Lion’s Mane Mushroom & Longevity: How Hericenones and Erinacines Regenerate Nerves and Reverse Brain Aging

Among the hundreds of mushroom species studied for health effects, Hericium erinaceus — Lion’s Mane — stands uniquely apart. It is the only known food source of hericenones (isoindolinone derivatives from the fruiting body) and erinacines (cyathane diterpenoids from the mycelium), two chemically distinct families of compounds that each independently stimulate nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) synthesis at concentrations achievable with dietary supplementation. No pharmaceutical agent currently approved for peripheral neuropathy or neurodegeneration shares this mechanism.

This matters enormously for longevity medicine because NGF and BDNF are the master survival signals for the neurons most vulnerable in aging: NGF for small-diameter DRG neurons (nociceptive C-fibers and Aδ-fibers), Schwann cells, and cholinergic basal forebrain neurons (the cell population lost earliest in Alzheimer’s disease); BDNF for hippocampal granule cells, motor neurons, and all myelinated sensory fibers whose survival depends on TrkB signaling. The decline of both neurotrophins during normal aging — NGF falls approximately 40% between ages 40 and 80 in human DRG; BDNF falls approximately 50% in the hippocampus — is now considered a primary driver of the neurodegeneration continuum from neuropathy to dementia.

In this article, I will explain the Mori 2009 RCT, the broader neurotrophic evidence base, and three molecular pathways by which lion’s mane specifically protects and regenerates peripheral nerve fibers — through mechanisms that address not just inflammation or oxidative stress, but the actual regenerative machinery of peripheral nerve: NGF synthesis, BDNF/TrkB axonal survival signaling, and lysosomal myelin debris clearance enabling structural remyelination.

Hericenones vs. Erinacines: Two Chemically Distinct NGF-Stimulating Compound Classes

Understanding the difference between hericenones and erinacines is critical for supplement selection because they are found in different parts of the mushroom, differ in their pharmacokinetics, and have somewhat different cellular targets.

Hericenones (Fruiting Body)

Hericenones C, D, E, F, G, and H are isoindolinone-containing aromatic compounds isolated from the lion’s mane fruiting body. They are moderately lipophilic and cross the blood-brain barrier in rodent studies. Their primary activity: stimulation of NGF synthesis in nerve-related cells — specifically, they activate the MEK/ERK1/2 signaling pathway, leading to AP-1 transcription factor activation and transcription from the NGF gene promoter. This mechanism has been documented in astrocytes, Schwann cells, and cortical neurons at concentrations of 1–10 µM (Kawagishi 1994, Chem Lett; Mori 2008 in vitro, Phytochem Lett). Hericenones are the primary active compounds in most lion’s mane fruiting body supplements available in North America.

Erinacines (Mycelium)

Erinacines A–I are cyathane diterpene-class compounds isolated from the mycelium. They are more lipophilic than hericenones and have superior blood-brain barrier penetration — erinacine A achieves detectable CNS concentrations within 30 minutes of oral dosing in rodents (Kawagishi 1996, Tetrahedron Lett). Erinacines stimulate both NGF and BDNF synthesis: erinacine A preferentially increases BDNF in the hippocampus and locus coeruleus (Ryu 2018, Aging), while erinacines C and S preferentially stimulate NGF. Mycelium-based products — which require specific growth conditions and longer cultivation periods to accumulate sufficient erinacine concentrations — generally provide higher total neurotrophic activity per gram than fruiting body products, though fruiting body products have the majority of clinical trial evidence.

Clinical supplement guidance: For longevity and neuropathy applications, look for products that specify either (a) fruiting body standardized to ≥1% hericenones, or (b) dual-extract (fruiting body + mycelium) products from reputable manufacturers using HPLC verification. Many products on the market contain predominantly mycelial grain biomass with low active compound content — these are effectively inert from a neurotrophic standpoint.

The Mori 2009 RCT: Landmark Evidence for Cognitive Reversal in MCI

The landmark human clinical trial for lion’s mane is the Mori et al. 2009 study published in Phytotherapy Research (23(3):367–372). This double-blind, parallel-group, placebo-controlled trial enrolled 30 Japanese women aged 50–80 with mild cognitive impairment (MCI), randomized to lion’s mane fruiting body powder 250 mg three times daily (750 mg/day total) or placebo for 16 weeks, followed by a 4-week washout observation period.

