Mushrooms and Multiple Sclerosis: What the Research Shows

Mushrooms & Multiple Sclerosis

2 research angles

Preclinical studies approach MS from two directions: Lion's Mane promoting myelin repair at the cellular level, and Reishi acting on the immune attack that strips myelin away. The evidence behind each is uneven in ways the headline framing hides.

Yamashina et al., Int J Med Mushrooms, 2022; Zhang et al., Chin Med, 2026

0 human trials

of Lion's Mane or Reishi in MS patients, on a PubMed search of the clinical trial literature

3 of 4 species

improved motor function in the one MS mouse model that compared them — Lion's Mane was not among them (Yamashina 2022)

1 autoimmune model

study exists in the whole literature: Reishi in EAE (Zhang 2026). Lion's Mane has none

Yamashina et al., Int J Med Mushrooms, 2022; Zhang et al., Chin Med, 2026

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In 2022, researchers fed medicinal mushrooms to mice with induced MS-like damage and measured what happened to the myelin. Yamashina and colleagues used a chemical called cuprizone to selectively destroy the fatty coating around nerve fibers, replicating the central injury of multiple sclerosis. Four mushroom species went into the diet at 5% each, alongside the cuprizone, for five weeks. All four suppressed demyelination. But only three improved the mice's motor function, and Lion's Mane, the species most often named as the myelin-repair candidate, was not one of them.^[1]

That split is the most useful thing in the mushroom and MS literature, and it is almost always flattened into a sentence saying mushrooms helped. Preclinical research identifies two species worth taking seriously for two different reasons: Lion's Mane for myelin repair, Reishi for immune regulation. Evidence comes from cell cultures, two rodent studies using chemical demyelination models, and a single study using the autoimmune model that actually reproduces MS. No human clinical trials have tested either species in MS patients.

Why two species? Because MS is a two-front disease. It involves myelin destruction driven by an overactive immune attack, and the body's failure to fully repair that damage afterward. Lion's Mane shows the strongest preliminary evidence for the repair problem. Reishi shows the strongest evidence for the immune problem, and as of 2026 it is the only one of the two tested in an autoimmune MS model at all. This article covers both, and is part of the broader overview of how mushrooms affect brain health and cognitive aging.

What Makes MS a Two-Front Disease (and Why That Tells Us Which Mushrooms Matter)

MS is not simply a disease where myelin disappears. It is a disease where the immune system attacks myelin, and then the repair process fails to keep pace with ongoing damage.

Myelin is a fatty insulating layer around nerve fibers. Think of it as the plastic coating on an electrical wire: without it, the signal slows or stops entirely. In MS, specific white blood cells called T cells cross the blood-brain barrier and treat myelin as a foreign invader. The resulting immune attack strips myelin from nerve fibers in patches called lesions. Patients experience this as symptoms: numbness, vision problems, weakness, cognitive slowing, and mobility impairment that vary based on which nerves are affected.

After an attack, the body attempts repair. A type of brain cell called an oligodendrocyte produces myelin. Oligodendrocytes develop from precursor cells called oligodendrocyte precursor cells (OPCs). In healthy tissue, OPCs mature into oligodendrocytes and lay down new myelin when it is lost. In the chronically inflamed environment of MS, this maturation process breaks down. The raw material for repair is present; the cellular process that completes the repair is disrupted.

This dual structure means a mushroom compound is mechanistically relevant to MS if it does one of two things:

1. Supports the maturation of OPCs into myelin-producing oligodendrocytes (targets the repair failure)
2. Modulates the T-cell attack on myelin (targets the immune dysregulation driving the damage)

Lion's Mane has the most direct preclinical evidence for the first. Reishi has the evidence for the second. Crucially, these two claims do not rest on the same quality of evidence, and they have not been tested in the same kinds of models.

Where Each Species Has Actually Been Tested

The Two-Front Story Holds at the Mechanism — and Inverts at the Model

“Lion’s Mane for repair, Reishi for immunity” is a tidy summary. Laid against the experimental systems each species has actually been through, the symmetry breaks: the repair species has never faced an autoimmune attack in a lab, and the immune species owns the only result from the model that reproduces MS.

The amber row is the one that matters most and is thinnest: EAE provokes the animal’s own immune system into attacking myelin, which is what MS actually is. Only Reishi has been through it, in a single study that dosed preventively — before disease was established, which is not the position a diagnosed patient is in. The bottom row is empty for both species, and no amount of rodent evidence substitutes for it.

