Exploring the Molecular Roots of Your Neuropathy

A closer look at the advanced science behind the Ayass Bioscience Transcriptomic Neuropathy Test

Discover the Science Behind the Ayass Bioscience Neuropathy Test

Welcome to a deeper look into the innovative science that powers the Ayass Bioscience Neuropathy Test.

This page explores the complex cellular systems, molecular components, and biological pathways analyzed through our advanced transcriptomic approach. By examining gene activity at this level, we can uncover the unique molecular patterns that contribute to each individual’s experience of neuropathy.

Our detailed analysis focuses on transcriptomic markers associated with Neurons, Schwann cells, Microglia, Fibroblasts, Endothelial cells, and Satellite Glial cells—all examined through PBMCs (Peripheral Blood Mononuclear Cells). These immune cells provide insight into the intricate pathophysiology of peripheral neuropathy. Changes in these markers can reflect both the progression of neuropathic sensory and motor dysfunction, as well as the body’s potential for nerve repair.

At the core of this powerful process is the Ayass Bioscience Transcriptome Data Center, where your sample is carefully processed and analyzed. The resulting data is interpreted using our Proprietary Agentic AI Platfor – a sophisticated artificial intelligence system developed in-house by Ayass Bioscience.

By combining high-precision lab work with advanced AI interpretation, we deliver an unmatched view of your molecular health.

Explore Key Molecular Pathways

Our test analyzes gene expression in several vital areas that offer deeper insight into the biological mechanisms behind neuropathy. Click on each category to learn more:

The Neuron’s Vital Communication & Supply Lines.

Neurons rely on long axonal projections, which demand highly efficient transport systems to shuttle essential molecules, organelles (such as mitochondria), and signaling elements between the cell body and axon terminals. Disruptions in this axonal transport process are a hallmark of many types of neuropathy.
Our analysis evaluates gene expression patterns linked to:

Kinesin Motors:

Role: Kinesins are motor proteins responsible for anterograde transport—moving cargo such as vesicles and mitochondria from the neuron’s cell body toward the axon terminals along microtubule pathways.

Neuropathy Insight: Disruptions in kinesin gene expression can hinder this transport, resulting in the buildup or shortage of essential components. This can lead to axonal dysfunction, energy deficits at nerve endings, and ultimately, nerve degeneration.

Cytoplasmic Dynei

Role: Dynein is a motor protein essential for retrograde transport—moving cellular materials from the axon terminals back to the cell body. This process recycles used components and delivers critical survival signals to the nucleus.

Neuropathy Insight: Impaired dynein function can cause waste buildup within axons and disrupt the flow of neurotrophic signals, leading to increased neuronal stress and potential damage.

Microtubules:

Role: Microtubules serve as structural “highways” for axonal transport, guiding motor proteins as they move cargo along the axon. Their stability and proper organization are critical for efficient transport.

Neuropathy Insight: Alterations in genes that regulate tubulin (the core building block of microtubules) or their assembly can destabilize these pathways, disrupting transport and impairing overall neuronal function.

Microtubule Stability Regulators:

Role: These proteins—such as microtubule-associated proteins (MAPs) like Tau—help regulate the stability and flexibility of microtubules. Maintaining the right balance between structural stability and dynamic remodeling is essential for healthy transport function.

Neuropathy Insight: Disruption in the expression of these regulatory proteins can result in microtubules that are either too rigid or too unstable. Both conditions interfere with axonal transport and are linked to nerve damage in disorders such as chemotherapy-induced neuropathy.

Architects of Nerve Insulation, Protection & Regeneration.

Schwann cells are the main glial cells of the peripheral nervous system. They play a critical role in insulating axons through myelination, enabling rapid nerve signal conduction, and in supporting nerve regeneration after injury. Dysfunction in Schwann cells is a key factor in many types of neuropathy.
Our analysis focuses on gene activity related to:

Myelin Proteins (e.g., P0, PMP22, MBP):

Role: These proteins are fundamental components of the myelin sheath, which insulates axons and enables fast, efficient nerve signal transmission.

Neuropathy Insight: Mutations or changes in the expression of genes encoding myelin proteins are directly linked to inherited demyelinating neuropathies such as Charcot-Marie-Tooth disease. These proteins can also be affected in acquired forms of neuropathy, leading to compromised myelination, slowed nerve conduction, and progressive axonal damage.

