neuroimmune
CGRP
Trigeminal and sensory neuropeptide that links migraine biology, vasodilation, and immune-adjacent tissue signaling
Review layer
Last reviewed 2026-07-03
Neuroimmune mediators are modeled as directional teaching nodes for threshold, reflex, sensory, vascular, and tissue-crosstalk behavior. Use as educational systems context, not diagnosis or treatment guidance.
4 review sources
State signature
Systems profile
System effects
Primary mapped axes from existing Atlas data.
Tissue
Organ, barrier, stromal, vascular, or local niche behavior.
Inflammation
Inflammatory alarm, recruitment, mediator release, or tissue-damaging amplification.
Neuroimmune
Nerve, neuropeptide, autonomic, microglial, pain, itch, fatigue, or sickness-behavior coupling.
Local map
Relationship field
Arrows point from the upstream source toward the receiving target. Restraint edges use a bar; association edges stay dashed because they are not causal arrows.
Selected relationship
CGRP is a vasoactive sensory neuropeptide that links trigeminovascular signaling with vascular tone and neurogenic inflammation
Read as source acts on or points toward the target.
What this relationship means
Read this as CGRP changing the local tissue setting around Vascular Immune Ecosystem, not as a stand-alone disease label.
Effect of source
CGRP carries nervous-system timing, sensory, or autonomic context.
Effect on target
Vascular Immune Ecosystem is where vascular tone, barrier behavior, trafficking, or sensitivity may show up.
Use with caution
This is a systems lens, not patient-specific prediction.
System effect
CGRP influences Vascular Immune Ecosystem; the axes below show which mapped systems carry that relationship.
Tissue
Organ, barrier, stromal, vascular, or local niche behavior.
Inflammation
Inflammatory alarm, recruitment, mediator release, or tissue-damaging amplification.
Metabolism
Energy allocation, glycolysis, mitochondrial strain, lipid signaling, or nutrient-sensitive behavior.
Axes are mapped cues from Atlas data, not clinical predictions.
Evidence context
Curated edge, reviewed endpoints, and mapped external anchors.
Graph neighborhood
Direct relationships
Arrow shows upstream source toward receiving target.
CGRP is a vasoactive sensory neuropeptide that links trigeminovascular signaling with vascular tone and neurogenic inflammation
Mediator interpretation
Effect Of and Effect On
CGRP is modeled as a vasoactive sensory neuropeptide with strong relevance to migraine and trigeminovascular signaling. In Atlas it acts as a bridge between neural threshold state, vascular tone, mast-cell-adjacent mediator release, and tissue sensitivity.
What this means
Effect of the nervous signal
Read CGRP as a sensory and trigeminal output signal: neural activation can be carrying vascular and tissue-threshold information into the immune map.
Effect on immune and tissue systems
On tissues it usually points toward vasodilation, meningeal or barrier sensitivity, and mast-cell-adjacent mediator context rather than a single inflammatory disease.
Use it in Atlas when
Use this node when migraine-threshold, vascular-tone, and neurogenic-inflammation questions need to be shown together.
Boundary
This is not a headache diagnosis, migraine treatment rule, or proof that mast cells are the primary driver.
Influence Trace
Nervous signal to immune behavior
What starts the signal?
Trigeminal activation, sensory gain, sleep debt, stress load, or other migraine-threshold pressure.
What receives it?
Vascular and meningeal-adjacent tissue systems, with mast-cell context shown as co-traveling rather than proven causal.
What changes in the system?
The map shifts toward vasodilation, tissue sensitivity, and neurogenic-inflammation context.
What should not be over-interpreted?
Do not use this as a headache diagnosis, medication recommendation, or proof that one trigger explains every migraine pattern.
- 1Trigeminal outputCGRP
CGRP marks a sensory-neuropeptide signal tied to trigeminovascular activation.
- 2Vascular toneVascular Immune Ecosystem
Vascular and meningeal contexts are the main receiving tissue layer in this trace.
- 3Mast-cell contextMast Cell
Mast-cell mediator release can co-travel in neurogenic inflammation models without proving causality.
Effect of
Regulated by
Signals through
Effect on immune cells
Effect on tissues
Nervous-system behavior
calcitonin-family neuropeptide