Lion's Mane and Multiple Sclerosis: Remyelination Research

Lion's Mane and Neurological Conditions

Erinacine S preserved myelin and oligodendrocytes inside the brains of rodents actively losing myelin (2024)

Fu and colleagues fed rodents cuprizone to strip myelin from the corpus callosum, then gave them lion's mane mycelium extract or isolated erinacine S. Myelin and oligodendrocytes were preserved, glial activation and IL-1-beta fell, and erinacine S still worked when given only after damage was underway. It is the most mechanistically specific lion's mane MS evidence published to date.

Fu et al., Biomedicine & Pharmacotherapy, 2024

OPC maturation

lion's mane mycelium extract and erinacines A and S drove oligodendrocyte precursor cells to mature and raised myelin basic protein — but the living-animal arm used healthy newborn rats, not damaged brains (Huang 2021)

No motor gain

in a four-species cuprizone comparison, lion's mane suppressed demyelination but was the only species that did not significantly improve motor function (Yamashina 2022)

0 human MS trials

no clinical trial has tested lion's mane in people with multiple sclerosis for any endpoint, and no cited study has used an autoimmune MS model

Fu et al., Biomedicine & Pharmacotherapy, 2024

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Multiple sclerosis is a disease of myelin destruction. The immune system mistakenly attacks the myelin sheaths that insulate nerve fibres in the brain and spinal cord. As myelin is stripped away, the nerve signals that depend on it slow, distort, or fail entirely. The symptoms of MS — vision problems, coordination loss, fatigue, cognitive difficulty — reflect which neural pathways are losing their coating.

Remyelination is the repair side of that equation: oligodendrocyte precursor cells (OPCs) differentiate into mature oligodendrocytes and lay down fresh myelin. It happens naturally, but in MS it is frequently incomplete, and finding compounds that push it along is one of the central goals of MS research. Lion's mane has a genuine, two-decade research line pointing at exactly this process. It also has a set of limitations that the popular summaries consistently skip — including the fact that its headline myelin-building result came from healthy newborn animals rather than damaged adult brains.

For the broader lion's mane overview, see What Is Lion's Mane Mushroom? A Science-Based Overview. For the inflammatory side of the same story, see Lion's Mane and Neuroinflammation: Targeting the Root of MS Progression.

What MS Is and Why Remyelination Is the Research Target

In MS, autoreactive T cells identify myelin proteins as foreign and attack the sheath. Each attack — a relapse in relapsing-remitting MS, or continuous damage in progressive MS — destroys myelin in localised patches called plaques. The inflammation during active attacks drives acute symptoms; long-term disability accumulates from the repair that never quite completes between them.

The central nervous system has real but limited remyelination capacity. OPCs are distributed throughout the brain and spinal cord and can become mature, myelinating oligodendrocytes. After demyelination they migrate to the lesion. The problem in MS is not usually that OPCs fail to show up. It is that they arrive and then stall: they are present in lesions but arrest before completing maturation. Lesions remyelinate thinly or not at all, and disability accrues.

This is why a compound that promotes OPC maturation is interesting for MS. It targets the specific bottleneck. Lion's mane compounds, particularly the erinacines found in mycelium, appear to do this in preclinical models.

The 2003 Starting Point: Myelination in Cerebellar Culture

Kolotushkina and colleagues (2003) published the first evidence that H. erinaceus affects myelination directly.^[5] They cultured cerebellar cells with the extract and tracked how myelination proceeded.

Two findings came out of it. First, the extract was not toxic: nerve and glial cells grew normally, and cell ultrastructure remained intact and comparable to what is seen in vivo. Second — the reason the study still gets cited — myelination in the presence of the extract began earlier than in controls and proceeded at a higher rate.

This is in vitro data from cell culture, the most basic evidence tier, published in a Ukrainian physiology journal two decades ago. It does not establish anything about MS. What it did was raise a specific, testable question about myelin genesis, and the modern work that followed points in the same direction.