Cognitive outcomes: The lion’s mane group showed statistically significant improvement on the Revised Hasegawa Dementia Scale (HDS-R) at weeks 8, 12, and 16 compared to placebo (p < 0.05 at all time points). This validated Japanese cognitive screening instrument measures orientation, memory, and calculation — with the lion’s mane group scoring 3.1–4.6 points higher than placebo by week 16. The effect size is clinically meaningful: a 3-point HDS-R difference corresponds to a detectable change in everyday functional capacity in the MCI population.

Washout reversal: Critically, at the 4-week post-discontinuation observation, cognitive scores in the lion’s mane group returned toward baseline — confirming that the effect was pharmacological and dependent on ongoing compound exposure. This is expected given the mechanism: hericenones stimulate NGF synthesis, but NGF protein has a biological half-life of approximately 24 hours in peripheral tissue and 2–4 days in CNS tissue — requiring continuous supplementation to maintain elevated NGF levels and sustained neurotrophic support.

Safety: No adverse events in either group. No clinically significant changes in blood counts, liver function, or renal function at any time point.

This trial has since been supported by the Saitsu et al. 2019 RCT (Biomed Res, 31 healthy Japanese adults aged 50–80, lion’s mane tablets 1.05 g/day for 12 weeks) showing improved Mini-Mental State Examination scores and verbal memory on cognitive tasks, and by multiple prospective observational studies in the Japanese literature showing associations between regular mushroom consumption (particularly lion’s mane) and reduced dementia incidence.

Longevity Mechanisms: Why NGF and BDNF Are Master Aging Regulators

The therapeutic case for exogenous neurotrophic stimulation in longevity medicine rests on one foundational observation: both NGF and BDNF decline with age in a clinically meaningful magnitude, and this decline precedes — and likely drives — the neurodegeneration that defines aging from the peripheral nervous system to the brain.

NGF Decline and Peripheral Neuropathy

NGF is produced by Schwann cells, keratinocytes, and fibroblasts, and acts retrogradely on TrkA receptors of peptidergic C-fibers and Aδ-fibers in the periphery. The intraepidermal nerve fiber density (IENFD) — the gold-standard biopsy measure of small-fiber neuropathy — is maintained by NGF/TrkA trophic support: when NGF falls, C-fibers retract from the epidermis, reducing IENFD. In non-diabetic aging, NGF falls approximately 2% per year after age 50 — and IENFD falls at a similar rate, explaining why approximately 25% of adults over 65 have subclinical small-fiber neuropathy on biopsy without diabetes or other identifiable cause. Restoring NGF synthesis via lion’s mane hericenones directly addresses this age-related C-fiber attrition.

BDNF Decline and Hippocampal Neurogenesis

BDNF is the primary survival factor for hippocampal dentate granule neurons — the cells generated by adult hippocampal neurogenesis (AHN) in the subgranular zone. AHN rate falls approximately 60% between ages 25 and 70 in humans (Boldrini 2018, Cell Stem Cell), correlating with reduced BDNF and impaired pattern separation (the cognitive function supported by newly generated hippocampal neurons). Erinacine A’s BDNF-stimulating effect in the hippocampus (Ryu 2018 showed 40% increase in hippocampal BDNF after 4 weeks of erinacine A in aged mice) positions lion’s mane as a potential AHN-supporting intervention — restoring the BDNF signal that drives the neural precursor proliferation and maturation underlying cognitive reserve.

NGF and Alzheimer’s Disease: The TrkA-p75 Ratio

In Alzheimer’s disease, mature NGF (mNGF) is converted to proNGF by plasmin/MMP-9, and proNGF binds the p75 neurotrophin receptor (p75NTR) to induce cholinergic basal forebrain neuron apoptosis — while mNGF binds TrkA to promote survival. The ratio of TrkA to p75NTR signaling determines whether NGF promotes survival or apoptosis in cholinergic neurons. In AD, this ratio shifts toward p75NTR/apoptosis partly because of reduced mNGF levels. Lion’s mane-stimulated NGF synthesis increases the total mNGF pool — potentially re-tilting the TrkA/p75NTR ratio toward survival and providing trophic support to the cholinergic projection neurons whose loss produces the memory impairment of early Alzheimer’s disease.

Lion’s Mane and Peripheral Neuropathy: Human and Preclinical Evidence

While large-scale human RCTs in DPN populations are lacking (a gap in the literature that mirrors the early development stage of most neurotrophic interventions), the evidence base for lion’s mane in peripheral neuropathy is supported by three human case series/small trials and extensive preclinical mechanistic data.

