaction with Neurons: Activated glial cells can influence neuronal function and contribute to the modulation of pain processing pathways. The glial cell activation transcriptome may uncover changes in genes involved in neuronal signaling, synaptic plasticity, and pain modulation.

Altered neurotrophin signaling refers to changes in the normal functioning and signaling pathways of neurotrophins, which are a family of proteins involved in the growth, development, and survival of neurons. Neurotrophins, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and others, play important roles in the central nervous system.

Here are some key points regarding altered neurotrophin signaling:
1. Decreased BDNF levels: Reduced levels of BDNF have been observed in certain conditions, including depression, chronic pain, and fibromyalgia. Decreased BDNF signaling may contribute to neuronal dysfunction, impaired synaptic plasticity, and altered pain processing pathways.
2. Dysregulated NGF levels: NGF is primarily involved in the growth and survival of sensory and sympathetic neurons. Dysregulation of NGF levels has been reported in various pain-related conditions, including fibromyalgia. Altered NGF signaling can influence pain sensitivity, sensory processing, and neuroinflammatory responses.
3. Impaired Trk receptor signaling: Neurotrophins exert their effects by binding to specific receptors called Trk receptors (e.g., TrkB for BDNF and TrkA for NGF). Changes in Trk receptor expression or function can disrupt normal neurotrophin signaling, affecting neuronal survival, synaptic plasticity, and pain modulation.
4. Impact on neuronal plasticity: Neurotrophins are critical for synaptic plasticity, the ability of neurons to change and adapt in response to experience. Altered neurotrophin signaling can impair neuronal plasticity, potentially contributing to cognitive difficulties, mood disorders, and abnormal sensory processing seen in conditions like fibromyalgia.

Fibromyalgia Evaluation Program

Utilizing AI analysis of the transcriptome proves advantageous in tackling Fibromyalgia

Transcriptome AI Genomic Analysis contributes to the development of personalized treatment strategies for fibromyalgia patients

By analyzing individual gene expression profiles, we are gaining insights into the unique molecular characteristics of each patient’s condition. This information assists in tailoring treatment plans and selecting therapies that are effective for each individual.

Fibromyalgia Transcriptome Analysis Sample Report

The report details a summary of the findings in the upper right-hand corner followed by data tables containing the identified biomarkers, pathways, and pathway-related therapies.
Example of short summary report: The report presented a characterization of Fibromyalgia through the identification of relevant biomarkers and pathways. The analysis revealed underlying characterization of Systemic Lupus Erythematosus in connection to Fibromyalgia. Pathway related treatment found: Belimumab (Benlysta), Pregabalin. READ MORE