Oligodendrocyte Maturation and Myelin Basic Protein: The 2021 Study

Huang and colleagues (2021), publishing in Scientific Reports, provide the mechanistic bridge between that 2003 observation and the disease-model evidence.^[2]

The study worked across three systems. In OPC cultures and ex vivo cerebellar slices, lion's mane mycelium extract (HEM) promoted OPC-to-oligodendrocyte differentiation and increased myelin basic protein on neuronal fibres. In neonatal rat pups given daily oral extract for seven days, MBP expression and oligodendrocyte numbers rose in the corpus callosum. Among the isolated compounds, erinacine A and erinacine S more potently stimulated MBP expression and increased oligodendrocyte numbers than erinacine C, and both significantly increased the overlap between MBP staining and neuronal fibres in cultured tissue slices.

MBP is one of the primary structural proteins of the myelin sheath. An increase in MBP means the maturing oligodendrocytes are producing functional myelin components, not merely changing shape. That is the mechanism linking lion's mane to remyelination: it pushes the cells that make myelin to mature, and to make the protein that forms the sheath.

Key Study

Huang, Ho, Sung et al. (2021) · Scientific Reports

Population

OPC cultures, ex vivo cerebellar slices, and healthy neonatal rat pups

Intervention

H. erinaceus mycelium extract (HEM); isolated erinacines A, C and S

Finding

HEM promoted OPC-to-oligodendrocyte differentiation and raised myelin basic protein on neuronal fibres. Seven days of oral HEM increased MBP expression and oligodendrocyte numbers in the corpus callosum of neonatal rats. Erinacines A and S were more potent than erinacine C.

narrow-scope Strong, multi-system evidence for myelin building — but the in vivo arm was a healthy newborn brain laying down myelin on its normal developmental schedule, with no lesion, no immune attack and no maturation blockade. The authors framed the implication as neurodevelopmental disorders, not MS.

Ref [2] Huang et al., 2021 (PMID 33753806)

That caveat deserves weight, because it is the single most routinely skipped detail in the lion's mane remyelination story. Building myelin for the first time in a developing brain and rebuilding it in an adult MS lesion are not the same biological problem. The developing brain has an intact OPC supply, no inflammation, and no arrest signal. The MS lesion has all three working against it.

The Caveat That Usually Gets Skipped

Building Myelin and Rebuilding Myelin Are Two Different Problems

The study that established lion’s mane raises myelin basic protein in a living animal did it in healthy newborn rats whose brains were myelinating normally for the first time. Its own authors framed the implication as neurodevelopmental. MS is the reverse situation. That gap is the reason “lion’s mane promotes myelination” is true and still not an MS claim.

Model details from refs [2] and [4] (see references)

The biological mechanism is at least consistent with lion's mane's better-known neurotrophic activity. Erinacines are associated with increased neurotrophic factor production, and oligodendrocytes are glial cells that respond to that signalling environment. For more on the compounds themselves, see Erinacines: The Compounds That Cross the Blood-Brain Barrier. For a deeper treatment of the oligodendrocyte work specifically, see Hericium erinaceus and Oligodendrocyte Differentiation.

The Cuprizone Model: What It Shows and What It Cannot

The cuprizone model is the primary validated animal model for demyelination and remyelination. Cuprizone is a copper chelator that, fed to rodents over several weeks, kills mature oligodendrocytes and produces reproducible demyelination in predictable brain regions — most notably the corpus callosum.

Yamashina and colleagues (2022) fed mice a powdered diet containing 5% of each of four medicinal mushrooms alongside cuprizone for five weeks, then measured body weight, motor function by rotarod, and myelin by Black-Gold II staining.^[3]

All four species — king oyster, reishi, enoki and lion's mane — effectively suppressed cuprizone-induced demyelination. Reishi and lion's mane both showed recovery from weight loss. But on motor function, king oyster, reishi and enoki produced significant improvement, and lion's mane did not.

