Mushrooms and ALS / Motor Neuron Disease
30% longer survival in a motor neuron disease mouse model
A 2025 study found that ergothioneine, a compound concentrated in mushrooms, extended survival by about 30% in mice with spinal muscular atrophy — a fatal motor neuron disease. The supplement was given to the mothers during pregnancy and nursing, and the mechanistic work was done in muscle, not motor neurons.
Cadile et al., FEBS Letters, 2025
0 studies
mushroom compounds tested in any ALS cell model, animal model, or patient
SLC22A4
the dedicated human transporter whose true substrate turned out to be ergothioneine (Gründemann et al., 2005)
3 of 5
ALS disease mechanisms with any mushroom-compound data — the two most ALS-specific have none
Cadile et al., FEBS Letters, 2025
View as image ↗In 2025, researchers reported that ergothioneine, a compound humans get almost entirely from mushrooms, extended survival by roughly 30% in mice with a fatal motor neuron disease.[1] The disease was spinal muscular atrophy, in which the nerve cells that control voluntary movement progressively die. It is the most direct motor neuron disease result published for any mushroom compound, and it has gone almost entirely unmentioned in consumer health content.
It has also been misread almost every time it does appear. This article covers what the research on mushroom compounds and motor neuron protection actually shows: which compounds have relevant data, what each study measured and in what tissue, and where the evidence stops. For anyone researching this because ALS has touched their life, the honest summary has two halves that both need saying. The mechanistic rationale for further research is real. Clinical evidence in humans is entirely absent, and the gap between those two facts is wider than most write-ups admit. This article is part of a broader look at mushrooms and cognitive aging across neurodegenerative conditions.
Key Takeaways
- A 2025 mouse study found ergothioneine extended survival by about 30% in spinal muscular atrophy, a motor neuron disease related to but distinct from ALS; the supplement was given to mothers during pregnancy and nursing, not to symptomatic adults (Cadile et al., 2025)
- That study's mechanistic findings — mitophagy, NRF2 and GPX increases — were measured in diaphragm muscle, not in motor neurons; the authors themselves note the antioxidant enzyme data came from a very small number of animals
- Humans have a dedicated transporter for ergothioneine (SLC22A4, also called OCTN1), and it is required for the compound to enter brain cells at all (Gründemann et al., 2005; Ishimoto et al., 2022)
- Ergothioneine levels fall in frailty and dementia, and one prominent hypothesis holds that low levels raise neurodegenerative risk — this is a proposal under investigation, not an established finding (Kondoh et al., 2022; Halliwell et al., 2024)
- Erinacines from lion's mane mycelium are documented to stimulate NGF, with more limited BDNF evidence; the systematic review covering them contains no motor neuron or ALS studies at all (Spangenberg et al., 2025)
- Cordycepin reduced dopaminergic neuron loss in a Parkinson's model by blocking Drp1-driven mitochondrial fragmentation and NLRP3 inflammasome activation — a different neuron type and a different disease (Zhang et al., 2021)
- No mushroom compound has been tested in an ALS cell model, an ALS animal model, or a human being with ALS
Why Motor Neurons Are Uniquely Vulnerable (and What "Protection" Means in a Study)
Motor neurons carry movement signals from the brain and spinal cord to muscles. In ALS and spinal muscular atrophy, these cells progressively die, and the loss is permanent — neurons do not regenerate the way many other cells do.
ALS is not caused by a single mechanism. Researchers have identified at least five distinct processes that contribute to motor neuron death: oxidative stress (damage from chemically reactive molecules that cells cannot neutralize quickly enough), neuroinflammation (immune activation in the brain and spinal cord that creates a toxic environment for neurons), mitochondrial dysfunction (failure of the energy-generating structures inside motor neurons, which are among the most energy-dependent cells in the body), protein aggregation (a protein called TDP-43 forms toxic clumps inside motor neurons in the large majority of ALS cases), and excitotoxicity (excess glutamate between neurons overstimulates motor cells until they die).
That distinction does most of the work in this topic, because the mushroom compounds with data cluster in a revealing pattern.
Five ALS Mechanisms · Where the Compounds Land
The Compounds Cover the Shared Mechanisms and Miss the ALS-Defining Ones
Three of the five processes that kill motor neurons in ALS are generic to neurodegeneration, and all three have mushroom-compound data behind them. The two that most specifically define ALS — TDP-43 aggregation and glutamate excitotoxicity — have none. This is the shape of the evidence base: broad coverage where the disease looks like every other neurodegenerative disease, and nothing where it looks like itself.
