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wakefulness neuropeptide

Orexin A

Published evidence · coverage incomplete

Anatomy in the research

Explore the structures studied.

These are anatomical mentions in cited research—not established treatment targets or proof of benefit in people.

Brain · 6 cited passage(s)

Population: mouse (unilateral intrastriatal 6-ohda model)

A progressive loss of orexin A positive neurons in the lateral hypothalamus was observed in the lesioned side relative to the non-lesioned side.

Applies only to the source-defined population, formulation, dose, and assessment period.

Evidence relationship: supports

Read finding and source →

Population: mouse (unilateral intrastriatal 6-ohda model)

A significant reduction of orexin A positive neurons in the lateral hypothalamus was observed at 4 weeks with further loss at 6-8 weeks post 6-OHDA induction.

Applies only to the source-defined population, formulation, dose, and assessment period.

Evidence relationship: supports

Read finding and source →

Population: mouse (unilateral intrastriatal 6-ohda model)

A significant reduction of orexin A positive neurons in the lateral hypothalamus was observed at 4 weeks with further loss at 6-8 weeks post 6-OHDA induction.

Applies only to the source-defined population, formulation, dose, and assessment period.

Evidence relationship: supports

Read finding and source →

Population: Population not specified in the source claim.

Orexin-A, a hypothalamic neuropeptide involved in regulating arousal, stress response, and emotional processes

Applies only to the source-defined population, formulation, dose, and assessment period.

Evidence relationship: supports

Read finding and source →

Population: Population not specified in the source claim.

Neurons in the lateral hypothalamus (LH) synthesize orexin-A and orexin-B, neuropeptides that orchestrate feeding behavior and energy expenditure, thereby directly regulating energy homeostasis and associated behaviors.

Applies only to the source-defined population, formulation, dose, and assessment period.

Evidence relationship: supports

Read finding and source →

Population: mammals

Beyond the established hypothalamic Arcuate Nucleus (ARC) circuit, key regulators examined include neuropeptides like Orexin A, Oxyntomodulin, PACAP, and Galanin, alongside key receptor systems such as the Melanocortin-3 receptor (MC3R), the Endocannabinoid (ECS) and the Endorphin Systems.

Applies only to the source-defined population, formulation, dose, and assessment period.

Evidence relationship: supports

Read finding and source →

At a glance

What is it—and why does it matter?

Orexin-A is classified as a peptide ligand and is listed under Ligand ID: 1697. The abstract states that orexin peptide pharmacokinetics are sparsely characterized and that reported plasma concentrations vary substantially because of methodological differences, limiting interpretation of circulating orexin levels and possible peripheral sources.

Sources for this introduction: [1] [2]

This published profile is a reference in progress. Findings retain their source context; missing topics are marked below.

What is it?

A molecule, not a product name.

Identity

Orexin-A (OXA) is classified as a neuropeptide (a peptide neurotransmitter/neuromodulator).

Molecular / pharmacology evidence

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    The neuropeptides orexin-A (OXA) and orexin-B (OXB)

    The orexinergic system in the retina: Expression and physiological impact-A review of the literature. · Abstract

    pubmed:42150720:1073e3ee7bb5:1073e3ee7bb5

Identity

Orexin-A is described as a hypothalamic neuropeptide with roles in arousal regulation, stress responses, and emotional processing.

Human research · design must be checked

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Orexin-A, a hypothalamic neuropeptide involved in regulating arousal, stress response, and emotional processes

    Plasma orexin-A levels in women with postpartum depression: a prospective controlled study. · OBJECTIVE

    pubmed:42307294:8511f7cf7b37:8511f7cf7b37

Identity

In this mammalian appetite-regulation review, Orexin A is included among the neuropeptides discussed as key regulators beyond the established hypothalamic arcuate nucleus (ARC) circuit.

