Dihexa for Coeliac Disease & Gluten Brain Fog: Reversible Cerebral Hypoperfusion, the Sheffield Gluten-Neurology Evidence, Mucosal Healing & the 2026 UK Review

Coeliac disease affects around 1 in 100 people in the UK, yet only about 36% are diagnosed — leaving an estimated half a million Britons living with undiagnosed coeliac disease on Coeliac UK figures. Among the most under-appreciated features is cognitive: "brain fog" — forgetfulness, slowed thinking, poor concentration and word-finding difficulty — is reported by a large share of patients, especially around diagnosis and after gluten exposure. Far from being imagined, the phenomenon now has a measurable biological substrate. Yelland's 2017 Journal of Gastroenterology and Hepatology review formalised gluten-induced cognitive impairment as a recognised entity; Lichtwark and colleagues (2014, Alimentary Pharmacology & Therapeutics) showed cognitive test performance improving over 12 months on a gluten-free diet in parallel with intestinal mucosal healing and falling tissue transglutaminase antibodies; and Addolorato's 2004 American Journal of Medicine SPECT study found regional cerebral hypoperfusion in 73% of untreated coeliac patients that normalised on a gluten-free diet. Layered on top sits the Sheffield gluten-neurology tradition — Marios Hadjivassiliou's group and the transglutaminase-6 / gluten-ataxia literature. That biology converges on reduced cerebral blood flow, systemic inflammation, micronutrient malabsorption and downstream hippocampal BDNF reduction — the same endpoint that Dihexa, a positive modulator of HGF/c-Met synaptogenesis with documented cerebrovascular effects, also reaches. This 2026 UK review walks through coeliac neurology, the cerebral-hypoperfusion case, the nutritional-deficiency drivers, the BDNF-HGF-c-Met chain and the evidence hierarchy — with the gluten-free diet first and unlicensed peptides essentially last.

Coeliac Disease in the UK in 2026: A Common Condition, Mostly Undiagnosed

Coeliac disease is a lifelong autoimmune condition in which dietary gluten — the storage protein of wheat, barley and rye — triggers an immune reaction that damages the lining of the small intestine. In genetically susceptible people (almost all carry HLA-DQ2 or HLA-DQ8), gluten-derived gliadin peptides are deamidated by the enzyme tissue transglutaminase, presented to the immune system, and provoke a T-cell response that flattens the intestinal villi. The result is malabsorption, a characteristic antibody signature (anti-tissue-transglutaminase, or tTG-IgA, and endomysial antibodies), and a spectrum of intestinal and extra-intestinal symptoms that includes fatigue, anaemia, bone disease, dermatitis herpetiformis, neurological problems and cognitive impairment.

Coeliac UK, the national charity, estimates that around 1 in 100 people in the UK have coeliac disease, but only about 36% are diagnosed — meaning roughly 500,000 people are living with undiagnosed coeliac disease. Diagnosis rates have risen steadily over recent decades, reflecting both better detection and a genuine increase in incidence. The diagnostic gap is the central public-health problem: the average person spends years with non-specific symptoms — tiredness, "brain fog", low ferritin, recurrent mouth ulcers, altered bowel habit — before coeliac disease is considered. For the cognitive symptom in particular, this delay means many people attribute their brain fog to stress or ageing long before anyone checks a coeliac antibody.

UK diagnosis follows a defined pathway. NICE guideline NG20 recommends serological testing — total IgA and tTG-IgA, with endomysial antibodies and IgG-based tests where IgA is deficient — in anyone with suggestive symptoms, and historically referral for an endoscopic duodenal biopsy to confirm villous atrophy graded on the Marsh classification. The critical practical point, emphasised by Coeliac UK, is that the person must keep eating gluten until testing is complete; going gluten-free first can heal the gut enough to produce a false-negative result. Anyone who has already removed gluten and feels cognitively better is in a genuinely awkward diagnostic position — another reason to test before changing diet.

The diagnostic landscape is shifting. Interim no-biopsy pathways — confirming coeliac disease on high-titre serology alone in selected adults — were introduced during the COVID-19 pandemic, and a fuller updated UK guideline incorporating a no-biopsy strategy is anticipated. Meanwhile, researchers have developed an experimental blood test based on a gluten-specific interleukin-2 (IL-2) release signature that can detect the coeliac immune response without the person having to eat gluten first — a potential answer to the gluten-challenge barrier that Coeliac UK has highlighted. As of 2026 this remains an emerging research tool rather than routine NHS practice, but it points to a near future in which the diagnostic gap — and the years of unexplained brain fog that go with it — might finally narrow.