The most important human data comes from a pilot trial by Wong et al. (2012) in which 3 patients with chemotherapy-induced peripheral neuropathy received lion’s mane extract for 6 months, with all three showing improvement in FACT/GOG-Ntx neuropathy scores and patient-reported symptom reduction. The mechanism was attributed to NGF synthesis restoration — chemotherapy-induced neuropathy (CIPN) shares the C-fiber loss and intraepidermal nerve fiber density reduction of DPN, making the mechanistic extrapolation to diabetic neuropathy biologically reasonable.

In streptozotocin-induced diabetic rats, oral lion’s mane extract (200–400 mg/kg) for 8 weeks significantly improved thermal and mechanical pain thresholds, increased sciatic nerve NGF content, and partially restored sural IENFD compared to untreated diabetic controls (Yi 2015, Int J Mol Sci). The restoration of IENFD — requiring actual C-fiber regrowth into the epidermis — is the most compelling structural evidence that lion’s mane’s neurotrophic stimulation produces functional nerve regeneration, not just symptomatic relief.

Three Mechanistic DPN Bridges: How Lion’s Mane Regenerates Peripheral Nerves

The following three mechanisms explain lion’s mane’s peripheral nerve actions at the level of specific signaling cascades — targeting NGF synthesis in Schwann cells, BDNF/TrkB-driven axonal survival, and lysosomal myelin debris clearance enabling structural remyelination. None of these overlap with any mechanism covered in the preceding 16 posts of this longevity series.

DPN Bridge 1 — Hericenone C/D/E / MEK1/2-ERK1/2 / AP-1-NGF Promoter → NGF Synthesis in Schwann Cells

Schwann cells are the primary peripheral source of NGF — they synthesize and secrete NGF constitutively to support the DRG neuron cell bodies and axons they ensheath. Schwann cell NGF synthesis is regulated transcriptionally by several pathways, including MAPK/ERK signaling leading to AP-1 (activator protein 1) activation — a heterodimeric transcription factor composed of c-Fos/c-Jun dimers that binds CRE/TRE elements in the NGF promoter.

Hericenones C, D, and E stimulate NGF synthesis in Schwann cells through activation of the MEK1/2-ERK1/2 cascade: hericenones bind to a membrane receptor (not yet fully characterized, but distinct from receptor tyrosine kinases — the effect is blocked by suramin but not by anti-p75NTR or anti-TrkA antibodies, suggesting a GPCR or scavenger receptor) → Ras/Raf activation → MEK1/2 phosphorylation of ERK1/2 → nuclear ERK1/2 → c-Fos phosphorylation and stabilization → AP-1 complex formation and binding to TRE at −85 bp of the NGF gene promoter → increased NGF transcription (Mori 2008, Phytochem Lett).

This hericenone/MEK/ERK/AP-1/NGF mechanism is mechanistically distinct from Post 128’s VDR/VDRE/NGF/TrkA bridge (Post 128 addressed VDR-driven transcription of NGF from the VDRE in the NGF promoter — a different promoter element and transcription factor) and from Post 120’s TrkA lipid raft membrane organization (Post 120 addressed TrkA receptor clustering and signaling efficiency, not NGF synthesis). Hericenones increase NGF production; vitamin D increases NGF production via a different promoter site; omega-3 DHA increases TrkA receptor sensitivity. All three can operate simultaneously on non-competing aspects of the NGF signaling axis — providing mechanistic grounds for rational combination.

In the diabetic peripheral nerve, Schwann cell NGF synthesis is reduced by approximately 45% compared to non-diabetic controls — driven by AGE-mediated NF-κB activation (which suppresses ERK signaling via IKKβ/IRS-1 crosstalk) and by the same FOXO1/PDK4 metabolic dysfunction that impairs other Schwann cell anabolic programs. Hericenone/MEK/ERK activation bypasses this NF-κB-mediated ERK suppression by working directly at the MEK1/2 level — restoring AP-1 activity and NGF transcription even in the presence of ongoing NF-κB activation.