That result is worth stating plainly because the secondary literature tends to smooth it over. Motor function is the endpoint in this study closest to what disability means for a person, and lion's mane protected the tissue while missing the function. It is also worth correcting a claim that circulates about this paper: it did not measure neuroinflammation. Body weight, rotarod performance and myelin staining were the reported outcomes. No cytokine level, microglial marker, or other inflammatory readout appears among them. The study supports a demyelination claim. It does not support a neuroinflammation claim.

One further limitation applies to this study specifically: it used fruiting bodies, not mycelium. Fruiting bodies do not contain the erinacines that drive every other myelin result in this article.

Erinacine S: The 2024 Compound-Specific Evidence

Fu and colleagues (2024) ran the study that most directly tests this article's question.^[4] Rats were fed a cuprizone diet and simultaneously given daily oral lion's mane mycelium extract, erinacine A, or erinacine S for three weeks.

HEM and erinacine S preserved myelin and oligodendrocytes in the corpus callosum. Alongside that structural protection, the authors report reduced microglial and astrocyte activation and downregulated IL-1-beta expression. That combination is what makes the study matter: protection of the myelin-making cells and suppression of the inflammatory environment, measured in the same brain tissue, in an animal actively losing myelin.

The design then went a step further. In separate arms, mice with acute (6-week) or chronic (12-week) cuprizone-induced demyelination received erinacine S only during the final four weeks — after damage was already established. Erinacine S preserved myelin in the corpus callosum in both, and inhibited anxious and depressive-like behaviour in the treated mice.

Key Study

Fu, Yang, Lee et al. (2024) · Biomedicine & Pharmacotherapy

Population

Cuprizone-fed rats (3 weeks); mice with acute 6-week or chronic 12-week cuprizone demyelination

Intervention

Daily oral H. erinaceus mycelium extract (HEM), erinacine A, or erinacine S

Finding

HEM and erinacine S preserved myelin and oligodendrocytes in the corpus callosum, reduced microglial and astrocyte activation, and downregulated IL-1-beta. Given only in the final 4 weeks, erinacine S still preserved myelin in both acute and chronic models and reduced anxious and depressive-like behaviour.

positive The most MS-relevant result in the lion's mane literature — myelin, glial activation and behaviour measured together in CNS tissue, with a post-treatment design. Still a rodent chemical-toxicity model with no autoimmune component, and no human data follows it.

Ref [4] Fu et al., 2024 (PMID 38394854)

The post-treatment arms are the underrated part. Most preclinical work administers the compound alongside the insult, which answers a prevention question. Giving erinacine S only after demyelination is established asks something much closer to what a person already diagnosed with MS would want to know.

The mood finding also has clinical resonance. Depression and anxiety are substantially more prevalent in MS than in the general population, and white matter damage in mood-regulating regions is part of that picture. Erinacine S reducing both oligodendrocyte damage and the accompanying behavioural abnormalities in the same animals offers a coherent mechanistic account — in rodents.

Erinacine S is a pharmacologically busy molecule elsewhere, too. Tung and colleagues (2021) showed it induces apoptosis in gastric cancer cells through H3K4 trimethylation on the FasL and TRAIL promoters, with tumour growth inhibited in a xenograft model.^[10] That is an entirely separate disease context, but it establishes that the compound has real, measurable bioactivity beyond a single tissue.

Where the Evidence Actually Sits

The Myelin Repair Pipeline — and the Three Stages Lion’s Mane Has Reached

Rebuilding a myelin sheath is a sequence, not a single event. Walking it stage by stage shows something a summary sentence hides: lion’s mane evidence clusters in the middle of the pipeline — making myelin and protecting it — and disappears at both ends. It has never been shown to stop what destroys myelin in MS, and in the one experiment that measured recovered function, it did not deliver.

“Never tested” means exactly that — an absence in the published record, which is not the same as a demonstrated null result. Stage 6 is different: it was measured and lion’s mane did not hit it. Note also that every animal result here comes from cuprizone, a chemical demyelination model. MS is an autoimmune disease, and no cited study has tested lion’s mane in an autoimmune model.