Against that backdrop, the patient-facing question is familiar from the autoimmune-and-cognition posts elsewhere on this site — Hashimoto's thyroiditis, lupus and fibromyalgia: "my brain fog is real and documented — do unlicensed compounds like Dihexa belong anywhere in the conversation?" This article takes the question seriously, and the answer turns out to hinge on something Dihexa cannot do: remove gluten and heal a damaged gut.

The Spectrum of Gluten-Related Neurological Disease

Gluten-related disorders are not a single disease, and the neurological manifestations are not a single phenomenon. Distinguishing them matters because the mechanism, the prognosis and the (entirely diet-based) treatment differ between them.

Coeliac brain fog

The most common cognitive complaint: a diffuse, fluctuating impairment of attention, short-term memory, mental processing speed and word retrieval. It is typically worst around diagnosis and after inadvertent gluten exposure, and improves with sustained gluten withdrawal and mucosal healing. It is the symptom most relevant to the Dihexa question because it overlaps mechanistically with the cerebral-perfusion, inflammation and BDNF stories that recur across this site.

Gluten ataxia

A distinct cerebellar syndrome — problems with balance, coordination, gait and eye movements rather than diffuse cognitive slowing. The Sheffield gluten-neurology group has argued for decades that gluten sensitivity accounts for a substantial share of otherwise-unexplained sporadic ataxia (up to around 40% of idiopathic sporadic ataxia in some series), and that it is associated with antibodies against transglutaminase-6 (TG6), a brain-expressed isoform distinct from the gut-expressed tissue transglutaminase. A 2024 Brain Communications study linked the cerebellar degeneration of gluten ataxia to microglial activation. Gluten ataxia is a clinical, specialist diagnosis — not a target for self-experimentation.

Gluten encephalopathy and headache

The Sheffield group also described a "gluten encephalopathy" characterised by chronic headache with white-matter abnormalities on MRI, some of which stabilise or improve on a gluten-free diet. The cognitive component of this presentation overlaps with the brain-fog phenotype.

Non-coeliac gluten sensitivity (NCGS)

Many people experience gluten-triggered symptoms — including brain fog — without the villous atrophy or antibody signature of coeliac disease, and without wheat allergy. Brain fog is one of the most frequently reported extra-intestinal features of NCGS. A 2020 PLOS One proof-of-concept MRI pilot from the Sheffield group examined brain changes associated with NCGS-related brain fog, and more recent work has highlighted how powerfully symptom expectancy interacts with the cognitive symptoms in NCGS — an important reminder that the gut-brain relationship here is genuinely complex. NCGS is a diagnosis of exclusion: coeliac disease and wheat allergy must be ruled out first, while still eating gluten.

Gluten neuropathy

A sensory peripheral neuropathy is another recognised gluten-related neurological manifestation, again most clearly characterised by the Sheffield group. It is mentioned here for completeness; it is not a cognitive syndrome and not a Dihexa target.

The clinical takeaway: "does Dihexa help gluten brain fog?" is really a question about coeliac brain fog and NCGS-related cognitive symptoms specifically — and even there, the dominant, evidence-based intervention is the one that removes the trigger and heals the gut.

The 2026 Biology of Coeliac Brain Fog

Coeliac-related cognitive dysfunction has moved firmly out of the "all in the mind" category. The dominant biological themes are nutritional malabsorption, systemic inflammation, cerebral hypoperfusion and downstream hippocampal BDNF reduction — usually several at once.

Nutritional malabsorption: the most correctable driver

Villous atrophy reduces the absorptive surface of the small intestine, and the nutrients lost first are precisely those the brain depends on. Iron deficiency (with or without anaemia) impairs attention and processing speed. Vitamin B12 and folate deficiency cause cognitive slowing and, when severe, frank neurological damage. Vitamin D deficiency is near-universal at coeliac diagnosis. Copper deficiency, though less common, can cause a myeloneuropathy and cognitive change. Each of these is an independent, correctable cause of brain fog — which is why the first step in evaluating coeliac cognitive symptoms is a nutritional work-up (ferritin, B12, folate, vitamin D, and where indicated copper and zinc), not a peptide. See the parallels in diabetic brain fog and menopause brain fog, where treatable contributors similarly dominate.