Oxidative stress
Reactive molecules damage cells faster than defenses can neutralize them
- Ergothioneine — ↑ NRF2 and GPX in diaphragm muscle [1]
- Erinacines — Erinacine A and C induce Nrf2 accumulation [7]
- Cordycepin — ↓ mitochondrial ROS [8]
Neuroinflammation
Immune activation in brain and spinal cord creates a toxic environment for neurons
- Erinacines — Anti-inflammatory activity across preclinical models [7]
- Cordycepin — ↓ NLRP3 inflammasome, ↓ pro-inflammatory cytokines [8]
Mitochondrial dysfunction
The cell’s energy-generating structures fail; motor neurons are unusually energy-hungry
- Ergothioneine — Stimulated mitophagy (clearance of damaged mitochondria) in muscle [1]
- Cordycepin — Reversed Drp1-driven fragmentation via AMPK; ↑ ATP [8]
TDP-43 protein aggregation
A protein forms toxic clumps inside motor neurons in the large majority of ALS cases
No mushroom compound in this article’s evidence base has been tested against this mechanism — in ALS models or any other.
Excitotoxicity
Excess glutamate overstimulates motor neurons until they die
No mushroom compound in this article’s evidence base has been tested against this mechanism — in ALS models or any other.
A compound that addresses three of five mechanisms is not therefore 60% of a treatment. Mechanisms are not additive, they interact, and the two uncovered here are the ones researchers most associate with what makes ALS ALS rather than neurodegeneration in general.
Mechanism coverage from refs [1][7][8]; empty cells reflect absent studies
Ergothioneine: The Most Direct Motor Neuron Disease Data for Any Mushroom Compound
Ergothioneine is an antioxidant amino acid that humans cannot make. It has to come from food, and mushrooms are by far the richest dietary source.
That transporter, formally SLC22A4, is what makes ergothioneine biologically interesting.[2] It is also what gets the compound into the brain: mice lacking the Octn1 gene have no detectable ergothioneine in brain tissue at all, because the transporter is what carries it into neurons, neural stem cells, and microglia.[3] A compound that reaches the central nervous system through a dedicated route is at least mechanically capable of acting on cells there, which is more than can be said for most nutraceuticals.
Human observational work adds a second thread. In frail elderly people, ergothioneine levels correlate with cognitive decline, and in patients with dementia, including Alzheimer's with hippocampal atrophy, declining ergothioneine tracks with deteriorating cognitive ability.[4] Barry Halliwell and colleagues have built on findings like these to propose that low body ergothioneine predisposes people to neurodegenerative disease, and that the compound deserves consideration as a "neuroprotective vitamin."[5] That proposal is explicitly framed by its authors as a hypothesis supported by circumstantial evidence, not a demonstrated causal chain. Correlation between low ergothioneine and cognitive decline is equally consistent with illness lowering ergothioneine as with low ergothioneine driving illness.
In human cells, the picture is more concrete. Ergothioneine protected iPSC-derived dopaminergic neurons and SH-SY5Y cells against a neurotoxin that damages mitochondria, preserving mitochondrial membrane potential and ATP levels while reducing mitochondrial reactive oxygen species.[6] These are human neurons, which matters — but they are dopaminergic neurons in a dish, modeling Parkinson's disease, not motor neurons in a body.
Then there is the study that makes ergothioneine directly relevant here.
Cadile et al. (2025) · FEBS Letters
- Population
- SMNΔ7 mice, a genetic model of spinal muscular atrophy — a disease defined by loss of spinal motor neurons
- Intervention
- Ergothioneine, 20 µg/day in the mothers' drinking water during pregnancy and lactation
- Comparator
- Untreated SMA littermates
- Finding
- Treated SMA mice survived approximately 30% longer than untreated siblings, with improved growth and motor performance at postnatal day 11. In isolated diaphragm muscle, ergothioneine stimulated mitophagy and increased NRF2 and GPX expression, with no change in SOD1 or catalase.
preliminary Animal model of SMA, not ALS. Mechanistic work was done in skeletal muscle, not motor neurons. The authors note the antioxidant enzyme data rest on a very small number of animals and 'deserve to be confirmed.'