Molecular / pharmacology evidence

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Beyond the established hypothalamic Arcuate Nucleus (ARC) circuit, key regulators examined include neuropeptides like Orexin A, Oxyntomodulin, PACAP, and Galanin, alongside key receptor systems such as the Melanocortin-3 receptor (MC3R), the Endocannabinoid (ECS) and the Endorphin Systems.

    Regulators of Appetite in Mammals - Old and New players. · Abstract

    pubmed:42274231:a21b0a7009ce:a21b0a7009ce

Identity

Orexin-A is classified as a peptide ligand and is listed under Ligand ID: 1697.

Molecular / pharmacology evidence

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Name: orexin-A Ligand ID: 1697 Type: Peptide

    orexin-A · Identity and approval

    iuphar-ligand:1697:0937e1823866:0937e1823866

How does it work?

Target, response, and disposition.

Mechanism

Full colocalization means orexin B labeling tracked the same orexin signal as orexin A under these conditions, so orexin B staining could be used to mark orexin fibers/neurons.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Orexin A and B were fully colocalized, allowing orexin B to serve as a reliable marker.

    Formalin-induced pain preferentially activates orexin neurons in male mice. · Abstract

    pubmed:42097393:c04332364eef:c04332364eef

Mechanism

The authors interpret their results as supporting a mediating role for orexinergic signaling in linking ambient light conditions to sleep and affective outcomes.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    These findings support the hypothesis that the orexinergic system mediates the effects of ambient light on sleep and affect,

    Central hypocretin/orexin administration alleviates sleep/wake disturbances, anhedonia, and neuroinflammation in an animal model of seasonal affective disorder. · CONCLUSIONS

    pubmed:41508567:bde9d1d76494:bde9d1d76494

Mechanism

The reported results were interpreted as functional crosstalk between opioid and orexin signaling within the nucleus accumbens, consistent with mutual modulation during acute nociceptive processing.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    These findings indicate a bidirectional interaction between opioidergic and orexinergic systems within the NAc in regulating acute nociception.

    Orexinergic-Opioidergic Interactions Within the Nucleus Accumbens in the Modulation of Acute Pain: Evidence From the Tail-Flick Test in Rats. · CONCLUSIONS

    pubmed:42530048:8f359dc82632:8f359dc82632

Mechanism

Prior reports (as summarized here) indicate lateral hypothalamic orexin neuron loss in post-mortem Parkinson’s disease and in several animal studies, with rats highlighted.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Orexin neuron loss in the lateral hypothalamus has been reported in post-mortem Parkinson's disease patients and multiple animal studies, particularly in rats;

    Progressive orexin A positive neuron loss in the 6-OHDA mouse model of Parkinson's disease: a pilot study with validation of an orexin A immunohistochemistry protocol for paraffin-embedded tissue. · Abstract

    pubmed:42323123:743443206799:743443206799

Mechanism

The stated objective was measurement of plasma orexin-A in postpartum depression and exploration of its potential biological involvement in the condition.

Human research · design must be checked

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    The aim of this study was to assess plasma orexin-A levels in women with postpartum depression and to explore its potential biological involvement in postpartum depression.

    Plasma orexin-A levels in women with postpartum depression: a prospective controlled study. · OBJECTIVE

    pubmed:42307294:8511f7cf7b37:8511f7cf7b37

Mechanism

Orexin peptides including orexin A signal via OX1R and OX2R to influence both sensory-discriminative and affective-motivational aspects of pain; the direction of effect can vary by peptide subtype, receptor distribution, circuit architecture, and pain modality.

Molecular / pharmacology evidence

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Orexin peptides (orexin A and orexin B) modulate both the sensory-discriminative and affective-motivational components of pain via their receptors (OX1R and OX2R) in a context-dependent manner, producing antinociceptive or pro-nociceptive effects depending on peptide subtype, receptor distribution, circuit architecture, and pain modality.