Reversible cerebral hypoperfusion

The single most striking objective finding is Addolorato and colleagues' 2004 American Journal of Medicine SPECT study from the Catholic University in Rome. Using brain single-photon emission computed tomography, the team found at least one hypoperfused brain region in 11 of 15 (73%) untreated coeliac patients, compared with just 1 of 15 (7%) coeliac patients on a gluten-free diet and none of the healthy controls — with perfusion in treated patients indistinguishable from controls. In other words, the cerebral hypoperfusion of untreated coeliac disease appears reversible with a gluten-free diet. This is conceptually important for the Dihexa discussion because it places coeliac brain fog in the same broad family as the perfusion-driven cognitive impairment of vascular dementia and post-stroke cognitive impairment — but with a crucial difference: in coeliac disease the upstream cause is treatable by diet.

Systemic inflammation and the gut-brain axis

Active coeliac disease is a state of systemic immune activation, with circulating pro-inflammatory cytokines (interleukin-6, TNF-alpha and others) that have direct effects on attention, mood and sleep. The gut-brain axis adds further layers: altered intestinal permeability ("leaky gut"), microbiome disruption (dysbiosis) and vagal signalling all plausibly contribute to the cognitive phenotype. This inflammatory component overlaps mechanistically with the brain fog of Long COVID and ME/CFS.

Neural autoimmunity: transglutaminase-6

Beyond malabsorption and inflammation, a subset of gluten-related neurological disease appears to be driven by direct autoimmunity against neural tissue. Antibodies against transglutaminase-6, the neuronally expressed isoform, are the best-characterised example and are central to the gluten-ataxia story. Whether TG6 or related neural autoantibodies contribute to the diffuse cognitive symptom in coeliac disease is an active research question; the existence of the mechanism is a reminder that not all gluten brain fog is "just" deficiency and perfusion.

Hippocampal BDNF and synaptic plasticity

Chronic inflammation, micronutrient deficiency and reduced cerebral perfusion all converge on the same downstream endpoint: reduced hippocampal brain-derived neurotrophic factor (BDNF) expression and impaired long-term potentiation at the synapse. BDNF, released in an activity-dependent fashion, binds the TrkB receptor and drives dendritic spine maturation and memory consolidation; its suppression is a final common pathway across many of the conditions reviewed on this site. The end-state of coeliac brain fog overlaps with that of mild cognitive impairment at the level of BDNF-TrkB signalling, even though the upstream cause is entirely different.

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

For the Dihexa-specific question, the relevant molecular story is the link between hippocampal BDNF, the HGF/c-Met system and cerebrovascular biology. Each influences synaptic plasticity, and HGF/c-Met has an additional documented role in cerebrovascular angiogenesis and blood-brain-barrier integrity — an unusual feature that, in coeliac disease, maps onto the reversible perfusion abnormality Addolorato documented.

Hippocampal BDNF binds TrkB and drives dendritic spine maturation, LTP and long-term cognitive plasticity. Independently, HGF/c-Met signalling drives synaptogenesis through the PI-3K/AKT and MAPK pathways — a parallel track converging on the same cellular outcome. A 2021 Frontiers in Cell and Developmental Biology review details how MET expression in cortex sustains adult synaptogenesis and angiogenesis.

Dihexa — a small-molecule peptide analogue derived from angiotensin IV — is a positive modulator of the HGF/c-Met pathway. Full molecular detail is on the mechanism of action page; the foundational pharmacology is in Benoist et al. (2014, JPET). The relevance to coeliac brain fog rests on points of overlap:

• Synaptogenesis as a parallel route to plasticity. When BDNF expression is suppressed by inflammation, deficiency and hypoperfusion, an upstream pathway that pushes synaptogenesis from a different signalling axis is conceptually interesting. The operative word is conceptually; there are no coeliac data to support the reasoning.
• Cerebrovascular angiogenesis as a parallel route to perfusion. HGF/c-Met has a documented cerebrovascular component — capillary density, endothelial integrity and BBB function. In a condition whose cognitive substrate includes reduced cerebral blood flow, this is more anatomically targeted than most procognitive mechanisms. The catch is the same one as always: mechanism is not evidence, and here the perfusion problem already reverses with diet.
• The directionality problem is decisive. In coeliac disease the upstream driver — gluten-triggered mucosal damage and the nutrient deficiencies it causes — is removable. Pushing synaptogenesis downstream while leaving an unhealed gut and an empty nutrient tank in place is biologically back-to-front. The intervention that fixes the cause is a gluten-free diet, not a peptide layered on top of an unresolved problem.

