Neurolis is exactly what I needed for staying focused and locked in while working. Neurolis works fast and kept me locked in, I had ideas, enhanced problem solving abilities, and overall cognitive enhancements. 10/10, will have to keep buying this.
NEUROLIS - Focus & Cognitive Precision Formula
The Formula, In Practice
Engineered. Not Marketed.
KEY BENEFITS INCLUDE:
NEUROLIS
SATORI — The Standard of Performance
Every ingredient in Neurolis is selected for a single reason:
demonstrated, mechanism-backed support for cognitive performance.
Neuroplasticity. Focus. Memory. Neuroprotection.
This document contains the science behind each ingredient,
its mechanism of action, and the research that backs it.
Saffron is derived from the stigmas of Crocus sativus and contains two principal bioactive fractions: crocin (a carotenoid glycoside) and safranal (a volatile aldehyde). Both fractions operate through distinct and complementary neurological mechanisms, together producing a broad-spectrum nootropic and neuroprotective profile. Historically used in Persian and Ayurvedic medicine, saffron has accumulated a substantial body of modern clinical research supporting its role in mood regulation, cognitive enhancement, and long-term brain health.
- DOPAMINE & SEROTONIN REUPTAKE INHIBITIONCrocin and safranal inhibit the reuptake transporters for both dopamine and serotonin, extending the duration these neurotransmitters remain active in the synapse. This dual-pathway inhibition supports mood stability, motivation, working memory, and executive function — areas governed by dopaminergic and serotonergic tone in the prefrontal cortex and limbic system.
- BDNF UPREGULATIONSaffron extracts have been shown to increase expression of brain-derived neurotrophic factor (BDNF), the primary signalling protein governing neuronal survival, synaptic growth, and long-term potentiation. Elevated BDNF supports the formation and consolidation of new memories and is critical for learning-related plasticity in the hippocampus.
- ANTI-INFLAMMATORY NEUROPROTECTIONCrocin exhibits direct anti-inflammatory activity in the CNS, suppressing pro-inflammatory cytokines and oxidative stress that contribute to neuronal damage and cognitive decline. This neuroprotective mechanism preserves synaptic integrity over time and supports cognitive longevity.
- Enhances mood, motivation, and emotional stability
- Supports working memory and executive function
- Upregulates BDNF for neuroplasticity and memory consolidation
- Provides antioxidant neuroprotection against CNS inflammation
- Dual monoamine reuptake inhibition via crocin and safranal
- Saffron (Crocus sativus) and Major Depressive Disorder: A Meta-Analysis of Randomised Clinical TrialsView study ↗
- Crocin, an Active Constituent of Saffron, Attenuates Oxidative Stress and NeuroinflammationView study ↗
- Effects of Saffron Extract on Mental Health and Cognitive Function: A Systematic ReviewView study ↗
7,8-Dihydroxyflavone (7,8-DHF) is a naturally occurring flavone that acts as a direct agonist at the TrkB receptor — the primary receptor through which BDNF exerts its neuroplasticity and neuroprotective effects. Unlike most botanical compounds that only modestly modulate BDNF expression, 7,8-DHF directly binds and activates TrkB, triggering downstream signalling cascades that drive synaptic growth, neuronal survival, and cognitive enhancement.
- DIRECT TrkB RECEPTOR AGONISM7,8-DHF binds directly to the TrkB tyrosine kinase receptor — the high-affinity receptor for BDNF — and activates it with a pharmacological profile analogous to BDNF itself. This direct agonism bypasses the need for endogenous BDNF synthesis and provides robust neuroplasticity signalling even under conditions of reduced BDNF expression.
- PI3K/Akt & MAPK/ERK PATHWAY ACTIVATIONTrkB activation by 7,8-DHF initiates both the PI3K/Akt and MAPK/ERK intracellular signalling cascades. The PI3K/Akt pathway promotes neuronal survival and inhibits apoptosis; the MAPK/ERK pathway drives synaptic protein synthesis, long-term potentiation (LTP), and the structural changes underlying memory consolidation. Together these cascades produce the full downstream profile of BDNF-mediated neuroplasticity.