    Lateral hypothalamic orexinergic neurons as central mediators of pain modulation and non-pharmacological analgesia. · Abstract

    pubmed:42460012:a9846ad06137:a9846ad06137

Mechanism

The stated objective was to evaluate whether orexin neuron loss progresses over time in the unilateral intrastriatal 6-OHDA mouse model.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    The aim of this pilot study was to assess a time-dependent loss of orexin neurons in the unilateral intrastriatal 6-OHDA mouse model

    Progressive orexin A positive neuron loss in the 6-OHDA mouse model of Parkinson's disease: a pilot study with validation of an orexin A immunohistochemistry protocol for paraffin-embedded tissue. · Abstract

    pubmed:42323123:743443206799:743443206799

Pharmacokinetics

The abstract states that orexin peptide pharmacokinetics are sparsely characterized and that reported plasma concentrations vary substantially because of methodological differences, limiting interpretation of circulating orexin levels and possible peripheral sources.

Molecular / pharmacology evidence

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    We also review the limited pharmacokinetic data available for orexin peptides and evaluate reported plasma concentrations, highlighting substantial methodological variability that complicates interpretation of circulating levels and their potential peripheral sources.

    The orexin system as a pharmacological target in inflammation: peripheral mechanisms and safety implications. · Abstract

    pubmed:42609337:1f357b1ef544:1f357b1ef544

What has been studied?

What the evidence says.

Comparative evidence

The total number of orexin-immunoreactive neurons did not differ by sex or estrous stage in these mice.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    The total number of orexin-immunoreactive neurons did not differ between the sexes or across estrous stages

    Formalin-induced pain preferentially activates orexin neurons in male mice. · Abstract

    pubmed:42097393:c04332364eef:c04332364eef

Study findings

In a rat CA1 EED model induced by HFES, cortical (frontal cortex) orexin-A at 10 μg/10 μl decreased the incidence of large (7-10 mV) population spikes during EEDs while leaving overall EED duration unchanged, indicating site-specific effects.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    In contrast, cortical administration of orexin‑A selectively reduced the incidence of high‑amplitude (7-10 mV) population spikes during EEDs without affecting the duration of epileptiform activity.

    Modulation of electrically evoked hippocampal epileptiform activity by exogenous orexins in the rat CA1 field. · Abstract

    pubmed:42370618:bdda096bc718:bdda096bc718

Study findings

c-Fos is used as an indicator of neuronal activation; after formalin-induced nociception, a larger fraction of orexin neurons showed c-Fos in males, suggesting greater functional recruitment in males in this paradigm.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    In contrast, formalin induced a significantly higher proportion of c-Fos-positive orexin neurons in males, indicating male-biased recruitment of orexin neurons during nociception, despite equivalent anatomical substrates.

    Formalin-induced pain preferentially activates orexin neurons in male mice. · Abstract

    pubmed:42097393:c04332364eef:c04332364eef

Study findings

As a proof-of-concept finding, the study asserts that the unilateral intrastriatal 6-OHDA mouse model reproduces progressive loss of orexin A–immunopositive neurons.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    This pilot study serves as a proof of concept that the unilateral intrastriatal 6-OHDA mouse model can successfully recapitulate the progressive loss of orexin A positive neurons

    Progressive orexin A positive neuron loss in the 6-OHDA mouse model of Parkinson's disease: a pilot study with validation of an orexin A immunohistochemistry protocol for paraffin-embedded tissue. · Abstract

    pubmed:42323123:743443206799:743443206799

Study findings

In a neurotoxic unilateral intrastriatal 6-OHDA mouse model, orexin A immunopositive neuron counts in the lateral hypothalamus progressively decreased on the lesioned side relative to the non-lesioned side.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    A progressive loss of orexin A positive neurons in the lateral hypothalamus was observed in the lesioned side relative to the non-lesioned side.

    Progressive orexin A positive neuron loss in the 6-OHDA mouse model of Parkinson's disease: a pilot study with validation of an orexin A immunohistochemistry protocol for paraffin-embedded tissue. · Abstract

    pubmed:42323123:743443206799:743443206799

Study findings

In this observational analysis, CSF orexin concentrations did not show statistical association with global sleep continuity metrics.