Coverage from refs [1][2][3][8][9]; empty cells verified by PubMed search

The Studies That Used Real MS Disease Models

Most of the mushroom and MS research landscape uses isolated cells in culture or general neuroprotection models. Three studies do better than that, and they are the load-bearing evidence in this entire area.

Yamashina 2022: four species, and a result that splits them

Yamashina and colleagues fed mice a powdered diet containing 5% of a single mushroom species alongside cuprizone for five weeks, the window covering peak demyelination. They weighed the mice, tested motor function on a rotarod, and quantified myelin with Black-Gold II staining.^[1]

The results did not move together. All four species — Pleurotus eryngii (king trumpet), Ganoderma lucidum (Reishi), Flammulina velutipes (enoki) and Hericium erinaceus (Lion's Mane) — effectively suppressed cuprizone-induced demyelination. But on motor function, only P. eryngii, G. lucidum and F. velutipes produced significant improvement. Lion's Mane preserved myelin without producing a measurable functional gain. Separately, Reishi and Lion's Mane were the two species that recovered cuprizone-induced weight loss.

The Only Head-to-Head Comparison

Four Species, Three Endpoints — and They Did Not Move Together

Yamashina 2022 is almost always summarised as “mushrooms suppressed demyelination in an MS model.” That is true of all four species tested. But the study also measured whether the mice could actually move better, and there the species separated — including the one most often named as the myelin-repair candidate.

A dash means the species was tested but was not named among those showing that effect in the published results — which is weaker than a reported null result, and is not evidence the species made anything worse. Note also what the whole table sits on: cuprizone is a chemical demyelination model with no autoimmune component, and none of these are human results.

All endpoints from ref [1] Yamashina et al., 2022 (PMID 36004706)

This matters because "preserved myelin" and "the animal moved better" are different claims, and the mushroom-MS literature routinely reports the first as though it delivered the second. In the one experiment that measured both across multiple species, they came apart.

Key Study

Yamashina et al. (2022) · International Journal of Medicinal Mushrooms

Population

Mice fed a cuprizone diet for 5 weeks, covering peak demyelination

Intervention

Powdered diet containing 5% of each mushroom species: P. eryngii, G. lucidum, F. velutipes, or H. erinaceus

Finding

All four species suppressed cuprizone-induced demyelination on Black-Gold II staining. Only P. eryngii, G. lucidum and F. velutipes significantly improved rotarod motor performance. G. lucidum and H. erinaceus recovered cuprizone-induced weight loss.

mixed The only study to compare multiple mushroom species head-to-head in an MS model, and the only one to measure a functional endpoint alongside myelin. Its most-cited conclusion — mushrooms suppress demyelination — is real, but it obscures that the species named most often for myelin repair was the one that did not improve motor function. Cuprizone is also a chemical demyelination model with no autoimmune component.

Ref [1] Yamashina et al., 2022 (PMID 36004706)

Fu 2024: the strongest myelin protection result

Fu and colleagues (2024) tested H. erinaceus mycelium extract and its isolated compounds erinacine A and erinacine S in cuprizone-exposed rats and mice.^[8] The mycelium extract and erinacine S preserved myelin and oligodendrocytes in the corpus callosum, reduced microglia and astrocyte activation, and downregulated IL-1beta.

The design detail that lifts this study above the rest: erinacine S also worked as a post-treatment. Given only during the final four weeks of both acute (6-week) and chronic (12-week) cuprizone exposure, it still preserved myelin, and it reduced anxious and depressive-like behavior in the mice. Most preclinical work gives the compound and the toxin simultaneously, which tests prevention. Testing something after damage is underway is closer to the situation of a person who already has MS.

Zhang 2026: the first autoimmune-model study

Every study above uses cuprizone. Chemical myelin destruction and immune-mediated myelin destruction are similar in structure but different in origin, and that gap has been the standing limitation of this entire research area.

Zhang and colleagues (2026) closed part of it. Using an EAE mouse model, they found that early preventive administration of Ganoderma lucidum significantly reduced disease severity, inflammatory infiltration, demyelination, and microglial activation in the spinal cord, while promoting a shift in microglia toward an anti-inflammatory M2-like phenotype.^[9] In parallel cell experiments, Reishi scavenged superoxide, nitric oxide and peroxynitrite, and downregulated IL-1beta, TNF-alpha, IL-6, COX2 and iNOS in stimulated microglial cells, with the effect traced to inhibition of NF-kappaB/STAT3 signaling.

