Dihexa for Gut-Brain Axis Brain Fog: IBS, SIBO, Leaky Gut, the Microbiome & the 2026 UK Review

The gut has become the most fashionable organ in neuroscience — and behind the “second brain” hype is a real cognitive story. Your digestive tract houses trillions of microbes and its own dense nervous system, and it talks to the brain constantly along the vagus nerve and through immune, hormonal and metabolic signals — the microbiota–gut–brain axis. When that system is disturbed, as it can be in irritable bowel syndrome (IBS) — which affects an estimated 10–20% of people — in small intestinal bacterial overgrowth (SIBO), after a gut infection, or in long COVID, many people notice the fatigue, poor concentration and fuzzy thinking they call brain fog. In 2024 the “Gut Feelings” randomised controlled trial found weak evidence that a probiotic improved working memory, and a clinical trial is now testing a probiotic (Lactobacillus paracasei PS23) specifically against long-COVID brain fog. Because the gut feeds the very BDNF-driven synaptic plasticity that Dihexa — a positive modulator of HGF/c-Met synaptogenesis — also targets, people increasingly ask whether a peptide belongs in the conversation. This 2026 UK review walks through the signalling routes, the new trial data, the microbiome–BDNF link, what genuinely helps, and where Dihexa really sits: behind a proper gut work-up and treatment, not in front of it.

The Gut-Brain Axis and Brain Fog in 2026: Why Everyone Is Talking About the Microbiome

For most of medical history the gut and the brain were treated as separate territories. That has changed completely. The intestine is now understood to house a vast microbial ecosystem — trillions of bacteria, archaea, viruses and fungi — alongside its own extensive nervous system, the enteric nervous system, sometimes nicknamed the “second brain.” These two systems are in constant dialogue with the central nervous system through what researchers call the microbiota–gut–brain axis: a bidirectional network that integrates neural, immune, endocrine and metabolic signalling. When people search for “leaky gut brain fog,” “IBS brain fog” or “gut bacteria and memory,” this axis is what they are reaching for.

The clinical backdrop is large. Irritable bowel syndrome alone affects an estimated 10–20% of the population, making it one of the most common conditions a GP sees, and functional gut symptoms — bloating, irregular bowel habit, discomfort — are even more widespread. A recurring theme in patient accounts of these conditions is that the symptoms are not confined to the abdomen: fatigue, low mood, poor concentration and a foggy, slowed-down quality of thinking travel with them. The gut-brain axis offers a biologically grounded reason why that might be more than coincidence.

The symptoms people notice — tiredness, difficulty focusing, a sense that thinking takes more effort — overlap heavily with what the public calls “brain fog.” That overlap is exactly what makes the microbiome a fashionable suspect, and also what makes it tricky: those same symptoms are produced by poor sleep, stress, alcohol, an underactive thyroid, and iron, B12 or vitamin D deficiency. So the gut is best treated as one common, addressable contributor on a longer list — worth investigating and improving before anything exotic is considered. The patient-facing question echoes the one running through the other reviews on this site: “my brain fog has a plausible gut cause — does something like Dihexa belong anywhere in the picture?”

The 2024–2026 News: Why the Gut-Brain Axis Is Back in the Headlines

Two developments pushed the gut-and-cognition story back into the wellness conversation. The first was the 2024 “Gut Feelings” randomised, controlled trial, which tested a prebiotic-rich diet and/or probiotic supplements against cognition in adults. As a secondary outcome it found weak evidence that the probiotic improved working memory — reported as roughly a 96% posterior probability of benefit. That is a genuine, carefully analysed signal, and it is also a long way from a cognitive drug: the effect was small, it was a secondary outcome, and “weak evidence” is the authors' own framing, not a marketing gloss.

The second is more pointed. A registered clinical trial, NCT06348212, is now testing the probiotic strain Lactobacillus paracasei PS23 specifically against brain fog in people with long COVID — the first time many people will have seen “brain fog” written as a formal trial endpoint with a gut-targeted intervention. It reflects a fast-growing literature: reviews through 2025 describe long-COVID gut dysbiosis — reduced microbial diversity and depletion of short-chain-fatty-acid producers such as Faecalibacterium prausnitzii and Bifidobacterium — as a leading hypothesis for the persistent cognitive symptoms, with brain fog described in up to a third of long-COVID patients.

