Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,991 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Tuesday, August 25, 2026
A Novel Curcumin-Based Formulation Offers Protection Against Neurodegeneration in Rat Models of AlCl3 Induced Alzheimer’s Disease
Tuesday, July 21, 2026
This Russian Peptide Regrew Brain Cells in Stroke Rats. The Human Data Is Thin But the Safety Record Spans 3 Decades
Three decades of incompetence in your doctor and hospital in not getting this to an interventional protocol! Aren't you glad of WORLD CLASS INCOMPETENCE in your facility?
Of course your competent? doctor already has EXACT PROTOCOLS that deliver all the BDNF you need. And has been for over a decade, right? But your doctor incompetently knew nothing and did nothing, right? Which means your board of directors is so incompetent they can't recognize incompetence in their staff!
- BDNF
(209 posts to April 2011)
This Russian Peptide Regrew Brain Cells in Stroke Rats. The Human Data Is Thin But the Safety Record Spans 3 Decades
The Air Force fed pilots “go pills”—pure dextroamphetamine—from Vietnam through Afghanistan, which may have contributed to a 2002 incident where two US pilots on Dexedrine accidentally bombed a Canadian unit.
The pattern never changes: every shortcut works, but every shortcut bills you—whether it’s your heart, sleep, or addiction risk.
Enter Soviet Neuroscience
Semax is a heptapeptide—seven amino acids strung together: methionine, glutamate, histidine, phenylalanine, proline, glycine, and proline.
Unlike other peptides extracted from animal tissue, Semax was designed on purpose by Soviet pharmacologists at Moscow’s Institute of Molecular Genetics starting in the 1980s.
Researchers started with a fragment of ACTH (adrenocorticotropic hormone), which normally tells adrenal glands to produce cortisol. A four-amino-acid fragment showed positive stress effects on brain function—think learning, attention, resistance to low oxygen—without hormonal downsides like muscle breakdown.
Scientists welded on a proline-glycine-proline tail to prevent enzymatic degradation, creating a brain-targeted stress hormone fragment with built-in stabilizer. A non-stimulant cognitive booster with no obvious addiction profile—exactly what everyone had been hunting for.
At roughly 814 daltons, Semax is relatively small (BPC-157 is about 1,419, semaglutide exceeds 4,000). Small enough that Russians believed nasal mucous membranes could deliver it directly to brain tissue—hence the nasal drop delivery method.
How Semax Actually Works
The headline mechanism involves BDNF—brain-derived neurotrophic factor. Think of it as fertilizer for neurons, helping them survive, connect, and rewire.
In rat studies, Semax increases BDNF and its receptor TrkB in hippocampus and forebrain. That’s the most coherent thread in Semax research and the basis for every neuroplasticity claim attached to it.
It also nudges monoamine neurotransmitters like dopamine and serotonin. But here’s critical nuance matching user reports: Semax is not a stimulant.
In rat studies, Semax alone barely moved dopamine but amplified response when something else was already driving it. That’s why most users describe feeling more motivation rather than a true buzz.
It’s Not NZT
The entire Limitless premise builds on the myth that we only use a fraction of our brains. Unfortunately, that’s fiction—we’re already using essentially 100% of our brains at baseline.
Semax doesn’t unlock dormant capacity waiting for activation. It optimizes signaling in tissue you’re already running.
What Does Science Actually Show
The evidence is present but lopsided in a very specific way.
Bench and animal data is surprisingly deep. Cell studies show BDNF and nerve growth factor genes activating. Rat stroke research is strongest—researchers literally tied off brain arteries in rats, administered Semax, then watched gene expression shift from inflammatory/injury patterns toward repair.
One study showed boosted cell proliferation in injured rat brains, spawning online claims that “Semax regrows your brain.” But again, this is in mice—not 35-year-old humans trying to focus on Excel spreadsheets.
Human Data Is Thin and Russian
A small fMRI study showed intranasal Semax measurably changed brain network activity in healthy volunteers. Older EEG and cognitive work from the 1990s exists, plus a stroke rehab study where Semax plus early rehabilitation raised blood BDNF and slightly accelerated recovery.
But large placebo-controlled trials examining cognitive improvements—how most people actually use it—are still lacking.
Russia has used Semax as an approved drug for over 30 years in stroke patients, giving it more real-world data than almost any non-FDA-approved substance. While not as robust as semaglutide trials, in some ways it’s better—GLP-1 agonists haven’t been around nearly as long.
