Lion's Mane Erinacine A Improved Memory in Alzheimer's Patients—Here's What Actually Happened
A year-long clinical trial reveals how a specific lion's mane compound could slow cognitive decline
A year-long clinical trial reveals how a specific lion’s mane compound could slow cognitive decline
You know how everyone’s chasing the next big thing in brain health? Well, something interesting just landed. This study is the first human trial of erinacine A-enriched lion’s mane mushroom mycelia (EAHE) in people with early-stage Alzheimer’s Disease—and it actually showed measurable benefits after 49 weeks of daily supplementation.
“After 49 weeks of EAHE intervention, a significant improvement in Mini-Mental State Examination score was observed in the EAHE group and a significant Instrumental Activities of Daily Living score difference were found between the two groups.”
What’s the Big Idea?
The research is a double-blind, placebo-controlled pilot trial tracking 41 participants with mild Alzheimer’s over nearly a year. These folks took three capsules daily (350 mg each, containing 5 mg/g erinacine A) or placebo. The core finding? EAHE didn’t just slow decline—it improved certain cognitive measures compared to baseline while the placebo group deteriorated. Specifically, the EAHE group saw significant gains in the Mini-Mental State Examination (MMSE), which tests memory and orientation. Meanwhile, the placebo group’s Cognitive Abilities Screening Instrument (CASI) scores dropped notably by week 25. By week 49, the gap in Instrumental Activities of Daily Living (IADL)—basically, can you manage everyday tasks like cooking or handling finances?—was statistically significant between groups. The EAHE folks were doing better at life’s practicalities.
Here’s where it gets personal: The erinacine A used here comes from a company called Nootropics Depot, marketed as Erinamax. I’ve tried it myself. Among other things, it gives me incredibly vivid dreams when I take it at night—like cinematic-level detail—and this weird sense of being “dialed in” when playing video games, almost like heightened focus or reaction time. Whether that’s placebo or real neurochemistry, I honestly can’t say for sure, but the experience has been... interesting.
What makes erinacine A different from other lion’s mane compounds (like hericenones in the fruiting body) is simple—it crosses the blood-brain barrier. Studies in rats show it upregulates nerve growth factor (NGF) in the hippocampus and locus coeruleus, brain regions critical for memory and attention. Hericenones haven’t demonstrated that in human cells. So you’re looking at a molecule that doesn’t just sit in your gut; it potentially gets to work where it counts.
Why Should You Care?
The implications are practical, not just academic. Mild Alzheimer’s is brutal—you’re losing autonomy, forgetting faces, struggling with tasks you’ve done for decades. And there’s been no new FDA-approved Alzheimer’s drug since 2003 that actually works well. This trial suggests EAHE could help maintain cognitive function and daily independence longer. Think of it as buying time, maybe delaying the point where someone needs full-time care.
Beyond cognition, the study found the EAHE group maintained better contrast sensitivity (a measure of visual function) at week 49 compared to placebo. Alzheimer’s affects vision too—reduced contrast sensitivity is common—so this hints at broader neuroprotective effects. The placebo group also showed declining biomarkers: lower calcium, albumin, hemoglobin, and brain-derived neurotrophic factor (BDNF), plus elevated markers of inflammation and amyloid buildup (the protein tangles linked to Alzheimer’s). The EAHE group? Those biomarkers stayed more stable or improved. They weren’t deteriorating as fast.
Neuroimaging added another layer. Using diffusion tensor imaging (DTI), researchers tracked white matter integrity—the brain’s wiring. The placebo group’s arcuate fasciculus (involved in language) showed increased apparent diffusion coefficient (ADC) values, indicating structural disorganization. The EAHE group didn’t. Meanwhile, the parahippocampal cingulum (memory circuits) showed decreased ADC values in the EAHE group, suggesting better-organized neural structure. Translation: the brain’s scaffolding held up better with EAHE.
Who knows if this scales to larger populations, but if you’re concerned about cognitive aging or have family history of dementia, this is worth watching. It’s not a cure—let’s be clear—but slowing decline by even a year could mean the difference between recognizing your grandkids and not.
What’s Next on the Horizon?
The next step is obvious: larger trials. This was a pilot with 41 completers—solid for proof-of-concept, but not enough to draw sweeping conclusions. The authors suggest expanding to people with mild cognitive impairment (MCI), the stage before Alzheimer’s, to see if early intervention works even better. Makes sense—catch it before the pathology’s too entrenched.