Alongside these, a steady stream of 2025–2026 reviews has consolidated the mechanistic picture. A 2025 Frontiers in Microbiology review mapped the microbiota–gut–brain axis from pathogenesis to therapy; a companion paper examined its impact on brain structure and function; and work on immune modulation and cognitive decline tied dysbiosis to neuroinflammation. The direction of travel is clear: the gut is a real input into cognition. What remains unsettled — and this is the crux for anyone considering a peptide — is how reliably changing the gut clears established fog in a given person.

What “Gut Brain Fog” Actually Is: IBS, SIBO and Leaky Gut Explained

The phrase covers several overlapping ideas, and it helps to separate them. Irritable bowel syndrome (IBS) is a common functional disorder of gut-brain interaction, diagnosed clinically from abdominal pain related to bowel habit, bloating and altered stool form, once red flags are excluded. It is real, it is disruptive, and many people with it report cognitive and fatigue symptoms — which makes sense if gut-brain signalling is disturbed. UK diagnosis and management are guided by NICE CG61.

Small intestinal bacterial overgrowth (SIBO) describes an excess of bacteria in the small intestine, where numbers should be low. It can cause bloating, wind, discomfort and altered bowel habit, and a 2020 meta-analysis found SIBO in around a third of people diagnosed with IBS. The honest caveat is that SIBO is hard to confirm: hydrogen and methane breath tests have poor sensitivity and specificity, are not recommended by some specialist guidelines, and have very limited NHS availability — so “I have SIBO” is frequently a self-diagnosis built on an unreliable test. That uncertainty matters when someone is deciding how aggressively to intervene.

“Leaky gut” — more precisely, increased intestinal permeability — is the idea that a compromised gut lining lets bacterial products such as lipopolysaccharide cross into the bloodstream, driving low-grade systemic inflammation that can reach the brain. Intestinal permeability is a genuine, measurable phenomenon studied in conditions from coeliac disease to inflammatory bowel disease, and it is biologically plausible as a route to neuroinflammation. But “leaky gut” as a stand-alone consumer diagnosis is far less well defined than the marketing implies, and it is often invoked to sell supplements. The useful version of all three concepts is the same: a disturbed gut can plausibly cloud thinking through the gut-brain axis — which is a reason to investigate and treat the gut properly, not a licence to reach past that toward an experimental compound.

How the Gut Talks to the Brain: Vagus Nerve, Short-Chain Fatty Acids, Immune & Endocrine Routes

Why would the state of the intestine affect thinking at all? The mechanistic story has become unusually detailed. The gut signals the brain along at least four interlocking routes. The first is neural: the vagus nerve carries information directly from gut to brainstem, and microbial metabolites can activate vagal afferent neurons within seconds to minutes, triggering brainstem and limbic responses that modulate working memory, cognitive flexibility and stress resilience. The second is metabolic: gut bacteria ferment dietary fibre into short-chain fatty acids (SCFAs) — chiefly butyrate, propionate and acetate — which are anti-inflammatory, help maintain the gut barrier and the blood-brain barrier, and influence neurotransmitter and neurotrophin signalling in the brain.

The third route is immune. A disrupted microbiome and a more permeable gut lining can raise circulating inflammatory signals, and chronic low-grade neuroinflammation is one of the most consistent biological correlates of brain fog across very different conditions — from long COVID to ME/CFS and fibromyalgia. The fourth is endocrine: the gut is the body's largest endocrine organ, releasing hormones such as GLP-1, peptide YY and serotonin precursors that feed into appetite, mood and the stress (HPA) axis. The interplay with gut hormones is part of why GLP-1 drugs and the gut-brain axis are increasingly discussed together.

The takeaway is that a disturbed gut plausibly nudges the brain toward raised neuroinflammation, altered neurotransmitter and SCFA signalling, and a dysregulated stress response — a soft, diffuse downgrade rather than a focal lesion, which fits the vague, generalised quality of brain fog. And it is precisely the plasticity end of this chain — how these signals affect BDNF and synaptic strength — that links the discussion to Dihexa.