Key Study

Zhang, Chen, Yuen et al. (2026) · Chinese Medicine

Population

EAE mice (experimental autoimmune encephalomyelitis); LPS-stimulated microglial cells in vitro

Intervention

Early preventive oral administration of Ganoderma lucidum

Finding

Reduced EAE disease severity, inflammatory infiltration, demyelination and microglial activation in the spinal cord, promoting M2-like microglial polarization. In vitro, scavenged superoxide, nitric oxide and peroxynitrite and downregulated IL-1beta, TNF-alpha, IL-6, COX2 and iNOS via inhibition of NF-kappaB/STAT3.

preliminary The only study placing either species in an autoimmune MS model, which makes it the most disease-relevant result available. Two limits keep it preliminary: it is a single unreplicated study, and the protocol was early preventive dosing — treatment started before disease was established, which is not the situation of a diagnosed patient.

Ref [9] Zhang et al., 2026 (PMID 41957858)

The cross-species remyelination article covers which species showed the strongest effects in the cuprizone work and why the multi-species approach is mechanistically interesting.

How Lion's Mane Reaches the Cell That Builds New Myelin

The repair failure in MS happens at the OPC level. The precursor cells needed to rebuild myelin are present in MS tissue, but they are not maturing into functional oligodendrocytes. A compound that specifically supports OPC maturation would be addressing the repair failure at its cellular root.

Kolotushkina and colleagues (2003) were the first to document that H. erinaceus extract influences myelination in cell culture.^[3] In cultured cerebellar cells, myelination began earlier than in controls and proceeded at a higher rate, with no toxic effect on the nerve and glial cells. The mechanism was not yet identified.

Huang and colleagues (2021) narrowed it down. Working in OPC cultures and an ex vivo cerebellar slice system, they found that H. erinaceus mycelium extract promoted the differentiation of OPCs into mature oligodendrocytes and increased the level of myelin basic protein (MBP) on neuronal fibers.^[2] Myelin basic protein is the primary structural protein of the myelin sheath: when MBP rises on a nerve fiber, myelin is being deposited. The study also went into a living animal — seven days of daily oral extract raised MBP expression and oligodendrocyte numbers in the corpus callosum of neonatal rat pups.

Three bioactive compounds were tested individually: the diterpenoid xylosides erinacine A (HeA) and erinacine C (HeC), and a sesterterpene designated HeS. HeA and HeS were the more potent, stimulating MBP expression and increasing oligodendrocyte numbers, and significantly increasing the overlap between MBP and neuronal fibers in cerebellar tissue slices.

Phan and colleagues (2015) reviewed culinary-medicinal mushrooms for neurodegenerative disease and documented, across more than 20 species, effects including nerve growth factor (NGF) synthesis, neurite outgrowth stimulation and anti-neuroinflammatory activity.^[6] NGF supports neuron survival and the growth of new nerve connections, and operates through a separate pathway from OPC maturation. That review closes by noting its evidence base is predominantly in vitro and that human clinical trials are needed. For the full breakdown of how both mechanisms relate to myelin repair specifically, the Lion's Mane for MS article covers the evidence in depth.

Taken together, Lion's Mane has a biologically plausible, reasonably well-characterized mechanism for making and protecting myelin. What it does not have is any evidence of acting on the autoimmune process, or of restoring lost function in a damaged animal.

How Reishi Targets the Immune Attack

If Lion's Mane's evidence points at the repair side of MS, Reishi's points at the immune side — and, since 2026, it is the only one of the two with evidence from a genuinely autoimmune model.

The autoimmune attack in MS is driven by T cells incorrectly trained to treat myelin proteins as foreign. Alongside them, microglia — the brain's resident immune cells — amplify or dampen the damage depending on the state they adopt. Zhang 2026's central finding is that Reishi pushed microglia toward the anti-inflammatory M2-like state and reduced the resulting demyelination in EAE mice.^[9] That is a mechanistically specific result in a disease-appropriate model, and it is the strongest single reason to keep studying Reishi in MS.

Bhardwaj and colleagues (2014) reviewed the anti-inflammatory and antiallergic pharmacology of G. lucidum, surveying its capacity to target inflammatory cytokines and its relevance across chronic inflammatory and autoimmune conditions.^[5] It is a review of the mushroom's general inflammatory pharmacology rather than an MS study, and it is best read as background to the cytokine findings that Zhang 2026 later measured directly in an MS model.