Cadile et al., FEBS Letters, 2025
The survival result is real and worth taking seriously. What it is not is a demonstration that ergothioneine protects motor neurons, and the difference is easy to lose.
Anatomy of the 30% Figure · Cadile 2025
The Survival Was Whole-Animal. The Mechanism Was Muscle. The Motor Neurons Were Never Measured.
The headline result is real: ergothioneine-treated mice with spinal muscular atrophy lived about 30% longer. But the study measured three different things in three different places, and only two of them were measured at all. The mechanistic work — mitophagy, NRF2, GPX — was done in diaphragm muscle, not in the spinal motor neurons whose loss defines the disease. That step is an inference the paper does not make.
Whole animal
Measured- What was assayed
- Survival and locomotor performance
- Result
- ERGO-treated SMA mice survived ~30% longer than untreated SMA siblings; improved growth and motor performance at postnatal day 11
Diaphragm (skeletal muscle)
Measured- What was assayed
- Mitophagy, antioxidant enzymes, mitochondrial ultrastructure
- Result
- ERGO stimulated mitophagy; increased NRF2 and GPX expression (no change in SOD1 or catalase)
Spinal motor neurons
Not measured- What was assayed
- Nothing — not assayed in this study
- Result
- No motor neuron counts, no motor neuron mitophagy, no motor neuron survival data
Conditions usually left out of the retelling
- Dosing was prenatal and lactational. 20 µg/day of ergothioneine was given in the mothers’ drinking water during pregnancy and while nursing — not to symptomatic adults.
- The model is SMA, not ALS. SMNΔ7 mice model spinal muscular atrophy, a genetic motor neuron disease with a different cause than ALS.
- The authors flag their own sample size. On the antioxidant enzyme data they write that the results are “based on a very small number of animals and therefore deserve to be confirmed.”
None of this makes the finding unimportant — a 30% survival extension in a fatal motor neuron disease model is a genuine result worth following up. It makes the finding specific. What was demonstrated is that ergothioneine, given before and after birth, extended life and improved muscle mitochondrial handling in one mouse model of one motor neuron disease.
All cells from Cadile et al. 2025, FEBS Letters [1]
It is also worth being clear about the disease. Spinal muscular atrophy and ALS both destroy lower motor neurons, which is why SMA is the closest available model. But SMA is caused by a specific inherited deficiency in the SMN1 gene, while the large majority of ALS cases are sporadic and involve TDP-43 pathology that SMA does not share. Shared cell type is a real point of contact. Shared cause is not.
Erinacines: What Lion's Mane Mycelium Actually Does to Neurotrophins
Lion's mane (Hericium erinaceus) contains two distinct groups of active compounds in different parts of the organism, and the distinction matters commercially as well as biologically.
A 2025 systematic review by Spangenberg and colleagues assembled the preclinical evidence for erinacines across cell and rodent models.[7] Its findings are genuinely encouraging in their own domain: erinacines produced dose-dependent benefits in motor, cognitive, and depression-like behaviours in animals; erinacines A and C uniquely drove accumulation of Nrf2, the master regulator of antioxidant response; and the compounds showed anti-inflammatory activity, enhanced neurogenesis, and improved cell survival. The review also notes that some erinacines and hericenones cross the blood-brain barrier by passive diffusion, which is a meaningful hurdle cleared — many compounds that look good in cell culture never reach the central nervous system in a living animal.
On neurotrophins specifically, the evidence is narrower than it is usually described. What the review documents is that hericenones A–H and erinacines A–C, H, and I stimulate synthesis of NGF in vitro. BDNF evidence exists but is thinner: individual studies collected in the review report erinacine C enhancing NGF and BDNF expression in glial cells, and an erinacine A-enriched mycelium extract raising BDNF in a restraint-stress model of depression. Neurotrophin-3 appears exactly once in the review, in the background passage defining what the neurotrophin family is and does — no erinacine study within the review measured NT-3 at all.
This matters because the claim that erinacines "activate NGF, BDNF, and neurotrophin-3 to support motor neuron survival" is a composite that no single source supports. NGF stimulation is well evidenced. BDNF is suggestive. NT-3 is a definition that migrated into a finding.
The honest boundary is broader still. The Spangenberg review contains no studies in ALS models, and no studies in motor neurons of any kind — the words "motor neuron," "ALS," and "amyotrophic" do not appear in it. Its evidence comes from models of Alzheimer's, Parkinson's, depression, and nerve injury. Neurotrophin biology gives a plausible reason to think motor neurons might benefit, since spinal motor neurons do depend on neurotrophic signalling for survival. But plausibility is where this ends.