Dedifferentiation Factors (e.g., c-Jun):

Role: After nerve injury, Schwann cells switch to a repair mode by activating genes like c-Jun. This process allows them to dedifferentiate, clear cellular debris, and support axon regeneration.

Neuropathy Insight: Evaluating the expression of these factors provides insight into the nerve’s repair capacity. Reduced activation may signal impaired healing, while persistent activation can suggest ongoing or unresolved nerve damage.

ER Stress Components (e.g., BiP, CHOP):

Role: The endoplasmic reticulum (ER) plays a vital role in proper protein folding. When myelin proteins misfold, it can trigger ER stress within Schwann cells.

Neuropathy Insight: Elevated expression of ER stress markers suggests that Schwann cells are under strain, potentially struggling to synthesize or maintain healthy myelin. This stress response is associated with certain hereditary neuropathies and painful acquired conditions.

Inflammatory Mediators:

Role: In response to nerve injury or immune challenges, Schwann cells can release signaling molecules that drive the local inflammatory response.

Neuropathy Insight: While short-term inflammation is a natural part of the healing process, prolonged or excessive production of pro-inflammatory mediators by Schwann cells can lead to ongoing nerve damage, heightened sensitivity, and persistent neuropathic pain.

Component

Description
Kinesin Motors Drive anterograde (cell body → axon terminal) transport of synaptic vesicles and mitochondria (PMC).
Cytoplasmic Dynein Facilitates retrograde (axon terminal → cell body) transport of signaling endosomes and waste (PMC).
Microtubules Polarized “tracks” composed of tubulin dimers, forming the structural basis for transport (PMC).
Microtubule Stability Regulators Proteins (e.g., tau, MAPs) that stabilize or sever microtubules, affecting transport efficiency (PMC).

Guardians of Neuronal Well-being in Sensory Ganglia.

SGCs surround the cell bodies of neurons within sensory ganglia and play a key role in regulating neuronal excitability. They are actively involved in the development and persistence of pain states. Activation of SGCs is a recognized feature of many neuropathic pain conditions.
Our analysis examines gene expression related to:

GFAP (Glial Fibrillary Acidic Protein):

Role: GFAP is an intermediate filament protein that becomes upregulated when Satellite Glial Cells are activated.

Neuropathy Insight: Elevated GFAP expression is a well-established marker of SGC activation in response to nerve injury and inflammation. Its increased levels often correlate with heightened neuronal excitability and the development of neuropathic pain.

Connexin 43:

Role: Connexin 43 is a key protein that forms gap junctions between Satellite Glial Cells, enabling direct intercellular communication and helping regulate ion and metabolite balance.

Neuropathy Insight: Altered expression of Connexin 43 can disrupt SGC coupling, impairing their ability to stabilize the neuronal environment. This dysfunction may contribute to increased neuronal excitability and the persistence of neuropathic pain.

P2X/P2Y Receptors (Purinergic Receptors):

Role: These receptors respond to ATP, which is released during cellular stress or injury. On Satellite Glial Cells, they help detect changes in the local environment.

Neuropathy Insight: Increased expression or altered sensitivity of P2X/P2Y receptors can trigger SGC activation and promote the release of pro-inflammatory molecules, intensifying pain signaling and contributing to chronic neuropathic pain.

Kir4.1 Channels:

Role: Kir4.1 channels are inwardly rectifying potassium channels that play a vital role in helping Satellite Glial Cells maintain extracellular potassium balance.

Neuropathy Insight: A decrease in Kir4.1 expression or function can disrupt potassium buffering, leading to heightened neuronal excitability. This dysregulation is strongly associated with the development and persistence of neuropathic pain.

Glutamate Transporters (e.g., GLAST, GLT1):

Role: These transporters help Satellite Glial Cells clear excess glutamate—an excitatory neurotransmitter—from the space around neurons, maintaining chemical balance and preventing overstimulation.

Neuropathy Insight: When glutamate uptake is impaired, excitotoxic levels can accumulate, leading to increased neuronal sensitivity and the development of chronic pain. Dysregulation of these transporters in SGCs is a contributing factor in neuropathic pain conditions.