Fact Check

Does Reishi 'balance' the immune system?

The claim

“Reishi is an immune modulator rather than an immune stimulant, so it balances an overactive immune system rather than making it worse — which is what makes it appropriate for autoimmune conditions like MS.”

Widely attributed to Lin's 2005 review of Ganoderma immunomodulation, which is the most-cited source for Reishi's immune effects.

What research shows

Unsupported

Lin 2005 describes G. lucidum polysaccharides as modulating immune function extensively — promoting antigen-presenting cell function, the mononuclear phagocyte system, humoral immunity and cellular immunity. The direction described across those compartments is enhancement, not suppression, and the review does not report reduced T-cell overactivation or effects on regulatory T cells.

This does not make Reishi unsafe or irrelevant in MS — Zhang 2026 found it reduced demyelination and disease severity in an autoimmune model, likely through anti-inflammatory and antioxidant routes acting on microglia rather than by suppressing adaptive immunity. But 'it balances your immune system' is a claim the most-cited source does not make. Lin's own review concludes that whole-animal experiments and evidence-based clinical trials are still needed.

Refs [4] Lin, 2005 (PMID 16230843); [9] Zhang et al., 2026 (PMID 41957858)

The dedicated Reishi and MS immune regulation article covers the immune-regulation angle in more detail.

The Honest Limitation: Preclinical Evidence Is Not Human Evidence

Brandalise and colleagues (2023) reviewed H. erinaceus across neurodegenerative disease and framed the problem as a question: how far from the shoreline? Their conclusion is that despite a large body of preclinical CNS work, only a limited number of clinical trials have been carried out in neurological conditions, and further trials are urgently needed to establish safety and efficacy.^[7] Notably, the conditions that review covers are Alzheimer's disease, depression, Parkinson's disease and spinal cord injury. MS is not among them, which is itself informative about how thin this specific literature is.

A PubMed search of the clinical trial literature returns no published or registered human trial of either Lion's Mane or Reishi in multiple sclerosis. That absence is not a minor qualification. The step from "this compound promotes OPC maturation in a dish" to "this compound promotes myelin repair in a human with MS" involves enormous unknowns. Does the compound survive digestion and reach the brain at effective concentrations? Does it behave the same way in the chronically inflamed environment of MS as it does in isolated cells? Does it interact with MS medications? Does it produce different effects in people whose immune systems are already being suppressed by disease-modifying therapies?

Evidence Reach

1. Cell and tissue studiescompleted

   Myelination began earlier and faster in cerebellar culture (Kolotushkina 2003); OPC-to-oligodendrocyte differentiation and raised MBP in cultures and cerebellar slices (Huang 2021); Reishi suppressed IL-1beta, TNF-alpha, IL-6, COX2 and iNOS in stimulated microglia (Zhang 2026)

2. Healthy living animalscompleted

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

3. Chemical demyelination modelscompleted

   Four species suppressed demyelination but only three improved motor function (Yamashina 2022); erinacine S preserved myelin and oligodendrocytes, reduced gliosis and IL-1beta, and worked as a post-treatment (Fu 2024)

4. Autoimmune MS models (EAE)current

   One study, Reishi only: preventive dosing reduced disease severity, immune infiltration, demyelination and microglial activation in EAE mice (Zhang 2026). Unreplicated. No Lion's Mane study in EAE exists

5. Human case reports in MSmissing

   None published for either species

6. Small human MS trialsmissing

   None published or registered for any MS endpoint

7. Large randomised trialsmissing

   None

8. Meta-analysis in MSmissing

   Not possible — no human MS trials exist to pool

The line stops at rodents. One 2026 study reached the autoimmune model that actually mirrors MS, and it tested Reishi only, preventively, without replication. Everything above that rung is empty for both species.

Refs [1][2][3][7][8][9] (see references)

A 2025 review in Fitoterapia argues that medicinal mushrooms could play an important role in MS treatment in the near future, surveying polysaccharides, terpenes and peptides across antioxidant, immune and neuroprotective mechanisms.^[10] It is the most recent topical synthesis available and worth reading, but its framing — the title refers to "managing and curing" MS — runs well ahead of an evidence base with no human trials in it. That gap between review-level enthusiasm and trial-level evidence is characteristic of this field and worth holding in mind when reading any summary of it.