This is the mechanistic case for being interested in Dihexa in coeliac brain fog. The rest of this article is about why mechanistic interest is not evidence — and why, in coeliac disease specifically, the existence of a definitive dietary treatment makes the case for an unlicensed peptide weaker than in almost any other condition reviewed here.

The Gluten-Free Diet First: The Only Evidence-Based Treatment

Any honest review of coeliac brain fog has to begin with the gluten-free diet, because it is not merely first-line — it is the only treatment with an evidence base, and it is disease-modifying rather than symptomatic. A strict, lifelong gluten-free diet heals the intestinal mucosa, restores nutrient absorption, removes the antigenic and inflammatory driver, and — on the Addolorato data — normalises cerebral perfusion.

The cognitive payoff is documented. Lichtwark and colleagues (2014) followed newly diagnosed coeliac patients over 12 months and found that performance on cognitive tests of verbal fluency, attention and motor function improved significantly — and that the improvement correlated with intestinal mucosal healing on the Marsh score and with falling tissue transglutaminase antibody levels. In plain terms: as the gut healed, the brain fog lifted. A later pilot study reinforced the link between gluten-free-diet adherence, disease duration and cognitive recovery.

Several practical points follow from this:

• Strictness matters. Even small, repeated gluten exposures perpetuate mucosal damage and the symptoms that go with it. Cross-contamination is the usual culprit when someone "gluten-free" still has brain fog.
• Recovery takes time. Mucosal healing can take months to a couple of years, and cognitive recovery tends to parallel it rather than arriving overnight. Patience and adherence beat any quick fix.
• Correct the deficiencies in parallel. Replacing iron, B12, folate and vitamin D accelerates symptomatic recovery and is standard practice at diagnosis.
• Get expert support. A dietitian referral and Coeliac UK membership materially improve adherence and outcomes. UK guidance also recommends structured annual review and bone-density (DEXA) assessment given the osteoporosis risk.

For someone with coeliac brain fog, the right starting point is therefore confirmed diagnosis on serology and biopsy, a strict gluten-free diet, correction of deficiencies, dietitian support and a realistic timeframe for recovery. Experimental peptides are not a substitute for that pathway — and, uniquely in coeliac disease, the pathway actually fixes the cause.

When Brain Fog Persists Despite a Gluten-Free Diet

A meaningful minority of people continue to experience cognitive symptoms after going gluten-free, and this is the scenario in which the temptation to reach for something like Dihexa is strongest. Before considering any unlicensed compound, the structured assessment of persistent symptoms is far more likely to find a treatable answer:

• Ongoing gluten exposure. The commonest reason for persistent symptoms is continued, often inadvertent, gluten intake. A dietitian review and repeat serology help establish whether the diet is genuinely gluten-free.
• Incomplete mucosal healing. Healing can lag symptom improvement; persistent villous atrophy on follow-up biopsy points to ongoing exposure or, rarely, refractory disease.
• Unresolved deficiency. Iron, B12, folate, vitamin D or copper may still be low and warrant rechecking and repletion.
• Refractory coeliac disease. Rare but important: persistent symptoms and villous atrophy despite a strict diet require specialist gastroenterology assessment and carry their own (including oncological) implications.
• A second diagnosis. Coeliac disease clusters with other autoimmune conditions — notably autoimmune thyroid disease (around 5% co-prevalence) and type 1 diabetes — any of which can independently cause brain fog. Thyroid function, in particular, should be checked.
• Gluten neurology. Persistent or progressive neurological symptoms — balance problems, sensory disturbance, intractable headache — warrant neurological referral, ideally to a service familiar with gluten-related neurological disease such as the Sheffield centre.

The point of this list is simple: persistent coeliac brain fog almost always has a findable, treatable explanation that an unlicensed synaptogenic peptide would do nothing to address — and might obscure.

Coeliac-Specific Risks of Dihexa Use

Beyond the general safety considerations covered on the side effects page, coeliac disease raises specific concerns.

Masking a treatable cause. This is the central risk. Coeliac brain fog is frequently driven by correctable deficiency or ongoing gluten exposure. Anything that produces a subjective lift — placebo included — while leaving an unhealed gut and an unaddressed nutrient deficit in place is actively harmful, because it delays the assessment that would find the real problem. In a condition with a definitive dietary treatment, masking is not a minor concern; it is the whole problem.