Component

Function
Glial Fibrillary Acidic Protein (GFAP) A well-established marker of Satellite Glial Cell activation, particularly in chronic pain states. Elevated GFAP levels in SGCs have been documented in multiple studies (PMC), reflecting their reactive state in neuropathic conditions.
Connexin 43 A gap-junction protein that facilitates direct communication between Satellite Glial Cells, including the propagation of intercellular calcium waves. Its upregulation has been linked to neuropathic pain states (PMC).
P2X/P2Y Receptors Purinergic receptors on Satellite Glial Cells that detect extracellular ATP released during stress or injury. They play a key role in neuron–glia communication and are implicated in the amplification of pain signaling (PMC).
Kir4.1 Channels

Inward-rectifying potassium channels that help maintain extracellular ionic balance around neurons. Their dysfunction in Satellite Glial Cells is linked to increased neuronal excitability and neuropathic pain (PMC).
Glutamate Transporters (e.g., GLAST, GLT1) Responsible for clearing excess glutamate from the ganglionic cleft, these transporters prevent excitotoxicity and help maintain neuronal stability. Impairment is associated with chronic pain conditions (PMC).

Critical Zones of Interaction & Signal Propagation.

The structural and functional organization at the junctions between neurons and their associated glial cells—such as Schwann cells and Satellite Glial Cells—is critical for maintaining healthy nerve signaling.
Our analysis focuses on gene expression related to:

Nodes of Ranvier:

Role: These are regularly spaced gaps in the myelin sheath that enable saltatory conduction—allowing nerve impulses to rapidly jump from one node to the next. They are rich in specialized ion channels and structural proteins.

Neuropathy Insight: Disruption in the organization or expression of key molecular components at the nodes—such as ion channels and cell adhesion molecules—can significantly impair nerve signal transmission and contribute to neuropathic dysfunction.

Paranodal Junctions:

Role: These specialized structures flank the Nodes of Ranvier and anchor the myelin sheath to the axon, ensuring stability and proper alignment of the nodal architecture.

Neuropathy Insight: Mutations or altered expression of proteins involved in these junctions—such as Caspr and Contactin—can lead to myelin instability and disorganized nodes, impairing nerve conduction and contributing to neuropathic symptoms.

Schmidt-Lanterman Incisures:

Role: These are cytoplasmic channels within the layers of the myelin sheath in Schwann cells, enabling communication and nutrient transport between the Schwann cell body and the innermost layers of myelin.

Neuropathy Insight: Although less commonly examined in transcriptomic studies, the expression of genes that support Schwann cell cytoplasmic integrity and intracellular transport may offer insight into the functional health of these structures and their role in myelin maintenance.

Perineuronal SGCs:

Role: This continuous layer of Satellite Glial Cells encases the neuronal cell body within sensory ganglia, playing a key role in regulating the local microenvironment and supporting neuronal function.

Neuropathy Insight: The overall gene expression profile of SGCs—outlined in the sections above—provides valuable insight into the health and activity of this essential glial sheath in neuropathic conditions.

Axon–Myelin Adhesion Molecules:

Role: These molecules mediate the critical interactions that keep the myelin sheath securely attached and properly aligned with the axon, ensuring stable and efficient nerve conduction.

Neuropathy Insight: Disruptions in the expression of key adhesion molecules can weaken the structural connection between axon and myelin, increasing the risk of demyelination and axonal injury—common features in many forms of neuropathy.

Component

Function
Nodes of Ranvier

Gaps in the myelin sheath enriched with voltage-gated sodium (Na⁺) channels, enabling the regeneration of action potentials along the axon and supporting rapid nerve conduction (PubMed).
Paranodal Junctions

Septate-like contacts that anchor the myelin sheath at the borders of the nodes of Ranvier, playing a vital role in maintaining efficient electrical insulation and nodal integrity (PubMed).
Schmidt–Lanterman Incisures

Cytoplasmic channels within the myelin sheath that support ongoing communication and metabolic exchange between Schwann cells and the axon they insulate (PubMed).
Perineuronal SGC Sheath

Satellite glial cells form protective, tightly organized layers around sensory neuron cell bodies, helping regulate the local environment and maintain neuronal stability (PMC).
Axon–Myelin Adhesion Molecules

Cell-adhesion proteins—such as neurofascin—anchor the myelin sheath to the axon surface, maintaining structural integrity and enabling stable nerve conduction (PubMed).

Molecular Targets & Neuropathy

Understanding the Broader Context
While the Ayass BioScience Neuropathy Test maps your individual gene expression patterns across key cellular systems, it also provides valuable insight when viewed in the context of well-established molecular targets and pathways studied in neuropathic pain research.
Our comprehensive analysis may uncover dysregulation in genes associated with:

Key drivers of neuronal excitability.

Target: Nav1.7, Nav1.8, Nav1.9

Involved in neurotransmitter release and neuronal sensitization.