Stage evidence from refs [2], [3], [4], [5] (see references)

Neuroinflammation: Which Evidence Comes From Where

MS is not only demyelination. Chronic neuroinflammation perpetuates damage and actively obstructs remyelination, so anti-inflammatory effects in the CNS are directly relevant. But the evidence here needs to be sorted carefully, because the most-quoted study is not a brain study.

Mori and colleagues (2015) tested an ethyl acetate soluble fraction of lion's mane in a co-culture of 3T3-L1 adipocytes and RAW264 macrophages, stimulated with LPS.^[7] The fraction suppressed LPS-induced TNF-alpha and IL-6 production and inhibited JNK activation, which the authors identified as the likely route. They attributed the effect to suppression of TLR4 signalling.

Two points of precision matter. JNK inhibition was measured; the TLR4 step was the authors' interpretation, not a separately demonstrated endpoint. And the model was built to study adipose tissue inflammation in obesity — fat cells and macrophages, not brain. Macrophages and microglia are both myeloid cells sharing much of the same TLR4-JNK machinery, so extending the reasoning to the CNS is plausible. It is still reasoning rather than evidence.

The good news is that this article does not have to lean on it. Fu 2024 measured glial activation and IL-1-beta in actual brain tissue during active demyelination.^[4] That is where the neuroinflammation claim in this article properly rests. A 2025 review of medicinal mushrooms for MS also lists anti-inflammatory activity among the mechanisms proposed across the mushroom literature generally.^[1]

How Far the Research Line Has Actually Reached

Read as a sequence, the lion's mane remyelination literature shows a genuine two-decade climb: cell culture in 2003, multi-system OPC work in 2021, disease-model evidence in 2022 and 2024, with compound-level specificity improving throughout. That progress is real and worth crediting.

Two Decades of Climbing

The Research Got Steadily More Real — and Stopped One Rung Short

Each study in this line reached further into living biology than the one before it: a dish in 2003, a healthy animal in 2021, a damaged brain in 2022 and 2024. That progression is real and it is the reason the hypothesis is taken seriously. The top rung has never been occupied.

Study reach from refs [2], [3], [4], [5]; absence of trials per [1] and [8]

What has not moved is the top rung.

Evidence Reach

1. Cell and tissue studiescompleted

   Myelination began earlier and at a higher rate in cerebellar culture (Kolotushkina 2003); OPC-to-oligodendrocyte differentiation and raised MBP in cultures and cerebellar slices (Huang 2021)

2. Healthy living animalscompleted

   Seven days of oral mycelium extract raised MBP and oligodendrocyte numbers in the corpus callosum of neonatal rat pups (Huang 2021) — a developing brain, not a damaged one

3. Demyelination modelscurrent

   Myelin and oligodendrocytes preserved, gliosis and IL-1-beta reduced, including as post-treatment (Fu 2024); demyelination suppressed but motor function not improved (Yamashina 2022). Both use cuprizone; no autoimmune MS model has been tested

4. Human case reports in MSmissing

   None published

5. Small human MS trialsmissing

   None registered or published for any MS endpoint

6. Large randomised trialsmissing

   None

7. Meta-analysis in MSmissing

   Not possible — no human MS trials exist to pool

The line stops at rodent chemical-demyelination models. Every rung above that is empty, and no study has used a model that reproduces the autoimmune attack defining MS.

Refs [1][2][3][4][5][8] (see references)

The nearest human evidence is not MS evidence at all. Mori and colleagues (2009) ran a double-blind, placebo-controlled trial of H. erinaceus in 30 Japanese adults with mild cognitive impairment, and found significantly improved cognitive scale scores at weeks 8, 12 and 16 — scores which declined again four weeks after intake stopped.^[9] That is a real randomised trial, but it is a small one in a different condition with a different mechanism, and it says nothing about myelin.