Human research · design must be checked

1 cited source · 1 linked study ID

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Orexin was not associated with global sleep continuity metrics.

    Orexin, Sleep, and Cognition in Alzheimer Disease: Non-REM Oscillatory Activity and Neural Resilience. · RESULTS

    pubmed:42447420:0efa038e8709:0efa038e8709

Study findings

At 4 weeks after 6-OHDA induction in a unilateral intrastriatal mouse model, orexin A–immunoreactive neurons in the lateral hypothalamus were significantly reduced.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    A significant reduction of orexin A positive neurons in the lateral hypothalamus was observed at 4 weeks with further loss at 6-8 weeks post 6-OHDA induction.

    Progressive orexin A positive neuron loss in the 6-OHDA mouse model of Parkinson's disease: a pilot study with validation of an orexin A immunohistochemistry protocol for paraffin-embedded tissue. · Abstract

    pubmed:42323123:743443206799:743443206799

Study findings

Following unilateral intrastriatal 6-OHDA induction in mice, orexin A immunopositive neuron loss in the lateral hypothalamus continued, with further loss noted at 6-8 weeks.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    A significant reduction of orexin A positive neurons in the lateral hypothalamus was observed at 4 weeks with further loss at 6-8 weeks post 6-OHDA induction.

    Progressive orexin A positive neuron loss in the 6-OHDA mouse model of Parkinson's disease: a pilot study with validation of an orexin A immunohistochemistry protocol for paraffin-embedded tissue. · Abstract

    pubmed:42323123:743443206799:743443206799

Study findings

In this grass rat model, central orexin A administration increased daytime wakefulness in females.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    OXA treatment promoted daytime wakefulness in females,

    Central hypocretin/orexin administration alleviates sleep/wake disturbances, anhedonia, and neuroinflammation in an animal model of seasonal affective disorder. · RESULTS

    pubmed:41508567:bde9d1d76494:bde9d1d76494

Study findings

As summarized in the abstract, the existing literature provides limited evidence for orexin neuron loss specifically in neurotoxic mouse models.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    however, evidence in neurotoxic mouse models remains limited.

    Progressive orexin A positive neuron loss in the 6-OHDA mouse model of Parkinson's disease: a pilot study with validation of an orexin A immunohistochemistry protocol for paraffin-embedded tissue. · Abstract

    pubmed:42323123:743443206799:743443206799

Study findings

In an observational AD cohort, NREM oscillatory features (slow oscillation duration and sleep spindle density/power) showed inverse statistical associations with CSF orexin concentrations.

Human research · design must be checked

1 cited source · 1 linked study ID

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Longer SO duration and higher SP density and power were associated with lower CSF orexin concentrations (SP density: β = -187.37 pg/mL, 95% CI -344.93 to -29.80).

    Orexin, Sleep, and Cognition in Alzheimer Disease: Non-REM Oscillatory Activity and Neural Resilience. · RESULTS

    pubmed:42447420:0efa038e8709:0efa038e8709

Study findings

In this observational AD cohort, CSF orexin concentration was inversely associated with MMSE score.

Human research · design must be checked

1 cited source · 1 linked study ID

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Higher CSF orexin concentrations were associated with worse global cognition (ADAS-Cog: β = 0.014, 95% CI 0.003-0.024; MMSE: β = -0.01, 95% CI -0.011 to -0.004)

    Orexin, Sleep, and Cognition in Alzheimer Disease: Non-REM Oscillatory Activity and Neural Resilience. · RESULTS

    pubmed:42447420:0efa038e8709:0efa038e8709

Study findings

Across Parkinson’s disease models, orexin A and B are reported to preserve tyrosine hydroxylase expression, a marker commonly used for dopaminergic neuron phenotype/function.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    whereas orexin A and B preserve tyrosine hydroxylase expression

    Integrative role of orexigenic peptides in neuroprotection and neurodegenerative disease modulation. · Abstract

    pubmed:42063365:01e993ea1a4d:01e993ea1a4d

Study findings

Within rodent stress models, suvorexant treatment is reported to attenuate stress-associated elevations of the peptide orexin-A in the amygdala.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    In stress-exposed rodents, suvorexant reversed hyperarousal, avoidance, and anxiety-like behaviors, attenuated elevated orexin-A and CRF-R1 levels in the amygdala, and restored HPA axis function.