The Microbiome-BDNF Link: Where the Plasticity Story Begins

The cleaner cognitive thread connects the gut to brain-derived neurotrophic factor (BDNF), the master regulator of synaptic plasticity. Across animal and human work, gut dysbiosis — the imbalance seen in stress, poor diet and some disease states — is associated with reduced BDNF expression and weaker hippocampal plasticity. The relationship runs the other way too: in models of stress-induced dysbiosis, restoring beneficial bacteria can rescue hippocampal BDNF–TrkB signalling. Germ-free animals, raised without a microbiome, show altered BDNF and abnormal anxiety and memory behaviours that partly normalise when a microbiome is introduced — some of the most striking evidence that gut microbes shape the brain's plasticity machinery.

SCFAs appear to be central to this. Butyrate in particular acts on gene expression in the brain in ways linked to BDNF and synaptic function, and SCFA-producing species are exactly the bacteria depleted in dysbiosis and in long-COVID gut profiles. A balanced microbiome, in short, supports BDNF-driven synaptic strengthening; a disrupted one tends to suppress it, alongside the inflammation that accompanies it. A 2025 review frames these pathways as opportunities for prevention and intervention in mental and neurodegenerative disorders.

This is the conceptual hinge of the whole article. Low BDNF and weakened plasticity are a shared endpoint: nutritional deficiencies reach it (covered in our magnesium, B12 and vitamin D reviews), chronic stress reaches it, and gut dysbiosis reaches it. Dihexa is interesting precisely because it aims at that same endpoint — but, as always, converging on an endpoint is not the same as fixing the upstream cause.

What the Treatment Evidence Actually Shows: Probiotics, Prebiotics, Diet and the Mixed Picture

Here is where honesty matters, because the gut-and-cognition literature is much stronger on mechanism and association than on hard clinical proof in humans. The observational and mechanistic data are genuinely compelling: dysbiosis tracks with cognitive and mood symptoms, SCFAs influence the brain, and the gut-brain axis is real. The interventional data — can we change cognition by changing the gut? — are more limited and decidedly mixed.

The 2024 “Gut Feelings” RCT found only weak evidence that a probiotic improved working memory, and no clear effect of a prebiotic-rich diet on the primary cognitive outcome. Trials of probiotics for cognition in older adults and people with mild cognitive impairment have produced a patchwork of small positive, null and inconclusive results, with effects that vary substantially between individuals depending on host genetics and baseline microbiota. For IBS specifically, probiotics may help gut symptoms in some people, but NICE is cautious about which strains and how much benefit, and recommends a four-week trial with monitoring rather than open-ended use. The clearest dietary tool for IBS, the low-FODMAP diet, can reduce symptoms but is restrictive and meant to be used with a dietitian.

The fair summary for 2026 is this: looking after the gut is clearly worth doing — for digestion, for inflammation, and plausibly for the cognitive symptoms that travel with gut disturbance — and the science is moving quickly. But no trial shows that a microbiome intervention rapidly and reliably clears established brain fog the way replacing severe B12 might, and the strongest cognitive signals are small and individual. That is the realistic backdrop against which any unlicensed peptide has to justify itself — and it is demanding, because the conventional interventions (diet, fibre, treating the underlying gut condition, managing stress and sleep) already capture most of the plausible benefit at very low risk.

Who Gets Gut-Related Brain Fog: The Overlaps That Matter

Gut-brain symptoms are not evenly distributed, and the overlaps are telling. The clearest cluster is the post-infectious and inflammatory group: long COVID, where gut dysbiosis is a leading hypothesis for persistent brain fog, and ME/CFS, which frequently follows infection and shows altered gut profiles. Fibromyalgia overlaps heavily with IBS and “fibro fog.” Coeliac disease is the cleanest example of a gut condition with a documented cognitive component — “coeliac fog” — and a definitive treatment, the gluten-free diet, which underlines the general principle: diagnose the gut problem and the cognitive symptoms often follow it down.

Several everyday factors disturb the microbiome and feed this loop. Diet low in fibre and diverse plants starves SCFA-producing bacteria. Chronic stress and poor sleep alter gut function and composition and overlap with anxiety. Antibiotics reshape the microbiome, sometimes for months. Alcohol increases intestinal permeability and inflammation (a theme in our alcohol brain fog review). And conditions such as type 2 diabetes and the hormonal shifts of menopause interact with both gut and brain. The clustering cuts two ways: the gut is worth reviewing in almost anyone with persistent fog, because it is so often involved and so amenable to low-risk change — but a gut disturbance rarely explains everything on its own, and the fog that remains usually has other, co-existing causes that also need attention.

