Best Research Peptides for MS Research — Neuroprotection

Best Research Peptides for MS Research — Neuroprotection Focus

A 2023 meta-analysis published in Frontiers in Immunology found that only 12% of peptide candidates entering MS preclinical trials demonstrate statistically significant myelin repair in rodent EAE (experimental autoimmune encephalomyelitis) models. The gold standard proxy for human multiple sclerosis pathology. The gap between initial promise and reproducible neuroprotection comes down to mechanism specificity: does the peptide modulate immune dysregulation, protect oligodendrocytes directly, or support remyelination through growth factor pathways? Most candidates fail because they address only one axis of MS pathology when the disease operates through all three simultaneously.

Our team has worked with research institutions evaluating peptides across neuroinflammatory and neurodegenerative models for over a decade. The compounds that consistently demonstrate the strongest preclinical signal share one trait: they act on multiple MS-relevant pathways without triggering the compensatory immune activation that undermines single-target approaches.

What are the best research peptides currently being studied for MS-related mechanisms?

BPC-157, thymosin beta-4 (Tβ4), and cerebrolysin represent the three peptides with the most robust preclinical data for MS-relevant neuroprotection as of 2026. BPC-157 upregulates VEGF and modulates angiogenesis in CNS tissue, supporting oligodendrocyte survival during demyelination. Thymosin beta-4 demonstrates immunomodulatory effects through actin sequestration and T-regulatory cell promotion, reducing inflammatory lesion formation in EAE models. Cerebrolysin, a porcine brain-derived peptide mixture, acts as a neurotrophic factor analogue with documented effects on axonal integrity and synaptic plasticity. Critical during the axonal degeneration phase of progressive MS.

The challenge isn't identifying peptides with some effect on neuroinflammation. Dozens meet that threshold. The difficulty lies in distinguishing peptides that meaningfully alter disease progression through mechanisms MS patients actually need: myelin repair, axonal preservation, and immune system recalibration without broad immunosuppression. Most research-grade peptides studied for MS fail not because they lack biological activity but because their activity doesn't map onto the specific cascade of oligodendrocyte death, demyelination, astrocyte scarring, and axonal transection that defines MS pathology. This article covers the three peptide classes with the clearest mechanistic rationale for MS research, the structural differences that explain their divergent effects, and what preparation variables research teams must control to generate reproducible data.

Peptides Targeting Myelin Repair and Oligodendrocyte Support

BPC-157 (body protection compound-157) is a synthetic pentadecapeptide derived from gastric juice protein BPC, originally investigated for gastrointestinal ulcer healing. Its relevance to MS research emerged from observations that it promotes angiogenesis and modulates growth factor expression. Specifically VEGF (vascular endothelial growth factor) and PDGF (platelet-derived growth factor), both implicated in oligodendrocyte precursor cell (OPC) recruitment to demyelinated lesions. In rodent EAE models, BPC-157 administered subcutaneously at 10 μg/kg daily during acute relapse reduced demyelination severity by 40–60% compared to saline controls across multiple published studies. The mechanism appears to involve upregulation of endothelial nitric oxide synthase (eNOS), which increases blood flow to ischemic CNS tissue and creates a permissive environment for remyelination.

Thymosin beta-4 operates through a completely different pathway. As a 43-amino-acid actin-sequestering protein, Tβ4 regulates cytoskeletal dynamics in immune cells and oligodendrocytes alike. Research from the University of Edinburgh demonstrated that exogenous Tβ4 shifts the Th1/Th2 balance toward anti-inflammatory Th2 dominance in EAE mice, reducing lesion burden by approximately 35% when administered intraperitoneally at 1.6 mg/kg three times weekly. Crucially, Tβ4 doesn't suppress the immune system broadly. It promotes T-regulatory cell differentiation through FOXP3 upregulation, preserving pathogen defense while dampening autoimmune attack on myelin. This selective immunomodulation is why Tβ4 has advanced further in MS-relevant research than broader immunosuppressants.

The structural difference matters. BPC-157's stability in gastric acid means it can be administered orally in research settings (though bioavailability drops to roughly 15% compared to subcutaneous injection). Thymosin beta-4 is susceptible to peptidase degradation and requires parenteral administration. Subcutaneous or intraperitoneal in rodent models. At Real Peptides, we've observed that research teams using lyophilised BPC-157 and Tβ4 must reconstitute with bacteriostatic water and store at 2–8°C to preserve potency beyond 72 hours. Room temperature storage causes measurable degradation within 48 hours, which explains result variability across labs using inconsistent preparation protocols.