Target: Alpha2delta subunits

Important for descending pain modulation pathways.

Target: Serotonin, norepinephrine

Involved in pain sensation (heat, capsaicin).

Target: Nociceptors

Cellular responses to electrical or magnetic modulation.

Target: Dorsal columns, DRG

Play a role in pain processing.

Target: Acetylcholine pathways

Identifying whether genes related to these targets are differentially expressed in your profile can offer meaningful insights and support more informed discussions with your healthcare provider about the underlying mechanisms of your neuropathy.

Target/Mechanism

Therapeutic Role
Voltage-gated Sodium Channels

Targeted by novel inhibitors such as sulzetrigine to reduce ectopic neuronal firing—an underlying driver of neuropathic pain (Chemistry World).
Calcium Channels (α2δ Subunits) Gabapentin and pregabalin bind to α2δ subunits of voltage-gated calcium channels, reducing neurotransmitter release and dampening pain transmission (PMC, nypep.nysdoh.suny.edu).
Monoamine Reuptake Serotonin-norepinephrine reuptake inhibitors (SNRIs), such as duloxetine, boost serotonin and norepinephrine activity to support descending pain inhibition pathways (nypep.nysdoh.suny.edu).
TRPV1 Receptors High-dose capsaicin patches (Qutenza) target TRPV1 receptors to desensitize nociceptors and reduce pain signaling (Accessdata).
Neurostimulation Spinal cord and dorsal root ganglion stimulators emit electrical pulses to interfere with pain signaling pathways (U.S. Food and Drug Administration).
Muscarinic Acetylcholine Receptors Cholinergic modulation via muscarinic receptors helps suppress nociceptive signaling within spinal cord circuits (PMC).
Fatty Acid Binding Proteins (FABPs) Inhibiting FABP5 increases endocannabinoid levels, leading to analgesic effects in dorsal root ganglion (DRG) neurons (PMC).
Thermal Nerve Modulation Cryoneurolysis uses targeted cold application to temporarily ablate peripheral pain fibers and reduce pain (PMC).

Disclaimer: This information is provided for general educational purposes only. The Ayass Bioscience Neuropathy Test does not diagnose specific conditions or recommend particular treatments. All medical decisions should be made in consultation with a qualified healthcare provider who can assess your full medical history and other diagnostic findings.

To offer a more complete understanding, it’s helpful to consider the current strategies used in managing neuropathic pain:

  • Pregabalin (Lyrica): Binds to α2δ subunits of voltage-gated calcium channels; approved for diabetic neuropathy and postherpetic neuralgia.

  • Gabapentin (Neurontin): Acts on the same α2δ subunits; commonly used off-label for various types of neuropathic pain.

  • Duloxetine (Cymbalta): A serotonin-norepinephrine reuptake inhibitor (SNRI) approved for diabetic peripheral neuropathy and fibromyalgia.

  • Capsaicin 8% Patch (Qutenza): A high-dose topical TRPV1 receptor agonist approved for postherpetic neuralgia and diabetic neuropathy.

  • Spinal Cord Stimulation (SCS): An implantable device that delivers electrical impulses to the dorsal columns of the spinal cord; used for treatment-resistant neuropathic pain.

  • Cebranopadol: A dual NOP/mu-opioid receptor agonist demonstrating efficacy in Phase 3 trials for diabetic neuropathy.

  • Scrambler Therapy: A non-invasive electro-analgesia technique that reprograms pain signaling pathways; currently undergoing multiple late-phase clinical trials.

  • Stem Cell–Derived Therapies: Use of autologous skin fibroblasts reprogrammed into Schwann-like cells, under investigation for hereditary neuropathies (Phase 2/3 trials).

  • Closed-Loop Spinal Cord Stimulation (Inceptiv): An advanced SCS system that senses spinal cord activity and dynamically adjusts stimulation; FDA-approved in 2024 for chronic pain.

Research is active in areas like selective Nav channel blockers (e.g., Nav1.7, Nav1.8 inhibitors), HCN channel blockers, AAK1 inhibitors, new drug delivery systems, and therapies targeting specific inflammatory or neurotrophic pathways.

Frequently Asked Questions

Find answers to common questions about our Advanced Neuropathy Transcriptome Analysis.

What does this test specifically address? Is it suitable for all types of nerve problems?

This test is specifically designed to investigate the molecular and cellular factors that may contribute to neuropathy. It offers detailed insights into your unique gene expression patterns related to nerve health, rather than serving as a general nerve function test or a diagnostic tool for nerve injuries caused by trauma or other conditions.