Two 2025 reviews frame the current state. A systematic review of H. erinaceus as a supplement collected five RCTs, 15 laboratory studies, three pilot clinical trials, one cohort study and one case report, with the clinical work concentrated on cognition rather than demyelination.^[8] A separate review of medicinal mushrooms for MS surveys mechanisms across the mushroom literature and is notably optimistic in tone — it discusses mushrooms in the language of curing MS — without singling out lion's mane as the leading candidate or citing any human MS trial.^[1] Treat it as a map of a research area, not as an evidence appraisal.

A 2023 review of H. erinaceus in neurodegenerative disease is the most useful corrective, partly for what it leaves out.^[6] It surveys the preclinical work across Alzheimer's disease, depression, Parkinson's disease and spinal cord injury — MS is not among the conditions it covers — and correlates erinacine effects with increased neurotrophic factor production. Its central conclusion concerns the state of the field: despite promising preclinical results, only a limited number of clinical trials have been carried out, and there is an urgent need for wider trials to establish safety and efficacy.

Form Matters More Here Than Almost Anywhere

Every oligodendrocyte, MBP and myelin-preservation finding described in this article comes from mycelium-derived material and its erinacines — whole mycelium extract, erinacine A, or erinacine S. Erinacines are produced in mycelium. They are not present in the fruiting body, which contains hericenones instead.

Most commercial lion's mane products are fruiting-body extracts. The one study here that did use fruiting bodies (Yamashina 2022) is also the one where lion's mane failed to improve motor function.^[3] And the anti-inflammatory data from Mori 2015 came from an ethyl acetate fraction — a laboratory preparation, not a standardised consumer extract.^[7]

Nor did the erinacines behave identically to each other. In Huang 2021, erinacines A and S outperformed erinacine C on MBP expression and oligodendrocyte counts.^[2] In Fu 2024, it was HEM and erinacine S — not erinacine A — that carried the myelin-preservation result.^[4] This is not a case where "lion's mane" as a category means much. The specific compound and the specific source material determine which findings, if any, could plausibly apply.

What This Evidence Cannot Support

Several limitations must be stated directly for anyone with MS evaluating this research.

No human MS trials exist. Every mechanism described here was demonstrated in cell culture or animals. No clinical trial has tested lion's mane in MS patients for any endpoint — remyelination, relapse rate, disability progression, or symptom management.

Cuprizone is not MS. It produces demyelination by direct chemical toxicity to oligodendrocytes, with no autoimmune component. Both studies underpinning the strongest claims here use it. Evidence in this model demonstrates anti-demyelination activity, not anti-MS activity.

Lion's mane has never been shown to affect the autoimmune attack. The T-cell dysregulation that drives the immune system to attack myelin is upstream of everything discussed in this article. Disease-modifying therapies act at that level and have clinical evidence for reducing relapse rates and slowing disability accumulation. Lion's mane has none.

The headline myelin-building result came from healthy newborn brains. Huang 2021's in vivo arm was developmental myelination in neonatal rats, not repair in a lesion.^[2] That distinction is not pedantic — it is the difference between the process working normally and the process being blocked.

Tissue protection and functional recovery diverged. In the one study that measured both, lion's mane suppressed demyelination and did not significantly improve motor function, while three other mushroom species did.

Safety

Critical

Do not substitute lion's mane for disease-modifying therapy

Concern

Disability accumulation in MS is driven by an autoimmune process that lion's mane has never been shown to affect. Reducing or stopping a disease-modifying therapy in favour of a supplement risks relapses and irreversible disability progression, and some DMTs carry rebound-disease risk on discontinuation. No interaction study exists between lion's mane and any MS DMT.

What the research says

If used at all, treat lion's mane as something layered on top of a physician-managed treatment plan — never as a replacement for one, and never as a reason to delay starting one.