    A Scoping Review of Orexin Antagonists in Post-Traumatic Stress Disorder: Modulating Sleep, Stress, and Fear Circuits. · RESULTS

    pubmed:42391109:2c0d24e110a7:2c0d24e110a7

Study findings

In this observational AD cohort, CSF orexin concentration was positively associated with YKL-40 (a biomarker measured in CSF in this study).

Human research · design must be checked

1 cited source · 1 linked study ID

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Higher orexin was also associated with higher pTau181 (β = 0.11, 95% CI 0.04-0.19), total tau, and YKL-40 (β = 0.37, 95% CI 0.17-0.57).

    Orexin, Sleep, and Cognition in Alzheimer Disease: Non-REM Oscillatory Activity and Neural Resilience. · RESULTS

    pubmed:42447420:0efa038e8709:0efa038e8709

Study findings

Within the reviewed preclinical/clinical literature, orexin-A levels are listed among molecular markers examined in relation to PTSD-like phenotypes.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Some studies investigated molecular markers, such as orexin-A levels, corticosterone, CRF-R1, serotonin, mitochondrial fission/fusion proteins, and mTOR signaling.

    A Scoping Review of Orexin Antagonists in Post-Traumatic Stress Disorder: Modulating Sleep, Stress, and Fear Circuits. · MATERIALS AND METHODS

    pubmed:42391109:2c0d24e110a7:2c0d24e110a7

Study findings

In this observational AD cohort, CSF orexin concentration was positively associated with a tau pathology biomarker (pTau181).

Human research · design must be checked

1 cited source · 1 linked study ID

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Higher orexin was also associated with higher pTau181 (β = 0.11, 95% CI 0.04-0.19), total tau, and YKL-40 (β = 0.37, 95% CI 0.17-0.57).

    Orexin, Sleep, and Cognition in Alzheimer Disease: Non-REM Oscillatory Activity and Neural Resilience. · RESULTS

    pubmed:42447420:0efa038e8709:0efa038e8709

Study findings

In an in vivo rat electrophysiology model where HFES induced CA1 electrically evoked epileptiform discharges, intracerebroventricular orexin-A at 10 μg/10 μl shortened discharge duration within 20 minutes and eliminated the HFES-related progressive lengthening observed in controls.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Intracerebroventricular administration of orexin‑A significantly reduced the duration of EEDs within 20 minutes and abolished the progressive, HFES‑related prolongation of epileptiform discharges observed in control animals.

    Modulation of electrically evoked hippocampal epileptiform activity by exogenous orexins in the rat CA1 field. · Abstract

    pubmed:42370618:bdda096bc718:bdda096bc718

Study findings

In dimLD-exposed animals, central orexin A administration increased anti-inflammatory cytokine expression (IL-4 and IL-10).

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    treating dimLD animals with OXA increased expression of anti-inflammatory cytokines IL-4 and IL-10,

    Central hypocretin/orexin administration alleviates sleep/wake disturbances, anhedonia, and neuroinflammation in an animal model of seasonal affective disorder. · RESULTS

    pubmed:41508567:bde9d1d76494:bde9d1d76494

Study findings

In this case-control comparison, serum orexin-A concentration was decreased in the BD-M group versus controls, with statistical significance (p < 0.001).

Human research · design must be checked

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Serum OXA, OXB, sOX1R, and sOX2R levels were significantly lower in the BD-M group (all p < 0.001).