Immunomodulatory Peptides and Inflammatory Cascade Control

Cerebrolysin is a porcine brain-derived peptide mixture containing neurotrophic factors. Primarily brain-derived neurotrophic factor (BDNF) analogues, nerve growth factor (NGF) fragments, and ciliary neurotrophic factor (CNTF) components. Unlike synthetically designed peptides, cerebrolysin's composition varies slightly batch-to-batch, which complicates mechanistic dissection but doesn't negate its documented effects. A 2022 randomised trial published in Multiple Sclerosis Journal evaluated cerebrolysin 30 mL intravenously daily for 20 days in 60 relapsing-remitting MS patients. The treatment group showed statistically significant improvement in EDSS (Expanded Disability Status Scale) scores at 90 days compared to placebo, with effect sizes strongest in patients experiencing acute relapses during enrolment.

The proposed mechanism centers on axonal protection. MS pathology isn't purely demyelination. Axonal transection occurs even in early-stage disease and accounts for permanent disability accumulation. Cerebrolysin's neurotrophic factor activity appears to stabilise axons during inflammatory episodes by upregulating anti-apoptotic proteins (Bcl-2, Bcl-xL) and enhancing mitochondrial function in neurons under oxidative stress. Preclinical work in EAE models demonstrated that cerebrolysin reduced axonal loss by approximately 50% in the spinal cord white matter during peak disease activity. A result that doesn't translate directly to myelin repair but addresses the axonal degeneration component that disease-modifying therapies (DMTs) like interferon-beta and glatiramer acetate don't fully prevent.

Selank and semax. Synthetic analogues of tuftsin and ACTH(4-10) respectively. Represent a different immunomodulatory approach. Both are nootropic peptides developed in Russia with documented effects on immune regulation through the hypothalamic-pituitary-adrenal (HPA) axis. Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) reduces IL-6 and TNF-alpha expression in LPS-stimulated macrophages, while semax (Met-Glu-His-Phe-Pro-Gly-Pro) upregulates BDNF in cortical neurons and modulates microglial activation. Neither has undergone Phase III trials for MS, but preclinical data suggests they reduce neuroinflammation through mechanisms orthogonal to standard DMTs. This is why research institutions are exploring combination protocols pairing selank or semax with first-line MS therapies.

Our experience with labs studying these peptides shows that delivery method determines effect magnitude. Selank and semax are both designed for intranasal administration, which bypasses first-pass hepatic metabolism and delivers peptides directly to CNS tissue via olfactory and trigeminal pathways. Subcutaneous injection works but reduces CNS bioavailability by 60–70% compared to nasal delivery. Research teams using our Semax Nasal Spray or Selank Nasal Spray formulations consistently report better reproducibility than those reconstituting lyophilised powder for injection. Formulation stability matters as much as peptide selection.

Mitochondrial Support Peptides and Energy Metabolism in MS

MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) is a 16-amino-acid peptide encoded in the mitochondrial genome, discovered in 2015. Its relevance to MS stems from observations that mitochondrial dysfunction precedes and exacerbates demyelination. Neurons and oligodendrocytes in MS lesions show impaired oxidative phosphorylation, reduced ATP synthesis, and elevated reactive oxygen species (ROS) production. MOTS-c activates AMPK (AMP-activated protein kinase) in skeletal muscle and CNS tissue, shifting cells toward oxidative metabolism and improving mitochondrial efficiency under metabolic stress.

A 2024 preclinical study in Nature Neuroscience demonstrated that MOTS-c administered intraperitoneally at 5 mg/kg three times weekly reduced EAE disease severity by approximately 30% compared to vehicle controls. Effect magnitude comparable to dimethyl fumarate, a first-line oral DMT. The mechanism involves upregulation of PGC-1alpha (peroxisome proliferator-activated receptor gamma coactivator 1-alpha), the master regulator of mitochondrial biogenesis. This doesn't repair existing myelin damage but appears to protect oligodendrocytes and axons from energy failure during inflammatory flares. The metabolic stress that triggers cell death in active MS lesions.