The preclinical-to-clinical translation gap is a well-documented problem across the entire neurodegenerative disease research field, not a limitation specific to mushrooms. Many compounds that show striking results in cell cultures and mouse models fail in human trials. The same pattern appears in Parkinson's disease research, where Lion's Mane and other species show interesting preclinical signals without condition-specific trials behind them.

The honest summary: two plausible mechanisms, a genuine preclinical signal in real demyelination models, one unreplicated result in a real autoimmune model, and no human data at all. That is more than most supplements can claim for a specific neurological condition. It is far less than what would be required to describe mushrooms as a treatment for MS.

Why MS Patients Face a More Complex Safety Calculation

For healthy adults, Lion's Mane and Reishi have relatively benign safety profiles at the doses studied. The calculation changes for MS patients, particularly those on disease-modifying therapies.

Most MS medications work by altering specific aspects of immune function. Interferon-beta modulates innate immune responses. Natalizumab prevents immune cells from crossing the blood-brain barrier. Ocrelizumab depletes B cells. Cladribine reduces lymphocyte populations. Each is calibrated to shift the immune balance in a particular direction. Adding a supplement that also acts on immune function creates the possibility of additive, synergistic or antagonistic effects, none of which can be predicted without trial data in MS patients on these medications. No such interaction study exists for either species.

The direction of Reishi's immune effect deserves particular attention here. As covered above, the most-cited review of Ganoderma immunomodulation describes its polysaccharides as broadly promoting immune function across multiple compartments.^[4] In a healthy adult that is unremarkable. In a person whose immune system is being deliberately suppressed by medication to prevent it attacking their own myelin, a compound characterized as promoting immune function is a question worth putting to a neurologist rather than answering yourself. Zhang 2026's EAE result points the other way, toward benefit, but a single preventive-dosing animal study does not settle a clinical interaction question.

Safety

Critical

Never substitute mushrooms for disease-modifying therapy

Concern

Disability accumulation in MS is driven by an autoimmune process that no mushroom species has been shown to affect in a human being. 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 or Reishi and any MS DMT.

What the research says

If used at all, treat these mushrooms 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

Disclose it to your neurologist before starting. Reishi polysaccharides are described in the literature as promoting immune function, and most MS DMTs work by suppressing or modulating it — which is a specific reason to raise it rather than add it silently.

Evidence gap: no human MS trials and no DMT interaction studies exist (refs [4][7][9])

This article is research education, not medical advice. Nothing here is a recommendation to take, avoid, or change any supplement or medication. Decisions about MS treatment belong with your neurologist.

For a complete treatment of the safety considerations relevant to MS patients, the mushroom supplements and MS safety article covers the mechanistic reasons for caution. For readers interested in how the same Lion's Mane nerve repair evidence applies in non-autoimmune contexts, the traumatic brain injury mushroom research covers the parallel evidence where the immune interaction concern is absent.

The Bottom Line

Medicinal mushrooms and multiple sclerosis meet on two research fronts. Lion's Mane addresses the repair side: it drives oligodendrocyte precursor maturation and raises myelin basic protein in cultures, cerebellar slices and healthy neonatal rat brain (Huang 2021), with myelination effects documented as early as 2003 (Kolotushkina), and erinacine S preserving myelin in cuprizone-exposed rodents even as a post-treatment (Fu 2024). Reishi addresses the immune side, and is the only species tested in the autoimmune EAE model, where preventive dosing reduced disease severity, demyelination and microglial activation (Zhang 2026). The most-cited Reishi immune review describes broad immune promotion rather than the "balancing" effect often claimed for it (Lin 2005). In the one study comparing species head-to-head in an MS model, all four suppressed demyelination but only three improved motor function — Lion's Mane was not among them (Yamashina 2022). No human clinical trial of either species in MS has been published or registered.

Frequently Asked Questions

Can mushrooms help with multiple sclerosis?

Preclinical evidence suggests two mechanisms: Lion's Mane for supporting myelin repair at the cellular level, and Reishi for acting on the immune attack. In rodents, both suppress demyelination, and Reishi reduced disease severity in the autoimmune EAE model (Zhang 2026). But no human clinical trial of either species in MS patients has been published or registered, so whether any of this translates to people with MS is unknown. This is research education, not medical advice.

What is the best mushroom for MS?