How is this neuropathy test different from standard tests my doctor might order?

This test goes beyond typical nerve conduction studies or routine blood work. It uses transcriptome analysis to identify which genes related to nerve health are actively expressed in your body. The results are then analyzed using a state-of-the-art Agentic AI platform developed by F420.ai. This provides deeper insights into the cellular pathways and molecular mechanisms potentially driving your symptoms — insights not available through standard diagnostic tests.

What is transcriptome analysis in simple terms?

Think of your DNA as your body’s full instruction manual. Transcriptome analysis looks at the active messages — called RNA — that your cells are reading from that manual right now. For neuropathy, this helps us see which genes related to nerve health are currently “switched on” or “off,” giving a real-time view of what’s happening at the cellular level.

What is Agentic AI, and how does it help analyze my results?

Agentic AI is an advanced type of artificial intelligence designed to handle complex biological data. In this test, specialized AI “agents” study your transcriptome — the active gene messages in your cells — to identify patterns. They detect which genes are behaving differently, how those genes interact in biological pathways, and how all of this relates to known mechanisms involved in neuropathy. This allows for a much more detailed and personalized analysis than traditional methods.

Is the sample collection difficult or painful?

Not at all. The test uses a simple at-home collection kit. It usually just takes a few drops of blood from a quick finger prick. Step-by-step instructions are included, making the process easy and comfortable to do yourself.

How long will it take to receive my results after I send back my sample?

Once your sample arrives at our laboratory — Ayass Bioscience, using the Ayass Bioscience Transcriptome Data Center — it goes through detailed processing and advanced AI analysis. We aim to deliver your comprehensive report within 3 to 4 weeks, and you’ll be kept updated on the progress throughout the process.

What kind of information will I get in my report?

Your personalized report will highlight genes that are showing unusual activity in your sample, the biological pathways those genes are involved in, and how these patterns may relate to known mechanisms of neuropathy. It’s a detailed molecular snapshot — offering insights at the cellular level — rather than a list of symptoms or a simple yes/no result.

Can this test tell me exactly what type of neuropathy I have or which specific treatment will work for me?

This test is designed to provide deep insights into the molecular and cellular mechanisms that may be contributing to your neuropathy. It does not diagnose a specific type of neuropathy or recommend a particular treatment. Instead, it offers valuable information that you and your healthcare provider can use to better understand your condition and explore more personalized care options.

How can I use the information from this test?

The insights from your report can be a powerful tool for discussions with your doctor or specialist. They help reveal the unique biological factors involved in your case, which may guide further testing, support more informed decisions, or lead to more personalized treatment strategies.

You mentioned a “Proprietary Agentic AI Platform.” What makes this AI platform special for analyzing neuropathy?

Our proprietary Agentic AI Platform, developed by Ayass Bioscience’s F420.ai, is specifically designed to analyze the vast and complex data generated from transcriptome analysis — with a focus on neuropathy. Unlike general-purpose AI tools, this platform is trained to detect subtle patterns in gene expression across many interconnected cellular components and pathways that affect nerve health. It integrates these findings to deliver a comprehensive molecular view, offering far deeper insight than isolated data points alone.

Can I clarify the relationship between Ayass BioScience and F420.ai?

F420.ai is an integral part of Ayass BioScience. The advanced Agentic AI platform is developed and operated entirely in-house, ensuring seamless integration between our laboratory processes at the Ayass BioScience Transcriptome Data Center and the AI-powered data analysis. This direct connection allows for continuous refinement and a focused application of the technology to complex conditions like neuropathy.

How is this transcriptome analysis different from a standard genetic (DNA) test for neuropathy?

Standard genetic tests typically look for inherited mutations or variations in your DNA that may increase your risk for certain conditions. Transcriptome analysis, however, measures the current activity of your genes — showing which ones are “on” or “off” and to what extent. This provides a dynamic, real-time snapshot of what’s actively happening in your cells right now in relation to your neuropathy. It captures influences beyond inherited genetics, including environmental and biological factors affecting gene expression.

What is the specific role of the Ayass BioScience Transcriptome Data Center in this testing process?

The Ayass BioScience Transcriptome Data Center is our state-of-the-art molecular laboratory where your sample is physically processed. This includes extracting RNA from your blood sample and performing high-throughput sequencing to generate your raw transcriptome data. Once complete, this data is analyzed using our proprietary F420.ai Agentic AI Platform for deeper insights into gene activity and neuropathy-related pathways.