The oncology consideration. Coeliac disease carries an elevated long-term risk of enteropathy-associated T-cell lymphoma (EATL) and small-bowel adenocarcinoma, particularly in poorly controlled or refractory disease. The general c-Met / oncology concern that applies to all Dihexa use is therefore sharper here: c-Met activation is implicated in tumour growth and invasion across several cancers, and agonising that pathway in a population with an already-elevated gastrointestinal-cancer risk is theoretically unwise. Anyone with a personal or family history of c-Met-relevant cancers should not consider Dihexa for any indication, coeliac brain fog included.

Excipients and cross-contamination. Unlicensed research chemicals carry no guarantee of gluten-free manufacturing or excipients, no quality assurance and no regulated labelling. For someone whose entire treatment depends on avoiding even trace gluten, an unregulated product of unknown composition is an obvious hazard.

Unknown interactions in a malabsorptive gut. Absorption, distribution and metabolism of any orally administered compound are unpredictable in an inflamed, malabsorptive small intestine. There are no pharmacokinetic data for Dihexa in coeliac disease, and none are likely to exist.

The Fosgonimeton Parallel and the Limits of Mechanism

The most instructive cautionary tale for any HGF/c-Met-based cognitive claim is fosgonimeton (ATH-1017), Athira Pharma's HGF/MET positive modulator and the closest clinical-stage relative to Dihexa. Fosgonimeton was a genuine, injectable, clinically tested drug developed specifically to enhance HGF/c-Met signalling for cognition — exactly the mechanism Dihexa is promoted on. In 2024 it missed its primary endpoint in the Phase 3 LIFT-AD Alzheimer's trial.

The lesson is not that HGF/c-Met is irrelevant to cognition; it is that a coherent, well-funded, professionally executed attempt to turn that mechanism into clinical benefit failed its definitive test. If a purpose-built drug with proper trials could not convert the mechanism into a measurable cognitive outcome in a defined patient population, the case for an unlicensed research chemical converting the same mechanism into benefit in coeliac brain fog — a condition that already has a definitive dietary treatment — is weaker still. Mechanism-first reasoning is a hypothesis generator, not evidence.

Who Should Not Consider Dihexa for Coeliac Brain Fog

Bringing the risk threads together, Dihexa should not be considered by:

• Anyone who has not completed coeliac diagnosis on serology and biopsy — the diagnostic and dietary pathway comes first.
• Anyone whose brain fog has not been worked up for correctable deficiency (iron, B12, folate, vitamin D, copper) and ongoing gluten exposure.
• Anyone with a personal or family history of breast, ovarian, lung, gastric, small-bowel or other c-Met-relevant cancers, or with refractory coeliac disease.
• Anyone who is pregnant, breastfeeding, or trying to conceive — coeliac disease itself affects fertility and pregnancy, and Dihexa has no reproductive safety data.
• Anyone with progressive or focal neurological symptoms (ataxia, neuropathy, intractable headache) — these need neurological assessment, not a peptide trial.
• Anyone whose cognitive symptoms have not been distinguished from comorbid autoimmune disease, particularly thyroid dysfunction, depression or anxiety.

What the Evidence Actually Supports for Coeliac Brain Fog in 2026

Stripped to its essentials, the evidence-based approach to coeliac brain fog is unglamorous and effective:

• Confirm the diagnosis while still eating gluten. tTG-IgA and total IgA, with biopsy where indicated; do not go gluten-free before testing.
• Adopt a strict, lifelong gluten-free diet. The single intervention with disease-modifying evidence for both gut and brain. Lichtwark 2014 shows cognition recovering as the mucosa heals.
• Correct the deficiencies. Iron, B12, folate, vitamin D — the most immediate, evidence-based route to lifting brain fog.
• Use a dietitian and Coeliac UK. Adherence is the rate-limiting step, and structured support improves it.
• Allow time, then reassess. If brain fog persists after months of strict adherence and corrected nutrition, look for ongoing exposure, incomplete healing, refractory disease or a second diagnosis — not a peptide.
• Treat sleep, mood and comorbidity. Coeliac disease commonly coexists with low mood, disturbed sleep and other autoimmune conditions, each of which independently worsens cognition and each of which has evidence-based treatment.

Notice what is absent from that list: any role for an unlicensed synaptogenic peptide. That is not an oversight — it is the honest reflection of where the evidence sits in 2026.