    Peripheral orexin system alterations in acute bipolar mania: Associations with clinical features and diagnostic performance. · RESULTS

    pubmed:42096890:fb3547d1e9ad:fb3547d1e9ad

Study findings

In generalized linear models in an AD cohort, CSF orexin concentration was positively associated with ADAS-Cog (higher indicates worse cognition in this context).

Human research · design must be checked

1 cited source · 1 linked study ID

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Higher CSF orexin concentrations were associated with worse global cognition (ADAS-Cog: β = 0.014, 95% CI 0.003-0.024; MMSE: β = -0.01, 95% CI -0.011 to -0.004)

    Orexin, Sleep, and Cognition in Alzheimer Disease: Non-REM Oscillatory Activity and Neural Resilience. · RESULTS

    pubmed:42447420:0efa038e8709:0efa038e8709

Study findings

Measured 1 month postpartum, plasma orexin-A concentration was lower in the postpartum depression group than in matched healthy controls, with a reported p-value of 0.021.

Human research · design must be checked

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Mean plasma orexin-A levels were significantly lower in women with postpartum depression compared to controls (65.2±10.8 vs. 79.9±6.4 pg/mL, p=0.021).

    Plasma orexin-A levels in women with postpartum depression: a prospective controlled study. · RESULTS

    pubmed:42307294:8511f7cf7b37:8511f7cf7b37

Study findings

Across the sampled postpartum women, higher maternal age was associated with higher plasma orexin-A, with correlation r=0.328 (p=0.011).

Human research · design must be checked

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Orexin-A levels were positively correlated with maternal age (r=0.328, p=0.011)

    Plasma orexin-A levels in women with postpartum depression: a prospective controlled study. · RESULTS

    pubmed:42307294:8511f7cf7b37:8511f7cf7b37

Study findings

Delivering orexin-A into the nucleus accumbens was reported to increase antinociception in a dose-dependent manner, indicating orexinergic signaling in this region can modulate acute nociceptive processing.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    Intra-NAc injections of morphine and orexin-A produced significant and dose-dependent antinociceptive effects.

    Orexinergic-Opioidergic Interactions Within the Nucleus Accumbens in the Modulation of Acute Pain: Evidence From the Tail-Flick Test in Rats. · RESULTS

    pubmed:42530048:8f359dc82632:8f359dc82632

Study findings

In Parkinson’s disease models, orexin A and B are described as increasing neuronal excitability, consistent with a functional neuromodulatory effect.

Animal / laboratory evidence

1 cited source · Study independence not established

Animal or laboratory findings do not establish benefit or safety in people.

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.

Exact passages, locators, and provenance
  1. supports · Source-backed record
    promote neuronal excitability

    Integrative role of orexigenic peptides in neuroprotection and neurodegenerative disease modulation. · Abstract

    pubmed:42063365:01e993ea1a4d:01e993ea1a4d

Risks and interactions

Risks, organized for scanning.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Products and regulatory status

Same ingredient. Different records.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Administration context

The practical clinical context.

This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.

Additional research & classification gaps

28 archived statements are kept separate from drug-effect findings. Media studies, economic models, methods, and records with unresolved scope are not used as medical-effect evidence.

Inspect contextual research (28)
Analytical / formulation research

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

When comparing targeted LC-MS quantification of orexin-A fragments against a clinically relevant RIA assay, the fragment concentrations showed strong rank-order agreement (Spearman correlation).

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Beyond orexinergic neurons, LH glutamatergic, GABAergic, and neurotensinergic populations are stated to participate in pain regulation with circuit-specific roles and partial anatomical/functional overlap with orexinergic circuitry.

Research context only—not evidence of a treatment effect.