Semax’s efficacy as cognitive booster may be fuzzy, but its safety profile appears solid.
Dosing: Russian Medicine vs. Gray Market
Russian pharmaceutical Semax comes as nasal drops in two strengths: 0.1% solution for cognitive boost and stroke recovery, and stronger 1% reserved for acute hospital stroke treatment.
One drop of 0.1% delivers approximately 50 micrograms. Labeled daily range runs from a few hundred up to couple thousand micrograms, usually for only a few days at a time.
Gray market biohackers report using nasal sprays between 100-1,000 micrograms daily, typically 5 days on, 2 days off, because tolerance develops quickly and spray isn’t cheap.
Some insist they get better results from subcutaneous injection, though this has no obvious upside and adds another needle to weekly routine.
The Gray Market Problem
When buying “research use only” Semax, there’s decent chance you’re not buying Semax itself. There’s an entire family of remixes: N-acetyl Semax and N-acetyl Semax amidate (Adamax), each with chemical tweaks to extend half-life or intensify effects.
Those aren’t the molecules from Russian studies. Your mileage may vary—like buying a live bootleg concert recording where maybe it sounds better than studio version, or maybe the artist is drunk and slurring.
Side Effects and Safety
Semax is generally well-tolerated, which is major part of its appeal. But well-tolerated doesn’t mean risk-free.
Common user-reported complaints include:
- Anxiety and irritability
- Headaches
- Nausea
- Insomnia if taken late in day
- Unpleasant emotional intensity—like volume got cranked on whatever you were already feeling
The single most common complaint? Feeling absolutely nothing, even at high doses. Could mean bad product, incomplete absorption, wrong analog, or simply individual non-response.
Russian labeling contraindicates pregnancy, breastfeeding, acute psychiatric illness, and notably, history of seizures. Anything nudging brain excitability deserves respect—”naturally derived peptide” doesn’t automatically mean benign.
The scariest thing about Semax in the USA isn’t the peptide itself—it’s the bottle. Since it can’t be legally manufactured here for human consumption, there’s zero guarantee regarding purity, sterility, or whether labeled dose matches actual contents.
FDA Meeting Could Change Everything
On July 23-24, the FDA’s Pharmacy Compounding Advisory Committee (PCAC) meets to decide the fate of several peptides, including Semax.
BPC-157, KPV, TB-500, and MOTS-c are up day one. Semax joins Epitalon and Dihexa on day two, July 24th.
These peptides exist in regulatory limbo. This meeting decides whether they return to a list allowing compounding pharmacies to legally manufacture them under real oversight with quality control, or stay banished to gray market forever.
For Semax specifically, the committee reviews it for cerebral ischemia and trigeminal neuralgia. While PCAC votes are technically advisory, FDA won’t grant access to legitimate high-quality Semax from compounding pharmacies without it.
There’s a public comment docket at regulations.gov that committee members must consider. Comments submitted by July 9th get physically handed to committee before the meeting. After that deadline, FDA may still read them, but people casting votes won’t see them.
The Real Limitless Pill
Is Semax a real-life limitless pill? Probably not. We’re still waiting for actual NZT, and nothing flips your brain to 100% because you’re already running at 100%.
Remember how Limitless actually ends: even fictional NZT had a body count—tolerance, blackouts, withdrawal, people dying when supply runs dry. Even the fantasy came with a bill.
But is Semax a real molecule with genuine cognitive effects, legitimate neuroprotective properties, and 30 years of Russian clinical use? Absolutely. It emerged from legitimate pharmaceutical research in Moscow, not a Hollywood writer’s room.
Semax may be subtle and context-dependent, but positive signals appear exactly where they matter—in cognition and the injured, stressed brain.
Your Real NZT Already Exists
For those chasing focus, the closest thing to a real-life limitless pill is less exciting than movie trailers but costs nothing: sleep, blood pressure control, exercise, avoiding alcohol, treating sleep apnea, addressing depression.
That’s your NZT. Once those fundamentals are dialed, Semax might be reasonable value-add. But it isn’t the whole meal.
When fundamentals are out of whack, nothing else does the work for you. The fanciest Russian nasal spray on Earth will likely be one big expensive disappointment.
Semax is a real molecule with real effects and genuine potential—but it’s a tool, not magic. And if you want access to properly manufactured versions with quality control, make your voice heard at the FDA docket before July 9th.