The BDNF-HGF-c-Met Chain: Where Dihexa Enters the Picture

Now the part readers come for. If gut dysbiosis nudges the brain toward weaker BDNF-supported plasticity and higher neuroinflammation, is there a mechanistic case for a compound that pushes plasticity back up by another route? On paper, yes — and there is an unusual second layer to it here, because the same growth factor Dihexa targets is also involved in repairing the gut itself.

Dihexa (PNB-0408) is an orally active, blood-brain-barrier-penetrant peptide that acts as a positive modulator of hepatocyte growth factor (HGF) and its receptor c-Met. In preclinical work — most notably Benoist and colleagues (JPET, 2014) — activating HGF/c-Met drove synaptogenesis, the formation of new dendritic spines and functional synapses, and improved performance in cognitive tasks. The HGF/MET system also supports cerebrovascular health and the blood-brain barrier — relevant if gut-driven inflammation is undermining barrier integrity. Our mechanism of action page details the PI-3K/AKT and ERK signalling, and Dihexa vs BDNF unpacks the much-repeated “ten million times more potent than BDNF” claim and what it does and does not mean.

The intriguing extra wrinkle is that HGF is a well-recognised player in intestinal epithelial repair — it promotes the migration and healing of gut-lining cells (epithelial restitution) and has been studied in the context of inflammatory bowel disease and mucosal healing. So a reader could spin an appealing story: a compound that nudges a pathway involved in both gut-lining repair and brain synaptogenesis. The convergence is real and genuinely interesting — but it is not equivalence of cause. In gut-brain fog the upstream problem is a disturbed gut and microbiome with conventional treatments; restoring it addresses digestion, inflammation, nutrient absorption and the cognitive symptoms together. Dihexa does not rebalance the microbiome, has no human data for either the gut or the cognition, and amplifying a growth-factor pathway in inflamed gut tissue is exactly the kind of thing that needs trials, not enthusiasm. The mechanistic story is a reason to be curious, not a reason to substitute an unproven peptide for treating the gut.

Fix the Gut First: The Evidence-Based Steps

For anyone whose brain fog comes with gut symptoms, the evidence-based path is well-trodden, conventional and low-risk. The first move is diagnosis: see a GP, because the symptoms that look like IBS can sometimes be coeliac disease (a simple blood test), inflammatory bowel disease, or — with red-flag features — something that needs urgent investigation. Getting the right label is the single highest-value step, and it is the one a peptide cannot provide.

With serious causes excluded, the toolkit is dietary and behavioural. NICE CG61 and NHS guidance emphasise regular meals, adequate fluids (around two litres a day), limiting caffeine, alcohol and fizzy drinks, and adjusting fibre to symptoms. A low-FODMAP diet can meaningfully reduce IBS symptoms but is restrictive and should be done with a dietitian, not improvised indefinitely. Probiotics may be tried for at least four weeks while monitoring the effect, with the honest acknowledgement that the evidence on which strains help is still developing. Feeding the SCFA-producing bacteria with a diverse, plant-rich, fibre-rich diet is the least controversial lever of all, and it brings a package of other benefits with it.

Equally important is finding why the gut was disturbed and addressing the companions of fog. Because gut symptoms so often travel with other drivers, a sensible work-up for persistent fog also checks the obvious testable causes — vitamin D, B12, ferritin/iron and thyroid function — alongside the non-laboratory basics of cognition: sleep, mood, alcohol, activity and stress. None of that requires a research peptide, and all of it has a stronger evidence base than one. Our stacking guide discusses where everyday gut and nutritional foundations sit before anything experimental is considered.

When Brain Fog Persists Despite Treating the Gut

A common and frustrating scenario: the diet is better, the IBS is calmer, the probiotic has been running for weeks, and the fog has lifted only partly — or not at all. This is where the temptation to reach for something stronger is greatest, and where clear thinking pays off most. The first question is whether the gut was ever really the main driver. Because the microbiome is so often disturbed and so hard to pin down precisely, it is frequently a contributor rather than the cause; improving it was worth doing, but the real engine of the fog may be poor sleep, an undertreated mood disorder, a thyroid problem, ongoing iron, B12 or vitamin D deficiency, or a condition such as long COVID, ME/CFS or menopause that needs its own management.