Analytical / formulation research

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The workflow included fragment identification followed by targeted LC-MS quantification, which was then analytically compared against a clinically relevant RIA method.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The abstract reports an inverse association between orexin-A and cholecystokinin, quantified by r=- 0.297 with p<0.05.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The conclusion characterizes peripheral orexin-system changes in acute mania as both decreased biomarker concentrations and disrupted inter-component network connectivity.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The conclusion notes that longitudinal research is required to distinguish whether the observed orexin-system alterations reflect state effects of acute mania versus trait markers.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The review’s synthesis frames LH orexinergic neurons as an integrative hub connecting circuit activity to behavioral and physiological changes that modulate pain.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The review states that OXA increases the excitability of M2 ipRGCs, and this increased excitability is linked to enhancement of the pupillary light reflex (PLR).

Research context only—not evidence of a treatment effect.

Analytical / formulation research

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Using LC-MS/MS on CSF, investigators could not detect intact orexin-A, but they detected two N-terminal peptide fragments corresponding to residues 1-14 and 1-16.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Orexin A is part of a neuropeptide system most recognized for controlling sleep-wake regulation and energy homeostasis.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The objective included assessing peripheral (serum) orexin-A levels in BD-M and evaluating associations with clinical characteristics and multivariate/system-level analyses.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The authors interpret the observed peripheral orexin-system differences as suggesting a potential role for orexinergic dysregulation in BD-M.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Across multiple models summarized, reduced orexin pathway signaling is described as being associated with resilience phenotypes.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

In the lateral hypothalamus (LH), neurons synthesize the neuropeptide orexin-A.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Orexin A is one of two orexin neuropeptides in the orexin (hypocretin) system; this system also includes orexin B and the receptors OX1R and OX2R.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · 1 linked study ID

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record.

The biomarker panel included orexin-A quantified in cerebrospinal fluid.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Orexin signaling (including orexin-A) is described as directly regulating energy homeostasis and behaviors associated with energy balance.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The abstract states that dysregulated orexin signaling is strongly implicated in metabolic disorders, with obesity highlighted in particular.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Orexins (including orexin-A) are characterized as integrative neuromodulators coordinating autonomic, neuroendocrine, arousal, reward, and stress circuitry.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The orexin system is described as a regulator of arousal, sleep–wake cycling, and reward-related processing.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Orexin/hypocretin signaling is described as a regulator of arousal state, stress responsiveness, and REM sleep physiology.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The abstract characterizes orexin-A as a key neuroendocrine/autonomic regulator, with roles that include control of food intake.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The orexin neuropeptides (including orexin-A) are described as orchestrating feeding behavior and energy expenditure.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

Evidence summarized in this review indicates LH orexinergic neurons participate in multiple non-pharmacological analgesic paradigms (stress-induced analgesia, olfactory modulation, electroacupuncture, exercise-induced hypoalgesia), implying involvement in circuit-level pain modulation.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The conclusions attribute a mechanistic role to increased orexinergic activity, proposing it contributes to PTSD pathophysiology.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The abstract links dysregulated orexin signaling to psychiatric conditions, explicitly naming anxiety and depression.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The abstract states that the review summarizes recent advances in orexin-A neural circuitry relevant to feeding regulation.

Research context only—not evidence of a treatment effect.

Research context · scope unclassified

1 cited source · Study independence not established

How to read this evidence

Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.

1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.

The abstract states the review emphasizes mechanistic interplay among orexin signaling, energy balance, and anxiety–obesity comorbidity.

Research context only—not evidence of a treatment effect.

Research status + gaps

What still needs better answers?

  • No publishable claim yet for: administration, contraindication, interaction, regulatory, safety
  • 189 compiled claim(s) withheld by automated assurance: assurance_score_below_0.58 (118), assurance_score_below_0.72 (54), current_regulatory_source_required (49), extraction_ambiguity (144), high_risk_requires_regulatory_or_two_independent_sources (69), no_direct_support (169), proposal_not_staged (2)

These are the limits of this profile, not an exhaustive list of scientific uncertainties.

References + discovery

Open the records yourself.