Monday, May 25, 2026
Quinoa seed (Chenopodium quinoa W.) extract attenuates Alzheimer’s disease–like neurodegeneration: Targeting the SLC7A11/GPX4 pathway
Attenuates: Medicine & Biology: To make a virus or bacteria less virulent or harmful. You really think your competent? doctor and hospital will get human testing going?
Quinoa seed (Chenopodium quinoa W.) extract attenuates Alzheimer’s disease–like neurodegeneration: Targeting the SLC7A11/GPX4 pathway
- Maha O. Hammad,
- Tasneem Shady,
- Basma Moanes,
- Ayat R. El-sharkawy,
- Asmaa M. Galal,
- A’laa E. Tawfeek,
- Abd El-Kader M. El-sisi,
- Aya Sameh,
- Sara Mahrous,
- Nahed Atya,
- Amira Essam,
- Sara El-Desouky &
- Mohammed H. Abd El-Aziz
30 Accesses
Abstract
Background
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and hippocampal neuronal loss. Targeting ferroptosis-related pathways represents a promising therapeutic strategy.
Objective
This study aimed to investigate the potential effect of quinoa (Chenopodium Quinoa W.) seed extract in an aluminum chloride (AlCl₃)–induced rat model of AD, with a particular focus on the SLC7A11/GPX4 antioxidant axis and NCOA4-mediated ferritinophagy.
Methods
Adult male rats were randomly divided into four groups (n = 6): GI (Control), GII (AD), GIII (Quinoa + AD), and GIV (Alzemenda + AD). AD was induced by oral AlCl₃ administration. Quinoa extract and Alzemenda were administered concurrently with AlCl₃ throughout the experimental period. Behavioral performance was evaluated using the Morris Water Maze and Open Field Test. Oxidative stress markers, iron parameters, gene expression, and histopathological changes in the hippocampus were assessed.
Results
GII exhibited significant cognitive impairment, increased lipid peroxidation, depletion of antioxidant defenses, downregulation of SLC7A11, and marked hippocampal iron deposition compared with GI. Treatment with quinoa (GIII) significantly improved learning and memory, restored GPX4 activity and GSH levels, upregulated SLC7A11 expression, and attenuated hippocampal iron deposition. GIV showed comparable behavioral and histological improvement. Systemic iron indices, as well as hippocampal FPN1 and NCOA4 expression, did not differ significantly among groups.
Conclusion
Quinoa seed extract exerts ameliorating effects in AlCl₃-induced AD by suppressing oxidative stress-associated neurodegeneration through preservation of the SLC7A11/GSH/GPX4 axis rather than modulation of iron export or ferritinophagy pathways.
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Saturday, May 9, 2026
Atractylodin alleviates neuroinflammation and protects neurological function after ischemic stroke in association with reduced NLRP3 inflammasome activation
Your competent? doctor and hospital will need to get human testing going THAT ALSO CREATES EXACT REHAB PROTOCOLS!
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!
Atractylodin alleviates neuroinflammation and protects neurological function after ischemic stroke in association with reduced NLRP3 inflammasome activation
- Q
Qingyao Ouyang 1†
- Y
Yiying Yang 2†
Hoi Leong Lee 3
Ziyu Yan 1
- D
Dezhi Deng 4*
Wei Li 5*
1. College of Basic Medical Sciences, China Three Gorges University, Yichang, Hubei, China
2. Nanyang Second General Hospital, Nanyang, Henan, China
Abstract
Background:
NOD-like receptor protein 3 (NLRP3) inflammasome–driven neuroinflammation contributes to ischemic stroke injury. Atractylodin (ART) shows anti-inflammatory activity, but its neuroprotective potential and mechanistic links to NLRP3 signaling after cerebral ischemia–reperfusion (I/R) injury remain to be defined.
Materials and methods:
BV2 microglia were subjected to oxygen–glucose deprivation/reoxygenation (OGD/R), and rats underwent middle cerebral artery occlusion (MCAO) followed by reperfusion. ART was administered after reperfusion in vivo (10 or 30 mg/kg, once daily for 3 days) and during reoxygenation in vitro. Neurobehavioral outcomes and infarct volume were assessed in MCAO rats, along with measurements of neuronal apoptosis. NLRP3 inflammasome activation, gasdermin D (GSDMD)–dependent pyroptosis, pro-inflammatory cytokines, and microglial polarization markers were evaluated using immunoblotting, immunofluorescence, RT-qPCR, and enzyme-linked immunosorbent assay (ELISA).