The second question is whether enough has been done elsewhere. Where the gut was genuinely contributing, the benefit often comes as much through reduced inflammation, better nutrient absorption and improved sleep and mood as through any direct synaptic effect, and that takes consistency rather than a one-off intervention. Optimising the everyday cognitive basics and treating the co-existing causes systematically is unglamorous but effective. Only after that thorough, conventional work-up does it make sense to read about experimental agents — and even then, as our research and studies page sets out, the honest status of Dihexa for any cognitive indication is “mechanistically interesting, clinically unproven.”

Gut-Specific Risks of Dihexa Use

Beyond the general safety questions that apply to any unlicensed peptide, two issues are specific to the gut setting. The first is masking a diagnosable condition. Gut symptoms are one of the body's more important warning systems. NICE highlights red flags — unintentional weight loss, rectal bleeding, a change in bowel habit to looser or more frequent stools persisting in older adults, abdominal or rectal masses, iron-deficiency anaemia, and a family history of bowel or ovarian cancer — precisely because the things that mimic IBS include coeliac disease, inflammatory bowel disease and bowel cancer. Anything that produces a subjective cognitive lift while these go uninvestigated does real harm by delaying diagnosis.

The second is a pathway-specific oncology caution. The general c-Met / cancer concern that runs through all Dihexa discussion is sharper in the gut context, because c-Met (the MET receptor) is implicated in gastrointestinal cancers, including gastric and colorectal tumours, where MET signalling drives growth and invasion. Chronically amplifying that pathway in someone with an undiagnosed gut lesion, inflammatory bowel disease, or a strong family history of GI cancer is exactly the scenario where mechanistic enthusiasm is most dangerous. Add the fact that an orally dosed peptide passes through the gut itself, and the case for caution — and for proper diagnosis first — is stronger here than in almost any other indication on this site. The right answer to “could it be my gut?” is a medical assessment and conventional treatment, not a research chemical.

The Fosgonimeton Parallel and the Limits of Mechanism

The most important cautionary tale for anyone reasoning from mechanism to benefit is fosgonimeton (ATH-1017), the closest clinical-stage relative of Dihexa. Fosgonimeton is a small-molecule positive modulator of the same HGF/MET system, developed by Athira Pharma and taken all the way into human Alzheimer's trials precisely because the synaptogenic, neurotrophic rationale looked so compelling. In 2024 its pivotal Phase 3 LIFT-AD trial missed its primary cognitive endpoint.

The lesson is not that HGF/c-Met is uninteresting — it plainly is interesting, in the brain and in the gut alike — but that an elegant mechanism, even one carried into rigorous, well-funded human trials, does not guarantee a clinical benefit. If the most advanced drug targeting this exact pathway could not beat placebo on cognition in its main indication, the prior for an unlicensed, never-trialled peptide producing reliable gains in gut-brain fog should be set accordingly low. Mechanistic plausibility is a hypothesis, not a result — a point that applies just as much to the probiotic-and-cognition story, which is promising but, as the “Gut Feelings” trial showed, still weak and early.

Who Should Absolutely Not Consider Dihexa for Gut Brain Fog

Some situations make experimentation clearly inappropriate. Anyone who has not yet had their gut symptoms medically assessed should do that first — the answer may be coeliac disease, IBD or a condition that needs urgent attention, not a peptide. Anyone with any red-flag symptom — unintentional weight loss, rectal bleeding, anaemia, a persistent change in bowel habit, or a family history of bowel or ovarian cancer — needs investigation, not self-experimentation. Anyone with inflammatory bowel disease or a personal or family history of gastrointestinal cancer should weigh the c-Met / oncology caution extremely seriously, given MET's role in GI tumours. Anyone who is pregnant or breastfeeding should not use Dihexa under any circumstances; an unlicensed HGF/c-Met peptide has no safety data in pregnancy. And anyone whose fog might reflect a serious untreated condition — significant depression, a thyroid disorder, uncontrolled diabetes, sleep apnoea, or early dementia — needs proper assessment, because masking those with a subjective lift is dangerous.

This is the same conclusion reached across the reviews on this site: the more treatable and diagnosable the underlying cause, the weaker the argument for reaching past it toward an unproven compound. A disturbed gut is one of the more treatable — and one of the more important to diagnose correctly — causes of brain fog there is.