- SYNAPTIC PLASTICITY & NEUROPROTECTIONThrough sustained TrkB activation, 7,8-DHF promotes the growth and maintenance of dendritic spines, enhances synaptic density, and protects neurons against excitotoxic and oxidative damage. This produces measurable improvements in spatial memory, associative learning, and cognitive resilience under stress.
- Directly activates TrkB, mimicking BDNF's full neuroplasticity profile
- Drives synaptic plasticity and long-term potentiation
- Supports memory consolidation and associative learning
- Neuroprotection via PI3K/Akt anti-apoptotic signalling
- Effective even under conditions of diminished BDNF expression
- 7,8-Dihydroxyflavone, a Small-Molecule TrkB Agonist, Reverses Memory Deficits and BACE Activity in a Mouse Model of Alzheimer's DiseaseView study ↗
- A Small Molecule TrkB Ligand Reduces Motor and Cognitive Deficits and Decreases Amyloid-β and Tau Pathology in Mouse Models of Alzheimer's DiseaseView study ↗
- 7,8-Dihydroxyflavone Exhibits Therapeutic Efficacy in a Mouse Model of Rett SyndromeView study ↗
Polygala tenuifolia (Yuan Zhi) is a root herb with a 2,000-year history in Traditional Chinese Medicine, used primarily to sharpen cognition, support memory, and calm the mind. Its principal bioactive constituents — tenuifolin (a triterpenoid saponin) and onjisaponins — have been studied extensively for their acetylcholinesterase-inhibiting and neurotrophin-modulating properties. Polygala operates through mechanisms directly relevant to cholinergic tone, synaptic plasticity, and BDNF expression.
- ACETYLCHOLINESTERASE INHIBITIONTenuifolin inhibits acetylcholinesterase (AChE) — the enzyme responsible for degrading acetylcholine in the synapse. By reducing acetylcholine breakdown, Polygala elevates cholinergic tone in cognitive brain regions including the hippocampus and prefrontal cortex, supporting attention, working memory, and learning efficiency.
- BDNF EXPRESSION SUPPORTPolygala extracts have been shown to upregulate BDNF gene expression in the hippocampus, supporting neuronal survival and synaptic growth. This mechanism complements AChE inhibition by providing a growth factor-mediated route to long-term cognitive enhancement and neuroprotection.
- SYNAPTIC PLASTICITY ENHANCEMENTOnjisaponins from Polygala promote the release of BDNF and facilitate the induction of long-term potentiation (LTP) in hippocampal neurons. These effects support the encoding and consolidation of new memories and underpin Polygala's centuries of use as a cognitive tonic in traditional medicine systems.
- Elevates acetylcholine levels via AChE inhibition
- Enhances working memory, focus, and learning efficiency
- Upregulates hippocampal BDNF for neuroplasticity
- Supports long-term potentiation and memory consolidation
- Complementary cholinergic and neurotrophin-mediated mechanisms
- Tenuifolin, an Extract Derived from Polygala tenuifolia, Inhibits Amyloid-β Secretion and Tau AggregationView study ↗
- Onjisaponins, Active Principles of Polygala tenuifolia Root, Enhance Hippocampal BDNF and Improve Cognitive FunctionView study ↗
- Polygala tenuifolia Root Extract Improves Hippocampus-Dependent Learning and Memory in Rodent ModelsView study ↗
Scutellaria baicalensis (Chinese Skullcap) is a herb whose root contains a rich concentration of flavonoids — primarily baicalein, baicalin, and wogonin. These compounds have been studied for their ability to modulate GABAergic neurotransmission, suppress neuroinflammation, and stabilise dopaminergic signalling. The combined effect is a calming-without-sedating cognitive enhancement profile that reduces cognitive noise from excessive neuronal excitation and inflammatory stress.