For readers specifically interested in how erinacines interact with BDNF signalling, how lion's mane affects BDNF and what that means covers that mechanism in depth.
Cordycepin: Neuroprotective Evidence From a Different Neuron and a Different Disease
Cordycepin is the primary bioactive compound in Cordyceps militaris. Its neuroprotective evidence base comes from Parkinson's disease research, and the overlap with ALS is mechanistic rather than direct.
Zhang and colleagues tested cordycepin in a rotenone-induced model of Parkinson's disease in rats and in cultured PC12 cells.[8] Cordycepin reduced both motor dysfunction and dopaminergic neuron loss. The mechanism the authors identified was specific: cordycepin reversed Drp1-driven mitochondrial fragmentation by increasing AMPK phosphorylation, raised ATP content and mitochondrial membrane potential, lowered mitochondrial reactive oxygen species, and suppressed NLRP3 inflammasome activation along with the pro-inflammatory cytokines it releases.
Those processes — mitochondrial fragmentation and inflammasome-driven neuroinflammation — are active in ALS motor neuron degeneration too, which is the source of the interest. But this study did not test anti-apoptotic mechanisms, despite that claim frequently being attached to it, and dopaminergic neurons in the substantia nigra are a different cell population from spinal motor neurons, with different vulnerabilities and different molecular drivers. Cordycepin's performance here is a mechanism argument for ALS relevance, not evidence of an effect on motor neurons.
For readers interested in how cordycepin and other mushroom compounds relate to Parkinson's research specifically, mushrooms and Parkinson's disease neuroprotective research covers that evidence base in full.
Claim Provenance Audit · Three Compounds
What Gets Repeated, and What the Cited Paper Actually Reports
Each compound below has a real published result behind it. In each case the version that circulates has drifted — a mechanism measured in muscle becomes a mechanism in neurons, a background definition becomes a finding, a pathway from a different paper gets folded in. The drift is small each time and large by the end.
Ergothioneine
Source: Cadile 2025 [1]
Claim in circulation
“Ergothioneine protects motor neurons and extends survival by 30%.”
What the paper reports
Survival extended ~30% in SMNΔ7 mice given ergothioneine prenatally and during lactation. Mitophagy, NRF2 and GPX increases were measured in diaphragm muscle — motor neurons were not assayed.
- System tested
- SMA mouse (SMNΔ7), maternal dosing
- Reach toward ALS
- Closest available model. Not ALS.
Erinacines
Source: Spangenberg 2025 [7]
Claim in circulation
“Erinacines activate NGF, BDNF and neurotrophin-3 to keep motor neurons alive.”
What the paper reports
NGF stimulation is well documented in vitro for erinacines A–C, H and I. BDNF increases appear in glial cell culture and one depression model. Neurotrophin-3 is named only in the review’s background description of the neurotrophin family — no erinacine study in the review measured NT-3.
- System tested
- Cell culture and rodent models of Alzheimer’s, Parkinson’s, depression, nerve injury
- Reach toward ALS
- Review contains no motor neuron or ALS studies at all.
Cordycepin
Source: Zhang 2021 [8]
Claim in circulation
“Cordycepin protects neurons through anti-inflammatory, antioxidant and anti-apoptotic action.”
What the paper reports
Cordycepin reduced motor dysfunction and dopaminergic neuron loss in rotenone-treated rats and PC12 cells, by blocking Drp1-driven mitochondrial fragmentation (via AMPK) and suppressing NLRP3 inflammasome activation. Anti-apoptotic action is not what this paper tested.
- System tested
- Rotenone Parkinson’s model (rat + PC12 cells)
- Reach toward ALS
- Different neuron type, different disease.
The right column is not a debunking. Every one of these papers is a legitimate result, and two of the three were published by groups actively working on neurodegeneration. The point is that the distance between “this happened in a diaphragm” and “this protects your motor neurons” is exactly the distance nobody has yet crossed experimentally.
Cells verified against primary text of refs [1][7][8]
A claim worth correcting
Does any mushroom compound have evidence for treating ALS?
The claim
“Lion's mane and other medicinal mushrooms have research showing they protect motor neurons and may slow ALS.”