Beyond the Surface: Your Path to Molecular Insight

The Ayass BioScience Neuropathy Test, powered by comprehensive transcriptome analysis and the integrative strength of our proprietary Agentic AI Platform at the Ayass BioScience Transcriptome Data Center, offers a deep exploration into the complex molecular symphony — or discord — occurring within your nervous system.

By analyzing key cellular components, pathways, and their interactions, this test provides you and your healthcare provider with profound insights. This detailed molecular blueprint becomes a powerful tool for understanding the unique nature of your neuropathy, helping support more informed conversations and personalized care strategies on your health journey.

Beyond Symptoms: Gain Unprecedented Insight into Your Neuropathy’s Molecular Roots

Looking Deeper: A New Approach to Understanding Neuropathy

Are you navigating the challenging path of neuropathy, searching for more than just surface-level answers?
We offer an advanced testing service designed to uncover the deep biological drivers behind neuropathy — not just symptoms. This isn’t just another test. It’s a molecular-level investigation into the unique gene activity within your body that may be contributing to nerve dysfunction, pain, or impaired healing.

A Molecular Blueprint of Nerve Health

Using high-resolution transcriptome analysis, our test expands upon key markers related to neurons, Schwann cells, microglia, fibroblasts, endothelial cells, and satellite glial cells — all analyzed through PBMCs (peripheral blood mononuclear cells).

Changes in these immune cells reflect the complex biology of peripheral neuropathy. These cellular players are deeply involved not only in the development of sensory and motor dysfunction, but also in the body’s potential for nerve repair — and their status can now be monitored through your blood.

Unparalleled Depth. Just One Sample.

With just a small blood sample (approx. 1ml from fingerstick or 4ml from venous draw), your test begins at the Ayass BioScience Transcriptome Data Center (ABS TDC) in Dallas–Fort Worth.
There, our proprietary Agentic AI platform begins analyzing over 200 million potential pathway combinations, uniquely relevant to your nervous system.

This extraordinary depth uncovers molecular patterns, connections, and disruptions that traditional nerve tests simply can’t detect.

The Neuropathy Enigma: Why Deeper Cellular Understanding is Key

Neuropathy is deeply personal, rooted in the intricate fabric of your cellular and molecular biology.
Standard diagnostic tests often only scratch the surface. To achieve a truly comprehensive understanding, we must look deeper — into the inner workings of critical biological systems.

This includes a vast array of neural cell types, from motor and sensory neurons to glial cells such as Schwann cells, oligodendrocytes, astrocytes, and microglia. It also involves their complex subcomponents, including axonal transport systems, myelin sheaths, and synaptic dynamics.
Layered on top are numerous dynamic molecular pathways — from neuroinflammation and oxidative stress to neurotrophic factor signaling — all of which may contribute to the development or progression of neuropathy.

Our advanced analysis is designed to do exactly that. We investigate:

We examine the cells most critical to nerve health — including Schwann cells, which are responsible for producing and maintaining the myelin sheath; satellite glial cells, which support and regulate neurons in peripheral ganglia; and the core axonal structures of your neurons, which are essential for signal transmission and cellular communication.

We also delve deeper into the essential machinery and elements within these cells — such as the axonal transport systems that shuttle vital materials, the myelin sheath components that insulate and protect nerve fibers, and the synaptic structures that govern how signals are transmitted between neurons. Disruptions in any of these can contribute to neuropathic symptoms, and our analysis is designed to detect these subtle yet significant molecular shifts.

We map the active communication lines and functional processes that govern nerve health and response to damage — including pathways involved in neuroinflammation, oxidative stress, immune signaling, and the regulation of neurotrophic factors. These dynamic networks play a central role in how nerves respond to injury, repair themselves, or deteriorate over time.

This sophisticated integration of transcriptomic data and AI analysis delivers a level of detail and understanding that is truly cutting-edge.
By uniting molecular precision with advanced computational insight, we go beyond conventional diagnostics — offering a clearer, deeper view into the root causes of your neuropathy.

Crucially, these multifaceted biological insights — spanning cellular components, their substructures, and dynamic molecular pathways — are meticulously analyzed and integrated through our proprietary Agentic AI Platform.
This sophisticated integration, developed in-house at Ayass BioScience, is what truly sets our analysis apart. It enables a level of molecular precision and contextual understanding that is genuinely cutting-edge, offering insights far beyond the reach of conventional diagnostic tools.