- GABA-A RECEPTOR POSITIVE MODULATIONBaicalein and wogonin act as positive allosteric modulators at the GABA-A receptor, enhancing the effect of GABA — the brain's primary inhibitory neurotransmitter. This mechanism reduces excessive neuronal firing, attenuates anxiety-driven cognitive interference, and promotes a calm, focused mental state without the sedative or dependency risks of pharmaceutical GABAergic agents.
- NEUROINFLAMMATION SUPPRESSIONBaicalin potently inhibits pro-inflammatory cytokine production (TNF-α, IL-1β, IL-6) in microglia — the brain's resident immune cells. Chronic low-grade neuroinflammation impairs synaptic function, disrupts neurotransmitter balance, and contributes to cognitive fatigue and decline. Baicalin suppresses this inflammatory burden, supporting clearer, more efficient cognitive processing.
- DOPAMINE PATHWAY STABILISATIONWogonin has demonstrated the ability to modulate dopamine metabolism and protect dopaminergic neurons from oxidative stress. This stabilising effect on the dopamine pathway supports consistent motivational drive, focus, and reward processing — domains that deteriorate under chronic stress or neuroinflammatory conditions.
- Promotes calm focus via GABA-A positive modulation
- Reduces anxiety and cognitive interference without sedation
- Suppresses neuroinflammation for clearer cognitive processing
- Stabilises dopamine signalling for consistent motivation and drive
- Neuroprotective flavonoid profile: baicalein, baicalin, wogonin
- Baicalein and Baicalin Promote Antioxidant Defences and Inhibit Neuroinflammation in BrainView study ↗
- Wogonin, a Flavonoid from Scutellaria Baicalensis, Modulates GABA-A ReceptorsView study ↗
- Baicalin Inhibits Neuroinflammation and Oxidative Stress and Improves Cognitive Deficit in RatsView study ↗
Quercetin is one of the most abundant dietary flavonoids and one of the most extensively studied plant-derived anti-inflammatory and antioxidant compounds. In the context of cognitive performance, quercetin's primary relevance lies in its ability to reduce neuroinflammation, neutralise reactive oxygen species in neural tissue, and support mitochondrial energy production in neurons — which are among the most metabolically demanding cells in the body.
- ANTI-INFLAMMATORY ACTIVITYQuercetin inhibits NF-κB signalling — the central transcriptional pathway governing pro-inflammatory gene expression — as well as directly suppressing the production of TNF-α, IL-6, and other neuroinflammatory cytokines. This anti-inflammatory action protects synaptic function and neurotransmitter balance from the degrading effects of chronic low-grade CNS inflammation.
- ANTIOXIDANT NEUROPROTECTIONQuercetin is a potent radical scavenger with demonstrated ability to neutralise hydroxyl radicals, superoxide anions, and lipid peroxides in neural tissue. It also upregulates endogenous antioxidant enzymes including superoxide dismutase (SOD) and catalase. This dual-layer antioxidant action protects neuronal membranes and mitochondrial DNA from oxidative damage.
- MITOCHONDRIAL ATP SUPPORT IN NEURONSQuercetin supports mitochondrial membrane potential and electron transport chain efficiency in neurons, helping maintain the high ATP output required for sustained cognitive function. This bioenergetic support is particularly relevant during periods of prolonged mental effort, where neuronal energy demand is elevated and oxidative stress is highest.
- Reduces CNS neuroinflammation via NF-κB inhibition
- Potent antioxidant protection for neurons and synaptic structures
- Supports neuronal mitochondrial energy production
- Upregulates endogenous antioxidant enzyme systems
- Broad neuroprotective profile with extensive clinical backing
- Quercetin: A Flavonoid with Potential Neuroprotective Properties and MechanismsView study ↗
- Anti-inflammatory and Antioxidant Activities of Quercetin in the Central Nervous SystemView study ↗
- Quercetin and Its Anti-inflammatory Effects in Neurological Diseases: A Systematic ReviewView study ↗
Luteolin is a polyphenolic flavone found in a range of medicinal herbs and foods. It has emerged as a compound of significant interest in neuroscience for its exceptional ability to modulate microglial activation — a critical factor in controlling neuroinflammation — as well as its potent antioxidant profile in neural tissue. Luteolin's capacity to cross the blood-brain barrier makes it a uniquely effective neuroinflammation-targeting compound.