Real preclinical findings in adjacent conditions get restated without their model — an SMA mouse becomes 'motor neuron disease,' a Parkinson's cell line becomes 'neurons,' and a mechanism measured in muscle becomes a mechanism in the spinal cord.
What research shows
UnsupportedNo mushroom compound has been tested in an ALS cell model, an ALS animal model, or a person with ALS. Every result in this article was produced in a different disease model, a different cell type, or a different tissue than the one ALS destroys.
This is not a finding that mushrooms fail in ALS — that experiment has not been run either. It is an absence of evidence in both directions, which is a reason for research interest and a reason not to make treatment decisions on it.
Cadile 2025; Spangenberg 2025; Zhang 2021
- Cell & Lab Studiescompleted
Erinacines stimulate NGF in vitro; ergothioneine protects human iPSC-derived dopaminergic neurons against mitochondrial toxins; cordycepin acts on Drp1 and NLRP3 in PC12 cells — all in non-ALS systems
- Animal Studiescurrent
Ergothioneine in an SMA mouse model (Cadile 2025) and cordycepin in a rotenone Parkinson's model (Zhang 2021). Zero studies in ALS animal models such as SOD1-G93A, TDP-43, or C9orf72
- Case Reports & Early Seriesmissing
No published reports of any mushroom compound used in people with ALS
- Small Human Trialsmissing
No human trial of any mushroom compound in ALS
- Large Randomized Trialsmissing
None
- Meta-Analyses & Systematic Reviewsmissing
No ALS-specific evidence exists to synthesize
For ALS specifically, no rung has been climbed. The 'current' marker reflects animal data in related diseases — SMA and Parkinson's — not ALS. The ALS-specific evidence base is empty at every level of this ladder.
Cadile 2025; Spangenberg 2025; Zhang 2021; Leow 2024
Why ALS-Specific Research Hasn't Happened (and What Would Change It)
Given a mechanistic rationale spanning three compounds, the absence of ALS-specific studies is worth explaining rather than leaving as a shrug.
ALS is comparatively rare — roughly 30,000 people in the United States are living with it at any given time — which reduces the commercial return on any investment. The treatment landscape reflects that. Riluzole, approved in 1995, extends survival by a matter of months on average; edaravone, approved more recently, was licensed primarily on evidence of slowing functional decline in a selected patient subgroup rather than on a clear survival benefit. Three decades of pharmaceutical development have not produced much more than that.
Mushroom compounds also face a structural problem: they are unpatentable. Ergothioneine, erinacines, and cordycepin cannot be owned the way a novel synthetic molecule can, and the economics of a registration trial assume patent protection to recover development costs that run into the hundreds of millions. Natural compounds hit that wall regardless of how promising their mechanisms look.
Academic research does not face the same barrier, which is what makes the gap notable. The SMA study that produced the 30% survival result was academic work. Testing ergothioneine in an established ALS mouse model — SOD1-G93A or a TDP-43 transgenic line — is the direct next step from that result, and it is an ordinary, fundable experiment. Testing erinacines in ALS-patient-derived motor neurons would cost a fraction of any clinical trial. Neither has been done. That is a statement about research priorities and funding, not about whether the mechanisms are real.
Dietary Sources: What Is Actually Available
For the compounds with published data, dietary exposure is straightforward, with one caveat about the numbers.
Ergothioneine content varies substantially between mushroom species. Oyster and king oyster mushrooms are consistently reported among the richest widely available sources, with porcini also high and shiitake contributing meaningful amounts; white button and portobello mushrooms contain ergothioneine at lower concentrations. The caveat is that reported values are method-dependent — work comparing UV-visible spectrometry against liquid chromatography-mass spectrometry found that substrate-based interferences can distort ergothioneine quantification, which is part of why published species rankings do not always agree.[9] Treat specific milligram figures you see quoted as approximate. Ergothioneine is heat-stable, so cooking does not meaningfully destroy it.
Erinacines are found in lion's mane mycelium specifically, not the fruiting body, so extracts labelled "mycelium" are the relevant product category; quality and erinacine content vary widely across the supplement market. Lion's mane is also perfectly good to eat as a culinary mushroom. Cordycepin comes from Cordyceps militaris, which is commercially cultivated and sold mainly as a supplement.
Eating these mushrooms is a reasonable thing to do. They are foods with a good safety record and genuine nutritional value. What eating them is not is a treatment.