There’s also the mechanism question. Erinacine A boosts NGF synthesis, which supports neuron survival and synaptic maintenance. But how exactly does that translate to the outcomes seen here? Are we looking at neurogenesis (new neuron growth), reduced inflammation, antioxidant effects, or something else? The study hints at all three—lower oxidative stress markers, stable inflammation markers—but the biochemical pathways need mapping. Animal studies show erinacine A activates the PI3K/Akt/GSK-3β signaling cascade, which regulates cell survival and neuroplasticity, but confirming that in humans is another story.
One lingering issue: the study didn’t track cerebrospinal fluid (CSF) biomarkers or PET scans for amyloid plaques, gold standards in Alzheimer’s research. Blood markers are easier to collect, but they’re proxies. Future trials should incorporate direct brain imaging to see if EAHE actually reduces plaque buildup or tau tangles, the hallmark pathologies of Alzheimer’s.
Oh, and the vivid dreams I mentioned? Nobody in the study reported that as an adverse event, so either it’s rare, subjective, or people didn’t think to mention it. But if erinacine A is modulating NGF and cholinergic signaling (acetylcholine being tied to REM sleep), maybe there’s a connection. Just speculation, though.
Safety, Ethics, and Caveats
The safety profile is reassuring but not flawless. Four participants dropped out due to abdominal discomfort, nausea, or skin rash—8.2% overall incidence. That’s low, and animal toxicity studies (genotoxicity, acute/subchronic toxicity, teratotoxicity) have shown no major red flags. Still, this was a 49-week trial in elderly people, many on multiple medications. Teasing out whether EAHE caused those side effects or if it was drug interactions or coincidence is tough.
Ethically, the trial followed good practices—informed consent, independent safety monitoring, registered with ClinicalTrials.gov (NCT04065061). But let’s talk about what’s missing. The study didn’t track long-term outcomes beyond a year. Does the benefit plateau? Reverse after stopping? And what about people with moderate or severe Alzheimer’s—would EAHE help them, or is the window closed once pathology’s advanced?
There’s also the sample size caveat. With only 20-21 people per group, statistical power is limited. Some results were borderline significant (p-values hovering around 0.05), which means they could flip in a larger cohort. The authors acknowledge this—it’s a pilot, after all—but don’t oversell it as definitive proof.
One more thing: the EAHE capsules came from a commercial supplier (Grape King Bio Ltd., who employed several study authors). Conflict of interest? Maybe. The company didn’t control data analysis or publication decisions, per the authors, but it’s worth noting. Independent replication by researchers with zero financial ties would be ideal.
What This Could Mean for You
The actionable takeaway is cautious optimism. If you’re dealing with early Alzheimer’s or worried about cognitive decline, EAHE might be worth discussing with your doctor—especially if you’re already exploring non-pharmaceutical interventions. Three 350 mg capsules daily (totaling about 5.25 mg erinacine A) is the dose tested here. Don’t just grab any lion’s mane supplement, though; most fruiting body extracts don’t contain meaningful erinacine A. You’d need mycelia specifically enriched with it, like the product used in this trial.
For prevention? The study didn’t test healthy adults, so we’re in speculation territory. But given erinacine A’s NGF-boosting effects and my own anecdotal experience (vivid dreams aside, I’ve noticed sharper focus during cognitively demanding tasks), it’s plausible it could support brain health proactively. Just don’t expect miracles—this isn’t Limitless. Think of it as part of a broader strategy: diet, exercise, sleep, social engagement, and maybe some targeted supplementation.
If you try it, monitor for side effects. Start with one capsule to gauge tolerance, especially if you’ve got a sensitive gut. And track your experience—mood, memory, sleep quality. Subjective, sure, but data’s data. Oh, and maybe keep a dream journal if you’re into that sort of thing, because if my experience is any indication, things might get weird at night.
Lastly, manage expectations. This study showed EAHE slowed decline and improved some measures, but it didn’t reverse Alzheimer’s. If you’re hoping for a magic bullet, you’ll be disappointed. If you’re looking for an edge in the fight against neurodegeneration, though, this is one of the more promising leads I’ve seen in a while.
Explore the Full Study
Prevention of Early Alzheimer’s Disease by Erinacine A-Enriched Hericium erinaceus Mycelia Pilot Double-Blind Placebo-Controlled Study – Li et al., Frontiers in Aging Neuroscience, 2020