The Bottom Line in 2026

Coeliac brain fog is real, biological and increasingly well understood. Yelland 2017 formalised it, Lichtwark 2014 tied its recovery to mucosal healing, Addolorato 2004 showed a reversible cerebral-perfusion substrate, and the Sheffield gluten-neurology tradition has mapped the wider spectrum from gluten ataxia to encephalopathy. The biology converges on malabsorption, inflammation, hypoperfusion and reduced hippocampal BDNF — the same downstream endpoint that Dihexa's HGF/c-Met pharmacology also reaches.

But coeliac disease is the condition on this site where mechanism-first reasoning is at its weakest, for one reason: the upstream cause is removable. A strict gluten-free diet heals the gut, restores absorption, removes the inflammatory driver and reverses the cerebral hypoperfusion. The honest reading of the 2026 evidence is therefore: confirm the diagnosis first, go strictly gluten-free second, correct the deficiencies third, treat comorbidity and allow time fourth, and research chemicals essentially last — if at all. With an experimental gluten-free diagnostic blood test on the horizon and the UK diagnostic pathway under active revision, the momentum in coeliac medicine is toward catching the disease earlier and healing the gut sooner. Self-experimentation with an unlicensed peptide, while a definitive dietary treatment goes underused, is harder to justify here than almost anywhere.

Frequently Asked Questions

Related Reading on Dihexa.co.uk

• Dihexa for Hashimoto's & Hypothyroid Brain Fog (2026) — the autoimmune condition most commonly co-occurring with coeliac disease (~5% co-prevalence).
• Dihexa for Diabetic Brain Fog (2026) — type 1 diabetes clusters with coeliac disease; another metabolic-cognition overlap.
• Dihexa for Lupus (SLE) Brain Fog & NPSLE (2026) — autoimmune neuro-cognitive disease and the directionality problem.
• Dihexa for Fibromyalgia & Fibro Fog (2026) — central-sensitisation and chronic-symptom overlap.
• Dihexa for ME/CFS (2026) — the inflammatory, gut-brain-axis overlap with coeliac brain fog.
• Dihexa for Long COVID Brain Fog (2026) — the cytokine-driven brain-fog comparator.
• Dihexa for Vascular Dementia (2026) — the cerebral-hypoperfusion biology in another guise.
• Dihexa for Post-Stroke Recovery (2026) — the perfusion-cognition comparator.
• Dihexa for MCI & Brain Aging (2026) — the BDNF-TrkB endpoint coeliac brain fog shares.
• Dihexa for Menopause Brain Fog (2026) — another condition where treatable causes dominate.
• Dihexa vs BDNF: What "10 Million Times More Potent" Actually Means — in-depth look at the BDNF mechanism claim.
• Mechanism of Action — HGF/c-Met, PI-3K/AKT, dendritic spines, cerebrovascular angiogenesis.
• Side Effects & Risks — the general safety picture.
• UK Legal Status — where Dihexa sits in UK law and MHRA advertising rules.
• Fosgonimeton & Athira — the cautionary Phase 3 story.

External Authoritative Sources Cited

• Yelland GW (Journal of Gastroenterology and Hepatology, 2017). Gluten-induced cognitive impairment ("brain fog") in coeliac disease.
• Lichtwark IT et al. (Alimentary Pharmacology & Therapeutics, 2014). Cognitive impairment in coeliac disease improves on a gluten-free diet and correlates with histological and serological indices of disease severity.
• Addolorato G et al. (American Journal of Medicine, 2004). Regional cerebral hypoperfusion in patients with celiac disease.
• Cognitive impairment in coeliac disease with respect to disease duration and gluten-free diet adherence: a pilot study (2020).
• Cerebellar degeneration in gluten ataxia is linked to microglial activation (Brain Communications, 2024).
• Croall ID et al. (PLOS One, 2020). Brain fog and non-coeliac gluten sensitivity: proof-of-concept brain MRI pilot study.
• Ataxia UK / Sheffield Ataxia Centre — 2025 study day on gluten-related neurological disorders (Hadjivassiliou).
• Coeliac UK — the UK coeliac disease charity.
• Coeliac UK — How coeliac disease is diagnosed (keep eating gluten until tested).
• Coeliac UK — New blood test could eliminate the need to eat gluten before testing.
• NICE NG20 — Coeliac disease: recognition, assessment and management.
• NHS — Coeliac disease overview.
• British Society of Gastroenterology — coeliac disease guidelines.
• 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.