- MICROGLIAL MODULATIONLuteolin directly suppresses excessive activation of microglia — the brain's resident immune cells — by inhibiting the MAPK and NF-κB signalling pathways that drive microglial-mediated neuroinflammation. When microglia become hyperactivated (as occurs with chronic stress, injury, or systemic inflammation), they release neurotoxic cytokines that impair synaptic transmission and damage neurons. Luteolin attenuates this process, maintaining a protective rather than destructive microglial phenotype.
- POTENT ANTIOXIDANT NEUROPROTECTIONLuteolin demonstrates superior radical-scavenging activity compared to many other flavonoids, with particular efficacy against superoxide and hydroxyl radicals in neural tissue. It also chelates metal ions that catalyse oxidative reactions in the brain and upregulates the Nrf2/ARE antioxidant pathway — triggering a systemic cellular antioxidant response that provides broad neuroprotection.
- Modulates microglial activation to prevent neuroinflammatory damage
- Superior radical-scavenging antioxidant activity in neural tissue
- Activates Nrf2/ARE pathway for systemic cellular neuroprotection
- Crosses the blood-brain barrier for direct CNS action
- Protects synaptic structures from inflammatory and oxidative degradation
- Luteolin Inhibits Microglial Activation and Provides Neuroprotection in LPS-Treated NeuronsView study ↗
- Luteolin as a Neuroprotective Agent: Mechanisms and Clinical PerspectivesView study ↗
- Luteolin Reduces Neuroinflammation and Cognitive Deficits in a Mouse ModelView study ↗
Icariin is the principal bioactive flavonoid glycoside of Epimedium (Yin Yang Huo), a herb with centuries of use in Traditional Chinese Medicine for its adaptogenic and cognitive-enhancing properties. In modern neuroscience research, icariin has been investigated for its ability to modulate dopaminergic receptor activity, upregulate BDNF, promote synaptic plasticity, and improve cerebral blood flow — producing a multi-mechanism cognitive enhancement profile.
- DOPAMINERGIC RECEPTOR ENHANCEMENTIcariin modulates dopamine receptor expression and sensitivity — particularly D1 and D2 receptors in the prefrontal cortex and striatum. By optimising dopaminergic receptor function, icariin supports consistent motivation, attention, and executive function, and helps buffer the cognitive fatigue associated with dopamine depletion under sustained mental demand.
- BDNF UPREGULATION & SYNAPTIC PLASTICITYIcariin has been shown to increase BDNF expression in the hippocampus and cortex, supporting the growth of new synaptic connections and the maintenance of existing ones. This neurotrophin-mediated effect promotes long-term potentiation and supports memory encoding and consolidation — the same downstream outcome targeted by 7,8-DHF in this formula, but through a transcriptional rather than receptor-agonist mechanism.
- CEREBRAL BLOOD FLOW IMPROVEMENTIcariin inhibits PDE5 (phosphodiesterase-5) in cerebral vasculature, increasing cGMP levels and promoting vasodilation of cerebral blood vessels. Enhanced cerebral blood flow delivers more oxygen and glucose to active neural tissue, directly supporting cognitive performance and reducing the neural fatigue associated with vascular insufficiency.