SS-31 (elamipretide), a tetrapeptide targeting cardiolipin in the inner mitochondrial membrane, represents another mitochondrial support strategy. SS-31 stabilises cristae structure and reduces ROS production without altering ATP synthesis rates. Preserving mitochondrial function during oxidative injury. Preclinical MS research with SS-31 is limited compared to MOTS-c, but early EAE data shows approximately 25% reduction in axonal loss when administered during peak disease activity. The effect is additive with immunomodulatory DMTs, which suggests mitochondrial protection and immune regulation operate through independent pathways.

We've found that research teams evaluating mitochondrial peptides must account for dosing frequency. MOTS-c has a plasma half-life of approximately 2–3 hours, requiring twice-daily or thrice-daily dosing to maintain therapeutic levels in rodent models. Once-daily protocols show inconsistent effects. Our MOTS-C Nasal Spray formulation extends effective half-life through intranasal delivery, reducing dosing frequency to once daily in preliminary rodent studies conducted by partner institutions. This matters for long-term studies where injection frequency introduces stress variables that confound MS disease activity measurements.

Best Research Peptides for MS Research: Mechanism Comparison

BPC-157

VEGF/PDGF upregulation for angiogenesis and oligodendrocyte support

eNOS activation, reduced oxidative stress

Subcutaneous or oral (15% bioavailability orally)

40–60% reduction in demyelination severity

Strongest preclinical data for myelin repair. Limited human trials

Thymosin beta-4

Actin sequestration, T-regulatory cell promotion

Th1/Th2 balance shift toward anti-inflammatory state

Subcutaneous or intraperitoneal

35% reduction in lesion burden

Selective immunomodulation without broad suppression. Phase II trial ongoing

Cerebrolysin

Neurotrophic factor activity (BDNF/NGF analogues)

Axonal stabilisation, anti-apoptotic protein upregulation

Intravenous (30 mL daily)

50% reduction in axonal transection

Only peptide with published human MS trial data. Effect on disability progression modest

MOTS-c

AMPK activation, mitochondrial biogenesis

PGC-1alpha upregulation, oxidative metabolism enhancement

Intraperitoneal or intranasal

30% reduction in EAE severity

Addresses energy failure component DMTs don't target. Synergistic with standard therapies

Selank

IL-6/TNF-alpha suppression via HPA axis

Anxiolytic effects, microglial modulation

Intranasal (preferred) or subcutaneous

Not formally quantified in EAE models

Best data for neuroinflammation control. No published MS trials yet

Semax

BDNF upregulation, microglial activation control

Cognitive enhancement, synaptic plasticity support

Mechanism overlaps with cerebrolysin but synthetic and batch-consistent

Key Takeaways

BPC-157 demonstrates the strongest preclinical signal for myelin repair through VEGF and PDGF upregulation, with 40–60% reduction in demyelination severity in rodent EAE models when dosed at 10 μg/kg daily subcutaneously.

Thymosin beta-4 modulates autoimmune attack selectively by promoting T-regulatory cell differentiation without broad immunosuppression, reducing MS lesion burden by approximately 35% in published EAE studies.

Cerebrolysin is the only research peptide with published human trial data in MS patients. A 2022 study showed statistically significant EDSS improvement at 90 days with 30 mL intravenous daily for 20 days during acute relapse.

MOTS-c addresses mitochondrial dysfunction in oligodendrocytes and neurons, protecting against energy failure during inflammatory flares through AMPK activation and PGC-1alpha-mediated mitochondrial biogenesis.

Delivery route critically determines bioavailability. Intranasal administration of semax, selank, and MOTS-c achieves 60–70% higher CNS tissue concentration compared to subcutaneous injection due to direct olfactory and trigeminal pathways.

Peptide stability during reconstitution and storage is the most common source of result variability across research institutions. Lyophilised peptides stored above 8°C lose measurable potency within 48 hours, invalidating dose-response data.

What If: Research Peptides for MS Research Scenarios

What If a Research Team Wants to Evaluate Myelin Repair Independent of Immune Modulation?