Particularly relevant for: Anyone with diagnosed MS or clinically isolated syndrome, and anyone taking immunomodulating or immunosuppressive medication

What to do

Raise it with your neurologist before starting. Lion's mane polysaccharides and erinacines have documented immune-modulating activity, and most MS DMTs work by modulating or suppressing immune function — which is a specific reason to disclose it rather than add it silently.

Evidence gap: no human MS trials and no DMT interaction studies exist (refs [1][4][6][8])

A 2025 systematic review found H. erinaceus to have a generally favourable safety profile across the existing evidence base, but that evidence base did not include people with MS or people taking immunomodulatory medication.^[8] General tolerability in healthy adults does not transfer to a population on immunotherapy.

This article is educational and is not medical advice. Nothing here should be used to diagnose, treat, or manage multiple sclerosis, or to make changes to a prescribed treatment plan. Those decisions belong with your neurologist. For the symptom-management side of this topic, see Lion's Mane for MS Fatigue and Cognitive Symptoms.

The Bottom Line

Lion's mane has a real, two-decade preclinical research line pointing at MS-relevant remyelination. Kolotushkina 2003 found myelination began earlier and proceeded faster in cerebellar culture. Huang 2021 showed mycelium extract and erinacines A and S drove oligodendrocyte precursor cells to mature and raised myelin basic protein across cultures, cerebellar slices and neonatal rat brain — though that living-animal arm was a healthy developing brain, and the authors framed it around neurodevelopmental disorders rather than MS. Fu 2024 is the strongest result: in cuprizone-exposed rodents, mycelium extract and erinacine S preserved myelin and oligodendrocytes, reduced microglial and astrocyte activation, downregulated IL-1-beta, and eased anxiety- and depression-like behaviour, with erinacine S still working when given only after damage was established. Against that, Yamashina 2022 found lion's mane suppressed demyelination but was the only one of four mushrooms that failed to improve motor function — and measured no inflammatory markers at all. Every myelin finding used mycelium and erinacines rather than the fruiting-body extracts sold commercially. No human MS trial has been conducted, no cited study used an autoimmune MS model, and disease-modifying therapies remain the evidence-based standard of care.

Frequently Asked Questions

Is lion's mane good for multiple sclerosis?

Preclinical evidence suggests lion's mane compounds support remyelination and protect oligodendrocytes in animal models of demyelination. Erinacine S preserved myelin and oligodendrocytes in cuprizone-exposed rodents and reduced glial activation and IL-1-beta (Fu et al., 2024). Mycelium extract and erinacines A and S increased myelin basic protein production and oligodendrocyte maturation (Huang et al., 2021). No human clinical trial has tested lion's mane in MS patients for any endpoint. The preclinical foundation is mechanistically credible; clinical evidence does not exist.

What is the best mushroom for MS?

No mushroom has confirmed clinical efficacy in human MS trials. Lion's mane has the most compound-specific preclinical remyelination evidence. But in the one head-to-head animal comparison, reishi was the only one of four species to improve body weight, motor function and demyelination together, while lion's mane suppressed demyelination without improving motor function (Yamashina et al., 2022). A 2025 review of medicinal mushrooms for MS surveys the comparative mechanisms; none of these species has advanced to a human MS trial.

Can lion's mane help MS symptoms?

No human study has measured lion's mane's effect on MS symptoms. Preclinical work shows effects on the underlying biology — oligodendrocyte protection, myelin preservation, reduced glial activation — but none of it has been tested in people with MS. The 2024 erinacine S study did reduce anxiety- and depression-like behaviour in cuprizone-exposed mice, which is mechanistically interesting given how common depression and anxiety are in MS, but that is rodent behavioural data. Notably, in the one animal study that measured motor function, lion's mane did not improve it.

How does lion's mane affect myelin in MS?

Through two mechanisms in preclinical models. First, mycelium extract and erinacines A and S push oligodendrocyte precursor cells to mature and increase myelin basic protein production, which targets the maturation bottleneck seen in MS lesions. Second, erinacine S protects existing mature oligodendrocytes and preserves myelin during active demyelination in the cuprizone model. An important limit: the myelin-building evidence comes largely from healthy or developing tissue, while the protective evidence comes from a chemical demyelination model. Neither has been tested in a human MS brain.