Results:
In OGD/R-stimulated BV2 microglia, ART suppressed NLRP3 inflammasome activation and reduced GSDMD cleavage, accompanied by decreased IL-1β and IL-18 production. In the MCAO model, ART significantly improved neurological outcomes and reduced infarct volume and neuronal apoptosis. These protective effects were linked to a reduction in the expression of NLRP3 pathway components (NLRP3, ASC, and caspase-1) and GSDMD-N. Additionally, there was a shift in microglial responses toward an anti-inflammatory (M2-like) profile, which led to a decrease in pro-inflammatory markers.
Conclusion:
ART confers neuroprotection in experimental ischemic stroke by inhibiting NLRP3 inflammasome–associated pyroptosis and modulating microglial inflammatory polarization, supporting its potential as a therapeutic candidate for ischemic stroke.
More at link.
Thursday, April 16, 2026
Clemizole Mitigates Traumatic Brain Injury by Inhibiting Oxidative Stress, Neuroinflammation, and Apoptosis
Will anyone in stroke actually think of and do human testing of this for stroke? Of course not, there aren't two functioning neurons anywhere in stroke!
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!
OH NO! your doctor KNOWS NOTHING AND DOES NOTHING!
Clemizole Mitigates Traumatic Brain Injury by Inhibiting Oxidative Stress, Neuroinflammation, and Apoptosis
Abstract

Traumatic brain injury (TBI) triggers complex secondary pathological mechanisms, including neuroinflammation, oxidative stress, and apoptosis, contributing to long-term cognitive and motor deficits. This study investigates the neuroprotective potential of Clemizole, a known TRPC5 inhibitor, in a weight-drop rat model of TBI. Target prediction analyses using Swiss Target Prediction and CTD databases identified 159 overlapping genes between Clemizole and TBI. Protein–protein interaction network and hub gene analyses highlighted key proteins, such as TNF-α, CASP3, MMP-9, and TRPC5, implicating them in TBI pathogenesis. KEGG pathway enrichment revealed Clemizole-targeted pathways, including PI3K-Akt, TNF signaling, and apoptosis. After TBI, behavioral assessments showed that Clemizole significantly improved neurological scores, grip strength, locomotor activity, and spatial learning deficits. Biochemical assays revealed that Clemizole dose-dependently reduced nitrite and MDA levels while restoring GSH, indicating attenuation of oxidative stress. H&E (hematoxylin and eosin) and cresyl violet staining confirmed reduced neuronal degeneration and preserved cortical integrity. Clemizole also downregulated inflammatory cytokines and glial markers (Iba-1 and GFAP), alongside restoring BBB integrity via upregulation of tight junction proteins and suppressing MMP-9 expression. Furthermore, Clemizole activated the PI3K-Akt signaling pathway, decreasing the expression of pro-apoptotic proteins (Bax, caspase-9 and caspase-3) and restoring Bcl-2 levels. Importantly, Clemizole decreased TRPC5 expression and attenuated CHOP-mediated ER stress, suggesting a mechanistic link between TRPC5 inhibition and PI3K-Akt-mediated neuroprotection. Collectively, these findings demonstrate that Clemizole confers multifaceted neuroprotection following TBI by targeting TRPC5-mediated calcium dysregulation, restoring PI3K-Akt signaling, and attenuating oxidative, inflammatory, and apoptotic cascades. This study identifies Clemizole as a promising therapeutic candidate for mitigating secondary brain injury and promoting functional recovery after TBI.
Tuesday, April 7, 2026
Copper depletion ameliorates neuronal damage after intracerebral hemorrhage
Will your competent? doctor DO ANYTHING AT ALL WITH THIS?
NO? So, doesn't care about your recovery at all! Won't get human testing going either?
Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!
OH NO! your doctor KNOWS NOTHING AND DOES NOTHING!
Copper depletion ameliorates neuronal damage after intracerebral hemorrhage
Highlights
- •Intracerebral hemorrhage (ICH) induces copper overload and cuproptosis in perihematomal brain tissue.
- •The copper chelator TTM mitigates copper accumulation and inhibits cuproptosis in vivo and in vitro.
- •Copper depletion with TTM alleviates ICH-induced brain injury and neuronal death.
- •TTM treatment promotes the expression of neurite regeneration-associated proteins GAP43 and MAP2.
- •Targeting copper-induced cuproptosis is a promising therapeutic strategy for ICH.