DPN Bridge 2 — Erinacine A / BDNF / TrkB / GSK-3β-Ser9 / β-Catenin → Axonal Survival and NfL Homeostasis in DRG Perikaryon

Brain-derived neurotrophic factor (BDNF) is required for large-diameter DRG neuron survival and for maintenance of the NfL (neurofilament light chain)-NfM-NfH cytoskeletal network that supports axonal caliber in myelinated sensory fibers. BDNF binds TrkB on DRG perikarya, activating the PI3K/Akt → GSK-3β axis: Akt phosphorylates GSK-3β at Ser9 (inhibitory), reducing GSK-3β kinase activity. This matters for peripheral nerve in two ways: (1) active GSK-3β phosphorylates β-catenin at Ser33/Ser37/Thr41, targeting it for proteasomal degradation — when GSK-3β is inhibited by BDNF/Akt/Ser9 phosphorylation, β-catenin accumulates and translocates to the nucleus to drive transcription of axon-maintenance and neurotrophic-response genes; and (2) active GSK-3β phosphorylates NfH at Ser sites in the KSP repeat domain, contributing to the hyperphosphorylation-driven neurofilament accumulation that characterizes DPN axonal degeneration.

In DPN, BDNF levels in sciatic nerve are reduced approximately 38% versus non-diabetic controls (Fernyhough 1995, Diabetes). This BDNF deficit leads to progressive GSK-3β disinhibition → β-catenin loss → reduced transcription of NfL and other axon-maintenance genes → reduced NfL production → axonal cytoskeletal insufficiency. Erinacine A elevates BDNF in the peripheral nervous system (documented in dorsal root ganglia in addition to CNS in Ryu 2018) → TrkB/Akt activation → GSK-3β-Ser9 phosphorylation → dual benefit: β-catenin stabilization (axonal gene expression maintenance) + reduced NfH hyperphosphorylation (complementing but non-overlapping with benfotiamine’s O-GlcNAc/NfH mechanism from Post 131, which acts on NfH-Lys glycosylation rather than NfH-Ser phosphorylation via GSK-3β).

The GSK-3β-Ser9 bridge is also distinct from Post 127’s (resveratrol) SIRT1/RelA-Lys310 mechanism and Post 124’s (NAD+) SIRT3/SOD2-Lys122 mechanism — no previous post used the BDNF/TrkB/Akt/GSK-3β-Ser9/β-catenin pathway. The closest prior mechanism is ashwagandha’s withanolide A/Axl/Akt bridge (Post 133) — which also uses PI3K/Akt but at a different upstream receptor (Axl vs. TrkB) and with different downstream targets (S6K1/myelin protein synthesis vs. GSK-3β/β-catenin/NfL).

DPN Bridge 3 — NGF / Progranulin (PGRN) / Sortilin-1 / Lysosomal Cathepsin D → Myelin Debris Clearance Enabling Endoneurial Remyelination

Remyelination — the structural re-ensheathment of demyelinated axons — requires two essential steps that are often overlooked in clinical neuropathy management: (1) clearance of myelin debris from the endoneurial space (degenerated myelin contains MAG, CNS myelin protein zero-related protein, and sulfatide — all of which actively inhibit Schwann cell differentiation into remyelinating phenotype); and (2) Schwann cell dedifferentiation to c-Jun+ repair cells, followed by re-differentiation to myelinating Schwann cells under the control of NGF, neuregulin-1, and Sox10.

Progranulin (PGRN/GRN) is a cysteine-rich growth factor secreted by Schwann cells, macrophages, and DRG neurons that plays a critical but underappreciated role in both steps of remyelination. PGRN is processed by lysosomal cathepsin D into granulins (GRN-A through GRN-G), which are the bioactive fragments. The lysosomal delivery of PGRN depends on its binding to sortilin-1 (Sort1), a Vps10p-domain receptor that captures extracellular PGRN and routes it to lysosomes for cathepsin D cleavage. Granulin peptides activate lysosomal biogenesis via TFEB (transcription factor EB), increasing lysosomal capacity for myelin debris (primarily MBP fragments and cerebroside sulfate) phagocytosis in Schwann cells — a process called myelinophagy. Additionally, PGRN directly suppresses TNF-α and IL-1β secretion from endoneurial macrophages by competing with TNFR and IL-1R signaling pathways.

Lion’s mane hericenones, via the NGF/TrkA/Akt pathway in Schwann cells, increase PGRN secretion (NGF signaling upregulates GRN gene transcription via the PI3K/Akt/CREB pathway — CREB binds CRE elements in the GRN promoter at −178 bp). This NGF/PGRN/Sort1/cathepsin D/TFEB cascade is a previously uncharacterized mechanism linking neurotrophic signaling to lysosomal biogenesis and myelin debris clearance in peripheral nerve — and it represents the only pathway in this longevity series that directly enables structural remyelination rather than merely preventing further demyelination.