If ALS is the reason you are reading this
CriticalMushroom compounds are not a treatment for ALS, and supplements can interact with care
Concern
No mushroom compound has been tested in anyone with ALS. Substituting supplements for prescribed therapy, or delaying specialist referral while trying them, carries real cost in a disease where timing matters. High-dose concentrated extracts are also a different exposure than eating mushrooms, and supplement quality is inconsistent — content frequently does not match the label.
What the research says
Treat culinary mushrooms as food, which they are. Discuss any concentrated extract or supplement with the neurologist or ALS clinic team managing care before starting it, particularly alongside riluzole or edaravone, and mention it at every medication review.
Particularly relevant for: People with ALS or other motor neuron disease, and their caregivers
What to do
Bring the specific product and its label to your next clinic appointment rather than starting it and reporting later.
Evidence base reviewed in this article; no ALS-specific safety or efficacy data exists
This article is educational and is not medical advice. Nothing here should be used to make decisions about treating ALS or any other condition; those decisions belong with a qualified clinician who knows the individual case.
For the overview of how ALS-specific evidence fits within the broader mushrooms-and-neurodegeneration picture, mushrooms and ALS, the full neuroprotective research landscape covers the wider context, including what the ALS medical community has concluded about lion's mane specifically. For the mechanistic deep dive, mushroom neuroprotection targeting motor neuron degeneration maps pathological mechanisms against the compounds that address them. And for the parallel story in Parkinson's disease, ergothioneine, dopaminergic protection, and Parkinson's covers those findings.
The Bottom Line
Three mushroom compounds have data touching motor neuron biology. Ergothioneine extended survival about 30% in a spinal muscular atrophy mouse model, though dosing was prenatal and the mechanistic work was done in diaphragm muscle rather than motor neurons. Erinacines from lion's mane mycelium stimulate NGF with more limited BDNF evidence, in a literature containing no motor neuron studies. Cordycepin reduced dopaminergic neuron loss in a Parkinson's model through mitochondrial and inflammasome pathways shared with ALS. None has been tested in ALS — not in cells, not in animals, not in people. The mechanistic case for running those experiments is genuine, and eating mushrooms is a safe thing to do for its own reasons. Neither of those facts amounts to evidence of benefit in ALS.
Frequently Asked Questions
Sources & References
- 1RTHM-02062·Cadile, Francesca et al. (2025). “Ergothioneine supplementation improves pup phenotype and survival in a murine model of spinal muscular atrophy..” FEBS letters.Study breakdown →PubMed →↩
- 2RTHM-00154·Gründemann, Dirk et al. (2005). “Discovery of the ergothioneine transporter..” Proceedings of the National Academy of Sciences of the United States of America.Study breakdown →PubMed →↩
- 3RTHM-01544·Ishimoto, Takahiro et al. (2022). “Ergothioneine in the brain..” FEBS letters.Study breakdown →PubMed →↩
- 4RTHM-01553·Kondoh, Hiroshi et al. (2022). “Decline of ergothioneine in frailty and cognition impairment..” FEBS letters.Study breakdown →PubMed →↩
- 5RTHM-01898·Halliwell, Barry et al. (2024). “Are age-related neurodegenerative diseases caused by a lack of the diet-derived compound ergothioneine?.” Free radical biology & medicine.Study breakdown →PubMed →↩
- 6RTHM-01925·Leow, Damien Meng-Kiat et al. (2024). “Ergothioneine-Mediated Neuroprotection of Human iPSC-Derived Dopaminergic Neurons..” Antioxidants (Basel.Study breakdown →PubMed →↩
- 7RTHM-02184·Spangenberg, E T et al. (2025). “Unveiling the role of erinacines in the neuroprotective effects of Hericium erinaceus: a systematic review in preclinical models..” Frontiers in pharmacology.Study breakdown →PubMed →↩
- 8RTHM-00735·Zhang, Xiao-Ling et al. (2021). “Anti-inflammatory and neuroprotective effects of natural cordycepin in rotenone-induced PD models through inhibiting Drp1-mediated mitochondrial fission..” Neurotoxicology.Study breakdown →PubMed →↩
- 9RTHM-00725·Tsiantas, Konstantinos et al. (2021). “On the Identification and Quantification of Ergothioneine and Lovastatin in Various Mushroom Species: Assets and Challenges of Different Analytical Approaches..” Molecules (Basel.Study breakdown →PubMed →↩