Transcriptome Analysis: Revealing Your Active Neural Instructions

If your DNA is the complete instruction manual for your body, the transcriptome is the real-time report of which instructions are actively being read and used by your cells. It captures the RNA “messages” that drive cellular function, offering a dynamic snapshot of your body’s current biological activity — especially as it relates to neural health.

Neuropathy isn’t a static condition — it’s an ongoing, active biological process. Transcriptome analysis allows us to see which genes are currently influencing processes like inflammation, nerve repair, myelin production, mitochondrial function, and ion channel activity. These insights go far beyond what static DNA testing can reveal.

This approach gives us the ability to observe what your body is doing right now, at a molecular level. It uncovers active mechanisms that may be driving your neuropathy and opens the door to more personalized therapeutic considerations.

Our Process

Order your kit online and collect your sample using a simple finger-prick method — or opt for a 4ml blood draw if preferred.
Clear, step-by-step instructions are included to guide you through the process with ease.

Return your sample using the prepaid FedEx packaging included in your kit.
It will be sent directly to our Dallas–Fort Worth Ayass BioScience Transcriptome Data Center (ABS TDC).
Shipping is fully covered.

At our laboratory, your sample’s RNA is extracted and sequenced to map your complete transcriptome — specifically focusing on pathways related to neuropathy.
This forms the foundation for analyzing over 200 million potential pathway combinations, revealing the complex molecular signals behind your condition.

The massive dataset generated from your transcriptome is analyzed by our proprietary Multi-Agent AI System, developed by F420.ai — an Ayass BioScience company.
This isn’t just a single algorithm. It’s an integrated network of specialized AI agents, each designed to focus on specific aspects of neurological analysis, working collaboratively to uncover meaningful patterns and insights.

How Our Multi-Agent AI System Works

Our proprietary Multi-Agent AI System from F420.ai (an Ayass BioScience company) uses a coordinated team of intelligent agents, each with a specific role in transforming your transcriptomic data into meaningful insights:

  • Data Orchestrator & Preprocessing Agents
    Ensure the integrity, accuracy, and quality of your sample data before analysis begins.

  • Expression & Pathway Analysis Agents
    Identify significant gene expression patterns and map them to both known and emerging neurological pathways and cellular subcomponents.

  • Machine Learning & Knowledge Integration Agents
    Discover novel correlations in your data and contextualize them using the latest findings from global neurological research.

  • Clinical Correlation & Therapeutic Insights Agents
    Link molecular findings to potential clinical implications and help suggest avenues for personalized therapeutic strategies — to be discussed with your healthcare provider.

  • Reporting Agent
    Synthesizes these complex insights into a clear, personalized report, making advanced molecular data understandable and actionable.

This sophisticated AI framework enables an unparalleled level of integrative analysis across cellular systems, substructures, and dynamic pathways — providing a depth of understanding far beyond traditional testing.

You’ll receive a detailed, personalized report designed to bring clarity to your condition.
It highlights key differentially expressed genes (DEGs), affected neuropathy-related pathways, and provides insights that may support personalized therapeutic considerations — helping guide meaningful conversations with your healthcare provider.

Access your results securely through our patient portal.
Importantly, your transcriptomic data becomes a future-oriented asset — as new discoveries in neurological research emerge, its relevance to your unique molecular profile can be re-evaluated, offering ongoing value over time.

The Ayass BioScience Difference

Your investment in our Neuropathy Transcriptome Analysis delivers extraordinary and unprecedented worth because it provides:

Our analysis explores over 200 million pathway combinations and gene expression patterns across more than 9 key neural cell types, numerous cellular subcomponents, and a wide array of molecular pathways involved in neuropathy.

Information that would traditionally require multiple, separate tests — often costing thousands of dollars — is now seamlessly integrated into a single, comprehensive analysis.

You benefit from an AI system that simulates the collaborative expertise of an entire neurological research team — analyzing your unique data with precision and depth.
This level of specialized integration is an exclusive capability of Ayass BioScience.

This analysis moves beyond generic approaches by delivering molecular insights that can help you and your doctor identify and discuss targeted therapeutic strategies — tailored to your unique biological profile.

Your detailed transcriptomic data can be revisited as new scientific discoveries emerge, potentially offering fresh insights and clinical relevance — even years into the future.