- Enhances dopaminergic receptor function for motivation and focus
- Upregulates BDNF to support synaptic plasticity and memory
- Increases cerebral blood flow via PDE5 inhibition
- Supports long-term potentiation in the hippocampus
- Multi-mechanism cognitive enhancement: dopamine, BDNF, and vascular
- Icariin Attenuates Cognitive Deficits and Increases Neurotrophic Factors in a Rat ModelView study ↗
- Icariin Promotes BDNF Expression and Inhibits Neuronal Apoptosis in HippocampusView study ↗
- Neuroprotective Effect of Icariin on Learning and Memory in Alzheimer's Disease ModelView study ↗
Bacopa monnieri is one of the most extensively researched nootropic herbs, with a long history of use in Ayurvedic medicine under the name Brahmi. Its principal bioactives — bacosides A and B — operate through multiple complementary mechanisms to enhance synaptic signalling, preserve cholinergic tone, and support the structural remodelling of dendritic networks that underlies memory formation and retention.
- BACOSIDE-DRIVEN SYNAPTIC PLASTICITYBacosides A and B enhance the release of synaptic vesicles and upregulate key proteins involved in synaptic transmission, including synapsin I and growth-associated protein GAP-43. This promotes dendritic branching, synaptogenesis, and the structural reorganisation of neural circuits that is required for learning, memory consolidation, and cognitive adaptability.
- ACETYLCHOLINE PRESERVATIONBacopa moderately inhibits acetylcholinesterase (AChE) and enhances choline acetyltransferase activity, supporting acetylcholine synthesis and preservation. The net effect is elevated cholinergic tone in the hippocampus and cortex — the brain regions most critical for declarative memory formation and retrieval, and the regions most affected by cognitive decline.
- Drives dendritic remodelling and synaptogenesis via bacosides
- Preserves acetylcholine levels for optimal memory function
- Improves memory consolidation and learning speed
- Reduces cognitive decline and protects against cholinergic deficit
- One of the most clinically validated nootropic herbs available
- Effects of a Standardised Bacopa monnieri Extract on Cognitive Performance, Anxiety, and Depression in the ElderlyView study ↗
- Bacopa monnieri and Cognitive Enhancement: A Comprehensive Review of Human Clinical StudiesView study ↗
- Synaptic Plasticity Enhancement by Bacopa monnieri in the HippocampusView study ↗
Rhodiola rosea is an adaptogenic root native to arctic and mountainous regions of Europe and Asia. Its principal bioactives — salidroside and rosavins — have been studied extensively for their ability to normalise the stress response via the hypothalamic-pituitary-adrenal (HPA) axis, maintain monoamine neurotransmitter balance under psychological and physical stress, and support cognitive performance during periods of high cognitive demand and fatigue.
- HPA AXIS & CORTISOL NORMALISATIONSalidroside modulates the HPA axis — the central neuroendocrine pathway governing the cortisol stress response — by reducing excessive cortisol secretion without blunting the adaptive stress response. Chronic cortisol elevation is neurotoxic, impairing hippocampal neurogenesis, degrading working memory, and disrupting prefrontal executive control. Salidroside's normalising effect protects these cognitive systems under sustained stress.
- DOPAMINE & SEROTONIN MAINTENANCE UNDER STRESSRosavins inhibit the enzyme monoamine oxidase (MAO), which degrades dopamine and serotonin in the synapse. Under conditions of chronic stress or high cognitive demand, accelerated monoamine turnover leads to fatigue, mood decline, and motivation loss. By slowing MAO activity, rosavins preserve dopaminergic and serotonergic tone, maintaining mental energy, focus, and emotional stability when stress is highest.
- Normalises cortisol and HPA axis response to chronic stress
- Preserves dopamine and serotonin under psychological and physical demand
- Reduces mental fatigue and supports sustained cognitive performance
- Protects hippocampal neurogenesis from cortisol-mediated damage
- Clinically validated adaptogen with decades of research backing
- Rhodiola rosea for Mental and Physical Fatigue in Nursing Students: A Randomised Controlled TrialView study ↗
- A Randomised Trial of Two Different Doses of a SHR-5 Rhodiola rosea Extract on Exhaustion in Burnout PatientsView study ↗
- Antistress Effect of Rhodiola rosea: Salidroside and HPA Axis ModulationView study ↗