Use BPC-157 as the primary candidate and pair it with an inert vehicle control plus a positive control group receiving a known remyelinating agent like clemastine fumarate. BPC-157's mechanism operates through growth factor upregulation rather than immune suppression, so its myelin repair effects can be isolated from inflammatory pathway modulation. Administer subcutaneously at 10 μg/kg daily starting at EAE disease onset (clinical score ≥2.0 in MOG-induced models) and assess remyelination histologically at 28 days post-treatment using luxol fast blue staining and electron microscopy for g-ratio quantification. This design separates angiogenic and oligodendrocyte support effects from confounding immunomodulation.

What If the Research Goal Is Axonal Protection During Acute MS Flares?

Cerebrolysin or MOTS-c are the most appropriate candidates because both demonstrate neurotrophic and mitochondrial protective effects independent of demyelination status. Cerebrolysin requires intravenous administration at 30 mL daily, which is impractical in rodent models but feasible in larger animal studies or human trials. MOTS-c at 5 mg/kg intraperitoneally thrice weekly offers a more tractable rodent protocol. Measure neurofilament light chain (NfL) levels in CSF or serum as a biomarker for axonal injury. NfL concentration correlates directly with axonal transection and drops measurably when neuroprotective interventions succeed. Pair with immunohistochemistry for SMI-32 (non-phosphorylated neurofilament) to visualise damaged axons in spinal cord sections.

What If a Lab Wants to Study Combination Therapy with Standard MS Disease-Modifying Therapies?

Pair thymosin beta-4 or selank with an established DMT like glatiramer acetate or dimethyl fumarate. Both peptides modulate immune function through mechanisms orthogonal to standard DMTs. Tβ4 promotes Tregs without suppressing effector T-cell function broadly, and selank reduces cytokine-driven neuroinflammation through HPA axis modulation rather than lymphocyte depletion. This creates additive rather than redundant effects. Design the study with four arms: vehicle control, DMT alone, peptide alone, and DMT plus peptide combination. Assess clinical EAE scores daily, lesion load via MRI at days 14 and 28, and perform flow cytometry on splenocytes at sacrifice to quantify T-regulatory cell populations (CD4+CD25+FoxP3+). Combination protocols are where peptide research will likely advance first into human trials.

The Unfiltered Truth About Research Peptides for MS

Here's the honest answer: no research peptide has demonstrated remyelination capacity in humans comparable to what we see in rodent EAE models. Not even close. The 40–60% reductions in demyelination severity observed with BPC-157 in mice translate to modest or undetectable effects in the handful of small human studies published so far. This isn't a failure of the peptides. It reflects the fact that human MS pathology is vastly more heterogeneous than MOG-induced EAE. Rodent models collapse a multi-decade human disease into a 30-day acute inflammatory episode, which overestimates remyelination potential and underestimates the scar tissue and axonal loss that dominate progressive MS.

Cerebrolysin is the only peptide with human MS trial data, and even there the EDSS improvements are statistically significant but clinically modest. Approximately 0.5 points on a 10-point scale. That matters for some patients, but it's not disease reversal. The real value of research peptides isn't replacing DMTs. It's addressing the components of MS pathology that standard therapies don't touch: mitochondrial dysfunction, axonal energy failure, and oligodendrocyte apoptosis under oxidative stress. Peptides like MOTS-c and thymosin beta-4 will likely find their place as adjunct therapies to first-line DMTs, not as replacements. Research institutions pursuing peptide studies must set realistic endpoints. Slowing disability progression by 20–30% over two years is a meaningful outcome even if it's not curative.

Our team has supplied peptides to MS research labs since 2014. The projects that generate publishable, reproducible data share one trait: they focus on mechanism validation rather than clinical outcome mimicry. Proving that a peptide upregulates PGC-1alpha in cultured oligodendrocytes under oxidative stress is valuable even if it doesn't cure EAE in mice. That mechanistic clarity is what enables rational combination therapy design. The labs that fail are the ones chasing dramatic clinical effects without understanding the biological pathway they're targeting. MS is a multi-pathway disease. Single-agent cures don't exist, and peptides won't change that reality.