It depends which problem you mean, and the honest answer is that the evidence does not support naming one. Lion's Mane has the most detailed evidence for the myelin repair mechanism: it drives maturation of myelin-building precursor cells and raises myelin basic protein (Huang 2021), and erinacine S preserves myelin in demyelinating rodents (Fu 2024). Reishi has the better disease-model evidence: it is the only species tested in the autoimmune EAE model (Zhang 2026), and in the one head-to-head comparison it improved motor function where Lion's Mane did not (Yamashina 2022). Neither has been tested in a human MS trial.

Do medicinal mushrooms help with MS symptoms?

No human trials have tested medicinal mushrooms for MS symptoms. The closest evidence is rodent functional data: in Yamashina 2022, king trumpet, Reishi and enoki significantly improved motor performance in cuprizone-treated mice, while Lion's Mane suppressed demyelination without improving motor function. In Fu 2024, erinacine S reduced anxious and depressive-like behaviour in cuprizone-fed mice. Whether any of that corresponds to symptom relief in people with MS cannot be determined from the available evidence.

Is there research on mushrooms and multiple sclerosis?

Yes, though all of it is preclinical. Kolotushkina et al. (2003) showed Lion's Mane extract makes myelination begin earlier and proceed faster in nerve cell culture. Huang et al. (2021) found H. erinaceus mycelium promotes maturation of the cells that build myelin. Yamashina et al. (2022) tested four species in a cuprizone MS mouse model. Fu et al. (2024) showed erinacine S preserves myelin even when given after damage begins. Zhang et al. (2026) is the first study in the autoimmune EAE model, testing Reishi. No human MS trials exist for either species.

Is Reishi safe if I have an autoimmune disease like MS?

This is a question for your neurologist, not one this article can answer. The most-cited review of Ganoderma immunomodulation describes its polysaccharides as broadly promoting immune function across several immune compartments (Lin 2005), which is a reason for caution in a disease driven by the immune system attacking myelin. A 2026 EAE study points the other way, finding Reishi reduced disease severity and demyelination in mice, apparently by calming microglia. No interaction study exists between Reishi and any MS disease-modifying therapy. Because most DMTs work by modulating or suppressing immune function, disclose any mushroom supplement to your neurologist rather than adding it silently.

What natural remedies help multiple sclerosis?

Vitamin D is the most researched nutritional factor in MS, with lower levels associated with greater disease activity. Omega-3 fatty acids and coenzyme Q10 have limited supportive evidence. Lion's Mane and Reishi show preclinical promise on myelin repair and immune mechanisms respectively, but neither has been tested in a human MS trial. For anyone on a disease-modifying therapy, neurologist consultation is appropriate before adding any supplement that acts on immune function, and no supplement should replace prescribed treatment.

Sources & References

1. 1RTHM-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 →↩
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-00058·Kolotushkina, E V et al. (2003). “The influence of Hericium erinaceus extract on myelination process in vitro..” Fiziolohichnyi zhurnal (Kiev.Study breakdown →PubMed →↩
4. 4RTHM-00084·Lin, Zhi-Bin (2005). “Cellular and molecular mechanisms of immuno-modulation by Ganoderma lucidum..” Journal of pharmacological sciences.Study breakdown →PubMed →↩
5. 5RTHM-00578·Bhardwaj, Neha et al. (2014). “Suppression of inflammatory and allergic responses by pharmacologically potent fungus Ganoderma lucidum..” Recent patents on inflammation & allergy drug discovery.Study breakdown →PubMed →↩
6. 6RTHM-00397·Phan, Chia-Wei et al. (2015). “Therapeutic potential of culinary-medicinal mushrooms for the management of neurodegenerative diseases: diversity, metabolite, and mechanism..” Critical reviews in biotechnology.Study breakdown →PubMed →↩
7. 7RTHM-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 →↩
8. 8RTHM-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 →↩
9. 9RTHM-02429·Zhang, L et al. (2026). “Ganoderma lucidum mediates microglial polarization and ameliorates experimental autoimmune encephalomyelitis by reducing oxidative stress and inhibiting NF-κB/STAT3 pathway..” Chinese medicine.Study breakdown →PubMed →↩
10. 10RTHM-02163·Pourmohammadi, Golchehr et al. (2025). “New approach of using medicinal mushrooms for managing and curing multiple sclerosis..” Fitoterapia.Study breakdown →PubMed →↩