What the Evidence Supports for Gut-Brain Brain Fog in 2026 — The Bottom Line

Pulling the threads together, the evidence-based approach in 2026 is straightforward and almost entirely conventional. Get the gut assessed if you have persistent gut symptoms and fog, so that coeliac disease, IBD and red-flag conditions are excluded. Treat the cause — IBS, a confirmed infection, a medication effect — on its own terms. Improve the diet: diverse, plant-rich and fibre-rich to feed the SCFA-producing bacteria, with a dietitian-supervised low-FODMAP trial if IBS symptoms warrant it, and a four-week probiotic trial if you choose. Check the companions — vitamin D, B12, iron and thyroid — because they cluster. And address the non-laboratory drivers of cognition: sleep, mood, alcohol, activity and stress, which between them explain a great deal of everyday brain fog and powerfully shape the gut too.

What the evidence does not yet support is treating any microbiome intervention as a proven cognitive drug, chasing an unreliable SIBO breath test into open-ended self-treatment, or substituting an experimental peptide for diagnosing and treating the gut. The 2024 “Gut Feelings” trial and the long-COVID brain-fog research make a genuinely interesting case that the gut matters for cognition; they make no case at all for a research chemical. Dihexa remains, for gut-brain fog as for every other indication on this site, a compound with an interesting mechanism — doubly interesting here, given HGF's role in gut repair — and no human efficacy or safety data in the condition, behind the medical work-up and conventional treatment, not in front of them. For the broader picture, see our cognitive enhancement overview and Dihexa vs other nootropics.

Frequently Asked Questions

Related Reading on Dihexa.co.uk

• Dihexa for Long COVID Brain Fog (2026) — where gut dysbiosis is a leading hypothesis for persistent fog.
• Dihexa for ME/CFS (2026) — post-infectious fatigue with altered gut profiles.
• Dihexa for Fibromyalgia & Fibro Fog (2026) — overlaps heavily with IBS.
• Dihexa for Coeliac Disease & Gluten Brain Fog (2026) — the clearest gut condition with a cognitive component and a definitive treatment.
• Dihexa for Alcohol Brain Fog & ARBD (2026) — alcohol increases gut permeability and inflammation.
• Dihexa for Anxiety & Stress (2026) — the stress–gut–HPA-axis loop.
• Dihexa & GLP-1 Drugs (Ozempic, Wegovy, Mounjaro) — gut hormones and the gut-brain axis.
• Dihexa for Magnesium Deficiency Brain Fog (2026) — a companion testable cause of fog.
• Dihexa for Vitamin B12 Deficiency Brain Fog (2026) — absorption depends on a healthy gut.
• Dihexa, Sleep & Memory Consolidation (2026) — sleep shapes the gut and vice versa.
• Dihexa vs BDNF: What “10 Million Times More Potent” Actually Means — the BDNF mechanism claim in depth.
• Mechanism of Action — HGF/c-Met, PI-3K/AKT, dendritic spines, cerebrovascular angiogenesis.
• Side Effects & Risks — the general safety picture, including the c-Met / oncology caution.
• Fosgonimeton & Athira — the cautionary Phase 3 story.

External Authoritative Sources Cited

• Berding K et al. The impact of a prebiotic-rich diet and/or probiotic supplements on human cognition: secondary outcomes from the “Gut Feelings” randomised controlled trial (2024).
• Effect of Probiotic Strain Lactobacillus paracasei PS23 on Brain Fog in People With Long COVID (ClinicalTrials.gov, NCT06348212).
• NICE Clinical Guideline CG61 — Irritable bowel syndrome in adults: diagnosis and management (recommendations, red flags, diet, probiotics).
• The microbiota-gut-brain axis and central nervous system diseases: from mechanisms of pathogenesis to therapeutic strategies (Frontiers in Microbiology, 2025).
• Exploring the microbiota-gut-brain axis: impact on brain structure and function (Frontiers in Neuroanatomy, 2025).
• The microbiota-gut-brain axis in mental and neurodegenerative disorders: opportunities for prevention and intervention (Frontiers in Aging Neuroscience, 2025).
• The gut microbiome, immune modulation, and cognitive decline: insights on the gut-brain axis (PMC, 2025).
• Long COVID and the gut microbiome: insights into pathogenesis and therapeutics (Gut Microbes, 2025).
• Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome — an update (SIBO prevalence in IBS, breath-test limitations).
• HGF and MET in brain development and neurological disorders (Frontiers in Cell and Developmental Biology, 2021).
• Benoist CC et al. (JPET, 2014). Dihexa procognitive effects via HGF/Met.