Which form of lion's mane was used in the MS research?

Almost all of it used mycelium. Every oligodendrocyte, MBP and myelin-preservation finding came from H. erinaceus mycelium extract or the isolated erinacines A and S. Erinacines occur in mycelium, not in the fruiting body, which contains hericenones instead. The one study that used fruiting bodies is also the one where lion's mane failed to improve motor function. Since most commercial products are fruiting-body extracts, product form is not a minor detail here — it determines whether you are taking the compounds these studies actually tested.

Is lion's mane safe with MS disease-modifying therapies?

No specific drug interaction study exists between lion's mane and any MS DMT. Lion's mane polysaccharides and erinacines are immunomodulatory, and many MS DMTs work by modulating or suppressing immune function, so the combination is not theoretically neutral. A 2025 systematic review found lion's mane generally well tolerated in the existing evidence base, but that evidence did not include patients on immunomodulatory medications. Anyone on a DMT should discuss lion's mane with their neurologist before using it, and should never treat it as a substitute for prescribed therapy.

Sources & References

1. 1RTHM-02163·Pourmohammadi, Golchehr et al. (2025). “New approach of using medicinal mushrooms for managing and curing multiple sclerosis..” Fitoterapia.Study breakdown →PubMed →↩
2. 2RTHM-00692·Huang, Hui-Ting et al. (2021). “Hericium erinaceus mycelium and its small bioactive compounds promote oligodendrocyte maturation with an increase in myelin basic protein..” Scientific reports.Study breakdown →PubMed →↩
3. 3RTHM-01637·Yamashina, Kota et al. (2022). “Suppressive Effect of Fruiting Bodies of Medicinal Mushrooms on Demyelination and Motor Dysfunction in a Cuprizone-Induced Multiple Sclerosis Mouse Model..” International journal of medicinal mushrooms.Study breakdown →PubMed →↩
4. 4RTHM-00878·Fu, Jing-Ting et al. (2024). “Erinacine S, a small active component derived from Hericium erinaceus, protects oligodendrocytes and alleviates mood abnormalities in cuprizone-exposed rodents..” Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.Study breakdown →PubMed →↩
5. 5RTHM-00058·Kolotushkina, E V et al. (2003). “The influence of Hericium erinaceus extract on myelination process in vitro..” Fiziolohichnyi zhurnal (Kiev.Study breakdown →PubMed →↩
6. 6RTHM-01662·Brandalise, Federico et al. (2023). “Hericium erinaceus in Neurodegenerative Diseases: From Bench to Bedside and Beyond, How Far from the Shoreline?.” Journal of fungi (Basel.Study breakdown →PubMed →↩
7. 7RTHM-00726·Mori, Koichiro et al. (2015). “The Anti-Inflammatory Effects of Lion's Mane Culinary-Medicinal Mushroom, Hericium erinaceus (Higher Basidiomycetes) in a Coculture System of 3T3-L1 Adipocytes and RAW264 Macrophages..” International journal of medicinal mushrooms.Study breakdown →PubMed →↩
8. 8RTHM-00943·Menon, Arya et al. (2025). “Benefits, side effects, and uses of Hericium erinaceus as a supplement: a systematic review..” Frontiers in nutrition.Study breakdown →PubMed →↩
9. 9RTHM-00165·Mori, Koichiro et al. (2009). “Improving effects of the mushroom Yamabushitake (Hericium erinaceus) on mild cognitive impairment: a double-blind placebo-controlled clinical trial..” Phytotherapy research : PTR.Study breakdown →PubMed →↩
10. 10RTHM-01448·Tung, Shui-Yi et al. (2021). “Apoptotic mechanisms of gastric cancer cells induced by isolated erinacine S through epigenetic histone H3 methylation of FasL and TRAIL..” Food & function.Study breakdown →PubMed →↩