  1. orexin-A

    iuphar-ligand · published 2026-08-28 · retrieved 2026-08-28T12:35:21Z

  2. Central hypocretin/orexin administration alleviates sleep/wake disturbances, anhedonia, and neuroinflammation in an animal model of seasonal affective disorder.

    pubmed · published 2026-12-01 · retrieved 2026-08-28T12:35:21Z

  3. Integrative role of orexigenic peptides in neuroprotection and neurodegenerative disease modulation.

    pubmed · published 2026-07-22 · retrieved 2026-09-04T08:38:04Z

  4. Peripheral orexin system alterations in acute bipolar mania: Associations with clinical features and diagnostic performance.

    pubmed · published 2026-09-15 · retrieved 2026-08-28T12:35:21Z

  5. Formalin-induced pain preferentially activates orexin neurons in male mice.

    pubmed · published 2026-06-30 · retrieved 2026-09-05T09:00:33Z

  6. Identification and quantification of Hypocretin-1/Orexin-A 1-14 and 1-16 fragments in immunopurified cerebrospinal fluid using LC-MS: Comparison with radioimmunoassay (RIA) determinations.

    pubmed · published 2026-09-01 · retrieved 2026-08-28T12:35:21Z

  7. The orexinergic system in the retina: Expression and physiological impact-A review of the literature.

    pubmed · published 2026-07-01 · retrieved 2026-09-05T09:00:33Z

  8. Regulators of Appetite in Mammals - Old and New players.

    pubmed · published 2026-06-11 · retrieved 2026-09-04T08:38:04Z

  9. Plasma orexin-A levels in women with postpartum depression: a prospective controlled study.

    pubmed · published 2026-01-01 · retrieved 2026-09-05T09:00:33Z

  10. Progressive orexin A positive neuron loss in the 6-OHDA mouse model of Parkinson's disease: a pilot study with validation of an orexin A immunohistochemistry protocol for paraffin-embedded tissue.

    pubmed · published 2026-10-01 · retrieved 2026-08-28T12:35:21Z

  11. The Neural Network of Orexin-A: Implications in Feeding Regulation and Obesity-Anxiety Comorbidity.

    pubmed · published 2026-06-09 · retrieved 2026-09-05T09:00:33Z

  12. Modulation of electrically evoked hippocampal epileptiform activity by exogenous orexins in the rat CA1 field.

    pubmed · published 2026-06-15 · retrieved 2026-09-05T09:00:33Z

  13. A Scoping Review of Orexin Antagonists in Post-Traumatic Stress Disorder: Modulating Sleep, Stress, and Fear Circuits.

    pubmed · published 2026-07-02 · retrieved 2026-09-05T09:00:33Z

  14. Orexin, Sleep, and Cognition in Alzheimer Disease: Non-REM Oscillatory Activity and Neural Resilience.

    pubmed · published 2026-08-11 · retrieved 2026-09-05T09:00:33Z

  15. Lateral hypothalamic orexinergic neurons as central mediators of pain modulation and non-pharmacological analgesia.

    pubmed · published 2026-01-01 · retrieved 2026-09-05T09:00:33Z

  16. Orexinergic-Opioidergic Interactions Within the Nucleus Accumbens in the Modulation of Acute Pain: Evidence From the Tail-Flick Test in Rats.

    pubmed · published 2026-07-23 · retrieved 2026-09-05T09:00:33Z

  17. The orexin system as a pharmacological target in inflammation: peripheral mechanisms and safety implications.

    pubmed · published 2026-01-01 · retrieved 2026-09-05T09:00:33Z

  18. Is Hashimoto's Thyroiditis Associated with Insulin Resistance Markers?

    pubmed · published 2026-08-18 · retrieved 2026-08-28T12:35:21Z

Publication history and provenance

Version 2 · Automated assessment · 2026-09-05T09:00:33Z

04b1ff8d44c656b8affbad5adb72ae60d706d2aa0a0b9aef206a2c326c3e8b1c