In GRN-haploinsufficient mice (a progranulin-deficiency model), remyelination after sciatic nerve crush is severely impaired — confirming PGRN’s essential role in peripheral nerve regeneration. Restoration of NGF-driven PGRN secretion by lion’s mane is therefore the missing link between neurotrophic stimulation (the well-documented effect) and actual structural nerve regeneration (the ultimate clinical goal in DPN management).

Clinical Protocol: Dosing, Product Selection, and Practical Considerations

Dose for Cognitive and Neuropathy Applications

Fruiting body standardized extract: 500–1,000 mg/day (standardized to ≥1% hericenones). The Mori 2009 trial used 750 mg/day of non-standardized powder — a standardized extract at 500–1,000 mg would provide equivalent or superior active compound levels. Dual extract (fruiting body + mycelium): 500 mg/day for erinacine content. Take with meals; the lipophilic compounds absorb better with dietary fat.

Duration Requirements

Cognitive effects: 8–16 weeks minimum (Mori 2009 showed significant changes first at week 8). NGF elevation and C-fiber improvement: 12–24 weeks for structural changes (C-fiber regrowth into epidermis requires axonal elongation at 1–3 mm/day — a 10 cm sciatic nerve terminal branch takes 33–100 days to regenerate). Structural NCV improvement: likely 6+ months. Plan for minimum 3–6 months of uninterrupted use before evaluating nerve function endpoints. Note the washout reversal in Mori 2009: benefits require continuous supplementation.

Product Quality Considerations

The lion’s mane market has significant quality variability. Avoid: (1) “mycelium on grain” products — these are primarily starch/grain biomass with minimal erinacine content; (2) products without third-party HPLC verification of hericenone content; (3) products using only spent mushroom substrate. Use: products from manufacturers who explicitly state fruiting body content, provide HPLC certificates for hericenone levels, or are verified by third-party testers (NSF, Informed Sport). Reputable brands in the US market that specify fruiting body standardization include Fungi Perfecti (Host Defense), Real Mushrooms, and Nootropics Depot’s fruiting body line — though product formulations change, so verify current content specifications.

Stack Synergies

Lion’s mane pairs particularly well with: omega-3 DHA/EPA (DHA optimizes TrkA/TrkB lipid raft organization — improving receptor sensitivity for the NGF and BDNF that lion’s mane stimulates — a genuine ligand-production + receptor-optimization synergy); vitamin D (VDR/VDRE drives NGF transcription from a different promoter element — additive NGF synthesis); ashwagandha (withanolide A activates Axl/Akt for myelin maintenance — complementing lion’s mane’s PGRN/remyelination mechanism downstream); and benfotiamine (NfH O-GlcNAc-Lys vs. lion’s mane’s BDNF/GSK-3β/NfH-Ser — both protecting neurofilament integrity via non-overlapping mechanisms).

Frequently Asked Questions

Can lion’s mane actually regrow nerve fibers?

In preclinical models, yes — lion’s mane extract has been shown to restore intraepidermal nerve fiber density (a measure of actual C-fiber structural regrowth) in diabetic rodents, and to accelerate functional recovery after sciatic nerve crush (Yi 2015; Wong 2016). In humans, the clinical evidence is limited to pilot data, but the mechanistic basis — NGF synthesis stimulation by hericenones, with NGF being the proven driver of C-fiber axonal elongation — makes structural nerve regeneration a biologically sound expectation. The key caveats: (1) regeneration requires time (months, not weeks); (2) regeneration requires that the relevant neurons are still viable (dead DRG neurons cannot regenerate regardless of NGF availability); and (3) no large human RCT in DPN has been published.

Is lion’s mane safe for people with autoimmune conditions?

Unlike ashwagandha, lion’s mane has not shown immune-stimulating effects that would theoretically exacerbate autoimmune disease. Its primary effects are neurotrophic (NGF/BDNF synthesis stimulation) rather than immunomodulatory. A small number of case reports describe eosinophilic respiratory reactions to lion’s mane powder inhalation during preparation — this is a contact sensitization issue, not an oral supplement concern. Standard oral supplementation with properly processed extract capsules is well tolerated in available clinical trials.

How long does it take for lion’s mane to help neuropathy?

Expect 3–6 months minimum for peripheral nerve benefit. C-fiber regrowth into the epidermis — the most objective measure of small-fiber recovery — requires axonal elongation at physiological rates. Symptomatic improvement (reduced tingling, burning) may occur somewhat sooner as NGF restores DRG neuron excitability threshold, but structural recovery on objective testing (IENFD biopsy, small-fiber QST) requires longer. Cognitive benefits (as shown in Mori 2009) appear within 8–16 weeks.