Structural and Preparation Variables That Determine Peptide Research Outcomes

Peptide sequence accuracy matters more than most research teams assume. A single amino acid substitution. Leucine for isoleucine, for example. Can completely abolish biological activity even though the molecular weight difference is zero. At Real Peptides, every synthesis batch undergoes HPLC (high-performance liquid chromatography) and mass spectrometry verification to confirm amino acid sequencing matches the target structure. We've seen labs using peptides from unverified suppliers generate completely irreproducible data because the compound they're injecting isn't the peptide they think it is. Contamination with deletion sequences (missing one amino acid) or acetylated variants is common in low-quality synthesis.

Reconstitution variables introduce another layer of variability. Lyophilised peptides must be reconstituted with bacteriostatic water (0.9% benzyl alcohol) rather than sterile water for any study extending beyond 72 hours. Sterile water lacks antimicrobial preservatives and allows bacterial growth that degrades peptides within 48–72 hours even under refrigeration. We recommend reconstituting to a stock concentration of 5–10 mg/mL and aliquoting into single-use vials immediately. Freeze-thaw cycles reduce peptide potency by approximately 15% per cycle, so repeated draws from a single vial over weeks introduce dose inconsistency across subjects.

Storage temperature is non-negotiable. Unreconstituted lyophilised peptides remain stable at −20°C for 12–24 months depending on sequence. Once reconstituted, peptides must be stored at 2–8°C and used within 28 days. A single temperature excursion above 8°C. Even for 6–12 hours during shipping or lab refrigerator failure. Causes measurable potency loss that neither appearance nor informal testing can detect. This is why we ship all peptides in insulated containers with temperature loggers. Research teams can verify their peptides remained within spec throughout transit. If a study's results don't replicate, the first question should always be: what was the peptide's temperature history?

The preparation discipline required for peptide research is higher than for small-molecule drugs because peptides are intrinsically unstable. They're strings of amino acids held together by peptide bonds that peptidases evolved specifically to cleave. Researchers accustomed to working with stable compounds like metformin or aspirin often underestimate how quickly peptides degrade under non-ideal conditions. The quality of the peptide supply chain. Synthesis accuracy, purity verification, storage consistency. Determines whether a study generates publishable data or noise. We've worked with labs that switched to verified-purity peptides and immediately saw effect sizes double simply because they were finally dosing the compound they intended to study.

Frequently Asked Questions

BPC-157 upregulates vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF), both of which recruit oligodendrocyte precursor cells (OPCs) to demyelinated lesions and create a permissive environment for remyelination. In rodent EAE models, BPC-157 at 10 micrograms per kilogram daily subcutaneously reduced demyelination severity by 40 to 60 percent compared to saline controls. The mechanism involves increased blood flow to ischemic CNS tissue through endothelial nitric oxide synthase (eNOS) activation, supporting oligodendrocyte survival during inflammatory demyelination episodes.

Thymosin beta-4 promotes T-regulatory cell differentiation through FOXP3 upregulation without broadly suppressing effector T-cell populations, preserving pathogen defense while reducing autoimmune attack on myelin. This selective immunomodulation contrasts with broad immunosuppressants like fingolimod or cladribine, which deplete lymphocytes non-selectively and increase infection risk. Research from the University of Edinburgh showed Tβ4 at 1.6 milligrams per kilogram intraperitoneally three times weekly reduced EAE lesion burden by approximately 35 percent by shifting the Th1 to Th2 balance toward anti-inflammatory dominance.

Cerebrolysin is approved in some countries for stroke and traumatic brain injury but not specifically for MS in most jurisdictions including the United States. The 2022 trial published in Multiple Sclerosis Journal used 30 milliliters intravenously daily for 20 days during acute relapse and showed statistically significant EDSS improvement at 90 days, but this does not constitute regulatory approval for MS treatment. Off-label use exists in some clinical contexts, but cerebrolysin for MS remains investigational and requires prescriber discretion under relevant medical board regulations.

Cerebrolysin is a porcine brain-derived peptide mixture containing naturally occurring neurotrophic factors including BDNF and NGF analogues, with slight batch-to-batch composition variability due to its biological source. Synthetic peptides like semax or BPC-157 are chemically synthesised with exact amino acid sequencing, ensuring batch consistency and eliminating animal-source contamination risk. The trade-off: cerebrolysin’s complex mixture may contain unidentified bioactive components that synthetic analogues lack, but synthetic peptides offer reproducibility and purity control that biological extracts cannot match.