Many find that the clarity and direction gained from this single, comprehensive analysis can save years of diagnostic uncertainty, trial-and-error treatments, and related expenses — making it a powerful investment in their long-term health journey.

Important Information

Please note: Our molecular testing is currently designated for Research Use Only (RUO) and has not yet received FDA approval.

What You Receive with Your Order

  • Blood collection kit with prepaid return shipping
    (Choose from finger prick or venipuncture options)

  • Full RNA sequencing focused on metabolism-related gene expression

  • Advanced analysis via our proprietary Multi-Agent AI system

  • A comprehensive, personalized metabolic assessment report

Peripheral Neuropathy and PBMC Transcriptome Analysis

Blood cells can reveal nerve damage occurring in distant locations. This groundbreaking approach from Ayass Bioscience uses PBMC transcriptome signatures to understand changes in the peripheral nervous system.

Core Concept

Transcriptome Signatures
PBMCs reflect changes happening in the peripheral nervous system.
Blood as a Window
Blood cells provide insights into nerve damage occurring in distant locations.
Diagnostic Potential
This approach may revolutionize how we detect and treat neuropathy.

Cellular Mechanisms in Neuropathic Pain: A Multi-Cell Perspective

Exploring key cellular players in neuropathic pain pathology and emerging therapeutic avenues.

Sensory Neurons: Hyperexcitability and Ion Channels

Membrane Hyperexcitability
Spontaneous firing and reduced thresholds
Ion Channel Dysregulation
Nav1.7/1.8/1.9 altered expression
Therapeutic Targets
Selective Nav blockers under development

Schwann Cells: From Support to Inflammation

Myelinating State
Normal supportive function
Dedifferentiation
P75 and GFAP upregulation
Pro-inflammatory
Cytokine production increases
Therapeutic Target
Remyelination promoters

Immune Cells: Inflammatory Mediators

Macrophages
M1 phenotype predominates in pain states
Microglia
Central sensitization contributors
T Lymphocytes
Sex-specific pain mechanisms
Therapeutic Approaches
Immune modulators show promise

Fibroblasts: Matrix Remodeling and Fibrosis

Activation Phase
Transformation to myofibroblasts
Remodeling Phase
Excessive ECM production
Fibrotic Phase
Nerve compression and ischemia
Therapeutic Targets
Anti-fibrotic agents under investigation

Endothelial Cells: Blood-Nerve Barrier Disruption

Tight Junction Loss
Claudin-5 and ZO-1 downregulation
Increased Permeability
Inflammatory mediator infiltration
Vascular Remodeling
Microvascular changes worsen perfusion
Therapeutic Approach
Barrier stabilizers show potential

Satellite Glial Cells: Activation in Pain States

Activation Markers
GFAP upregulation indicates reactivity
Altered Gap Junctions
Increased coupling between cells
Purinergic Signaling
P2X7 receptor expression increases
Therapeutic Potential
Gap junction blockers reduce pain signaling

Cellular Crosstalk: Integrated Pain Pathways

Sensory Neurons
Release neuropeptides activating adjacent cells
Vascular Components
Facilitate infiltration of blood-borne factors
Schwann Cells
Respond with cytokine production
Immune Cells
Amplify inflammatory cascade

Sex Differences: Cellular Mechanisms

Male-predominant Mechanisms

Microglia-mediated pathways:

  • P2X4R signaling critical
  • TLR4 activation prominent
  • BDNF release mechanism

Female-predominant Mechanisms

T-cell mediated responses:

  • Adaptive immunity involvement
  • Estrogen modulation effects
  • Distinct cytokine profiles

Temporal Dynamics: Acute vs. Chronic Pain

Acute Phase (Days 1-7)

  • Wallerian degeneration
  • Robust macrophage infiltration
  • Immediate Schwann cell dedifferentiation

Subacute Phase (Weeks 1-6)

  • T-cell recruitment increases
  • Satellite glial cell activation peaks
  • Fibroblast activation accelerates

Chronic Phase (Months+)

  • Persistent ion channel remodeling
  • Established fibrotic changes
  • Maladaptive neuronal plasticity

Therapeutic Landscape: Multi-cellular Targets

Emerging therapeutics based on cellular mechanisms target multiple pain pathways simultaneously.

Future Directions: Precision Medicine Approaches

Genetic Profiling
Ion channel variants predict drug response
Cellular Biomarkers
Personalized pain mechanism identification
Combinatorial Therapies
Multi-cell targeted approaches
AI-Guided Decisions
Treatment algorithms predict outcomes