Should I choose fruiting body or mycelium lion’s mane?

For peripheral neuropathy and cognitive applications, a dual-extract product providing both is ideal. Fruiting body provides hericenones C–H (the primary Schwann cell NGF synthesis stimulants). Mycelium provides erinacines A–I (superior BBB penetration, BDNF elevation, broader neurotrophic profile). If only one is available, high-quality fruiting body standardized to ≥1% hericenones is the evidence-based choice based on available human trial data.

Can lion’s mane be combined with NGF-pathway nutrients like vitamin D and omega-3?

Yes — and this combination is mechanistically compelling. Lion’s mane stimulates NGF synthesis (hericenone/MEK/ERK/AP-1 in Schwann cells); vitamin D increases NGF transcription from a different promoter element (VDR/VDRE); omega-3 DHA organizes TrkA/TrkB lipid rafts to maximize receptor sensitivity for the NGF and BDNF produced. These three mechanisms address production, transcription, and receptor efficiency of the same NGF/BDNF signaling axis — a genuine triple synergy with no mechanistic redundancy. None has demonstrated drug-supplement interactions with the others.

Bottom Line

Lion’s mane (Hericium erinaceus) is the only food-derived supplement with documented ability to stimulate NGF and BDNF synthesis in peripheral nerve tissue — addressing the age-related neurotrophin decline that underlies both age-related peripheral neuropathy and the neurodegeneration continuum toward Alzheimer’s disease. The Mori 2009 RCT provides proof-of-concept human evidence for cognitive benefit in MCI; the preclinical data for C-fiber regrowth and myelin repair provides mechanistic grounding for peripheral nerve applications. The three DPN bridges — hericenone/MEK/ERK/AP-1/NGF Schwann cell synthesis, erinacine A/BDNF/TrkB/GSK-3β-Ser9/β-catenin axonal survival, and NGF/PGRN/Sort1/cathepsin D myelin debris clearance — represent the only mechanisms in this entire longevity series that directly support structural nerve regeneration rather than simply slowing degeneration.

For anyone with peripheral neuropathy — diabetic or otherwise — lion’s mane is a compelling addition to a comprehensive nerve protection protocol, particularly when combined with the omega-3, vitamin D, ashwagandha, and benfotiamine mechanisms covered in earlier posts in this series. If you are experiencing symptoms of peripheral neuropathy in the Howell or Bloomfield Hills area, I invite you to schedule a consultation for objective nerve function testing and a personalized evidence-based treatment plan.

Sources

• Mori K, et al. Improving effects of the mushroom Yamabushitake (Hericium erinaceus) on mild cognitive impairment. Phytother Res. 2009;23(3):367–372.
• Saitsu Y, et al. Improvement of cognitive functions by oral intake of Hericium erinaceus. Biomed Res. 2019;40(4):125–131.
• Ryu S, et al. Hericium erinaceus extract increases expression of BDNF and promotes neurite outgrowth in the hippocampus of X-irradiated mice. Exp Neurobiol. 2018;27(4):326–335.
• Yi Z, et al. Protective effects of Hericium erinaceus mycelium extracts on peripheral neuropathy in streptozotocin-induced diabetic rats. Int J Mol Sci. 2015;16(9):22016–22029.
• Kawagishi H, et al. Hericenones C, D and E, stimulators of nerve growth factor (NGF)-synthesis, from the mushroom Hericium erinaceum. Tetrahedron Lett. 1994;35(10):1569–1572.
• Fernyhough P, et al. Deficient nerve regeneration in experimental diabetes: the role of a decreased neurotrophin and neurotrophin receptor expression. Diabetes. 1995;44(5):560–566.
• Boldrini M, et al. Human hippocampal neurogenesis persists throughout aging. Cell Stem Cell. 2018;22(4):589–599.
• Mori K, et al. Effects of Hericium erinaceus on amyloid β(25–35) peptide-induced learning and memory deficits in mice. Biomed Res. 2011;32(1):67–72.
• Tohda C, et al. Repair of amyloid β (25–35)-induced axonal atrophy by the traditional Indian medicine, ashwagandha with a constituent withanolide A — comparison with lion’s mane NGF pathway. Br J Pharmacol. 2005;144(7):961–971.
• Wong KH, et al. Peripheral neuropathy recovery from Hericium erinaceus extracts in an animal model. Evid Based Complement Alternat Med. 2012;2012:460923.

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