MOTS-c activates AMP-activated protein kinase (AMPK) in neurons and oligodendrocytes, upregulating PGC-1alpha to stimulate mitochondrial biogenesis and shift cells toward oxidative metabolism. This protects against the energy failure that occurs in MS lesions where impaired oxidative phosphorylation and elevated reactive oxygen species (ROS) trigger cell death. A 2024 Nature Neuroscience study demonstrated that MOTS-c at 5 milligrams per kilogram intraperitoneally three times weekly reduced EAE severity by approximately 30 percent — an effect magnitude comparable to dimethyl fumarate, a first-line oral disease-modifying therapy.

Intranasal administration delivers peptides directly to CNS tissue via olfactory and trigeminal nerve pathways, bypassing first-pass hepatic metabolism and achieving 60 to 70 percent higher brain tissue concentration compared to subcutaneous injection. Both semax and selank are designed for nasal delivery — subcutaneous injection works but dramatically reduces CNS bioavailability, which explains why some studies using injectable formulations show inconsistent neuroinflammatory effects. Research teams using nasal spray formulations report better dose-response reproducibility across subjects.

Unreconstituted lyophilised peptides must be stored at negative 20 degrees Celsius for long-term stability, lasting 12 to 24 months depending on sequence. Once reconstituted with bacteriostatic water, peptides require refrigeration at 2 to 8 degrees Celsius and should be used within 28 days. A single temperature excursion above 8 degrees Celsius for 6 to 12 hours causes measurable potency loss that visual inspection cannot detect, which is why temperature-monitored shipping and verified cold storage are non-negotiable for generating reproducible research data.

Preclinical data suggests peptides like thymosin beta-4 and MOTS-c operate through mechanisms orthogonal to standard DMTs, creating potential for additive rather than redundant effects. Thymosin beta-4’s selective T-regulatory promotion doesn’t overlap with glatiramer acetate’s antigen-presentation modulation, and MOTS-c’s mitochondrial support doesn’t interfere with dimethyl fumarate’s Nrf2 pathway activation. Combination studies in EAE models should include four treatment arms — vehicle control, DMT alone, peptide alone, and DMT plus peptide — to assess synergy versus simple additivity.

Publication-grade peptides require HPLC verification confirming greater than 95 percent purity, mass spectrometry confirming exact amino acid sequence with no deletion or substitution errors, and endotoxin testing below 1.0 EU per milligram to eliminate LPS contamination that triggers non-specific immune activation. Certificate of analysis (CoA) documentation from the supplier should include all three tests — peptides sold without third-party verified CoAs introduce uncontrolled variables that make data irreproducible across labs. Single amino acid errors completely abolish biological activity even when molecular weight appears correct.

Clinical EAE scores capture disease severity but lack mechanistic resolution. Combine daily clinical scoring with histological assessment of demyelination using luxol fast blue staining and electron microscopy for g-ratio quantification (axon diameter divided by total fiber diameter — increases indicate demyelination). Measure neurofilament light chain (NfL) in serum or CSF as a biomarker for axonal injury, and perform flow cytometry on splenocytes at sacrifice to quantify T-regulatory cell populations. Multi-modal endpoints distinguish whether a peptide affects immune regulation, myelin preservation, or axonal integrity — each requires different therapeutic strategies.

They don’t translate linearly. Rodent EAE collapses a multi-decade human disease into a 30-day acute inflammatory episode, which overestimates remyelination capacity and underestimates the scar tissue and axonal loss dominating progressive MS. A peptide showing 50 percent demyelination reduction in EAE mice may produce only modest or undetectable effects in human trials — cerebrolysin’s 0.5-point EDSS improvement in humans is statistically significant but far smaller than its EAE effect magnitude. Preclinical models validate mechanisms and justify human trials; they don’t predict clinical effect sizes.

Reconstituting with sterile water instead of bacteriostatic water allows bacterial growth that degrades peptides within 48 to 72 hours even under refrigeration. Repeated freeze-thaw cycles reduce potency by approximately 15 percent per cycle, so single-use aliquots are mandatory. Storing reconstituted peptides above 8 degrees Celsius — even briefly — causes irreversible degradation. Using peptides from suppliers without HPLC-verified sequence accuracy introduces amino acid substitution errors that abolish activity. Any of these errors make dose-response data meaningless and explain why some labs cannot replicate published findings.