Cerebral Key supplements neurotransmitter precursors, in other words, it ensures resources are constantly available resulting in optimal neurotransmitter function. These neurotransmitters include Dopamine, Acetylcholine, Serotonin, and GABA. Dopamine is responsible for motivation to get things done, to reach that next milestone or goal. Acetylcholine is lesser known but incredibly impactful, responsible for most aspects of learning, memory, and concentration. Serotonin plays a role in mood as well as memory consolidation and sleep quality. Glutamate is known to be the main mediator of excitatory signaling in the central nervous system and is crucial for cognition, memory, and learning. GABA is the primary inhibitory brain chemical, put more simply it stops the excess unnecessary neurotransmission resulting in a calm, collective state. Additionally, the brain uses proteins to strengthen your neural networks; the connections between neurons where memories are stored.

Noopept stimulates 2 of these proteins, BDNF and NGF, increasing neural network strength and leading to better functional performance. That means faster learning and improved memory. The details of cognitive enhancement mechanisms are complex but the results are simple. Users of Cerebral Key experience short term benefits of improved mood and increased productivity. Long term benefits onset after 4 weeks of use and include improved learning, memory, and general cognition.

Optimizing Neurotransmitter Levels

Why is it important to optimize neurotransmitters?

Dopamine Chemical Structure

Dopamine is responsible for cognitive alertness and motivation. Dopamine promotes feelings of enjoyment and reinforcement to motivate performance. Dopamine provides the drive to learn more and take that next step necessary to accomplish goals.[47]

Acetylcholine chemical structure

Acetylcholine is critical for learning and memory. Acetylcholine controls the ability to process sensory information  (Learning) and retrieve stored information (Memory). Acetylcholine is also responsible for sustained attention (Concentration).[1]

Serotonin Chemical Structure

Serotonin has very specific effects on cognition including executive function, learning and memory consolidation. Serotonin is known to have a strong impact on mood as well as processing short term memory to long term memory.[48]

Glutamic Acid chemical structure

Glutamate is the most abundantly found neurotransmitter in the body. Glutamate is the brains main excitatory neurotransmitter and is critical for neural communication, memory formation, and learning.

How does taking nootropics optimize neurotransmitters?

Acetylcholine

For the brain to synthesize acetylcholine it must have choline and acetyl-CoA available. Mean choline intake for most people are far below the Adequate Intake established by the Institute of Medicine [2]

Nootropics supplements can increase both of these required resources. Citicoline is a high-quality choline source one can intake which will allow for increased ACH synthesis. ALCAR contributes the necessary acetyl group required for Acetyl COA, thereby increasing the synthesis of Acetylcholine as well. By increasing the amount of acetylcholine available, the brain is more capable of storing new information, concentration on a single task, and retrieving stored memories for use. [3]

Serotonin

Vitamin D3 – Serotonin is synthesized tryptophan hydroxylase 2, which is activated by vitamin D3. During experiments conducted using synthesized DNA vitamin D3 enhanced the ability of brain cells to produce serotonin anywhere from 2 to 30 times as much.[4] Serotonin has very specific effects on cognition including executive function, learning memory, and relaxation.[48]

Glutamate

Glutamate is the main excitatory neurotransmitter accounting for greater than 90% of the synaptic connections in the brain.[46] Glutamate is involved in cognitive functions such as learning and memory, including synaptic plasticity.Long term potentiation is an important memory formation neural activity which takes place at glutamatergic synapses in the hippocampus. L-Theanine, being a form of L-Glutamic acid, is a precursor to Glutamate. L-Theanine supplementation helps to ensure adequate levels of glutamate are synthesized and available. Noopept stimulates the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) Glutamatergic receptors resulting in enhanced memory formation.

Improved Learning and Memory

Information Processing

Bacopa Monnieri, another key ingredient in the product, is a medicinal herb which has been used for thousands of years for its cognitive enhancement effects. It has been shown to result in a proliferation of dendritic intersections and branching points. Dendrites are projected branches which are formed off of a neuron. The manner in which dendrites are formed is directly responsible for what signals a neuron is able to receive.

Therefore increasing the size of the dendritic tree associated with a neuron is to increase its capacity to receive more signals. This is hypothesized to have an impact on the speed of information processing. [5] Bacopa Monnieri has been found to produce these results after four weeks of supplementation. [7]

Before and After comparison of Dendritic growth caused by Bacopa Monnieri supplementation

Neuroplasticity

The formula’s main ingredient Noopept, stimulates BDNF and NGF proteins, resulting in increased neuroplasticity. [10]

At the single cell level, synaptic plasticity refers to changes in the connections between neurons. Neuroplasticity is the capability to change connections as well as form new connections between neurons.Through repetition of experience or deliberate practice, the connections between neurons become reinforced. When this happens that becomes the default “path of thought.” Neuroplasticity is highly influenced by the expression of the proteins Nerve Growth Factor (NGF) and Brain Derived Neurotrophic Factor (BDNF). BDNF expression results in increasing the strength of the neural connection from one neuron to another.[7][8] This means that the higher the levels of BDNF expression, the faster new experiences and learning will be translated into memory. NGF expression is involved primarily in the growth, as well as the maintenance, proliferation, and survival of nerve cells (neurons). In fact, NGF is critical for the survival and maintenance of these neurons as they will undergo programmed cell death ( apoptosis ) in its absence.[9] 

 

Neurogenesis

Neurogenesis is the process of generating new neurons in the brain. In adults, neurogenesis occurs in two primary locations; the dentate gyrus of the hippocampus and the striatum. The hippocampus plays an important role in memory, more specifically long term memory. The expression of the protein NGF results in neurogenesis.[9]  More neurons equate to more physical resources for the brain to form new connections, thereby increasing the capacity to learn and have learned material stored as memory between neural connections. Noopept stimulates the expression of NGF resulting in increased formation of new neurons.[10]

 Long Term Potentiation

What is LTP?

Long Term Potentiation, or LTP, is a result of increased strength of the connection between two neurons, thereby allowing for stronger recall of the memory which is stored between these neurons. Simply stated, it is a chain of biochemical events which results in stronger memory of information or skill.

Full Process LTP

Full Process LTP:

1.Neurotransmission takes place between two neurons. In this interaction, we have the Sender (presynaptic cell ) and the receiver (postsynaptic cell). One studies material for 30 minutes. This causes glutamate to be released between two neurons (this represents the review of the material).Neurotransmission takes place between two neurons. In this interaction, we have the Sender (presynaptic cell ) and the receiver (postsynaptic cell). The glutamate released is partially absorbed into the postsynaptic cell while some remains in the postsynaptic cleft ( space between the 2 neurons ).

2. When one continues to study and the glutamate is released between neurons it gradually builds up, increasing the concentration of Sodium (Na+) in the Synaptic Cleft ( space between the neurons. The increase in concentration causes the postsynaptic cell membrane to allow a greater influx of Sodium (Na+).

3. This leads to a larger concentration of Na+ inside the postsynaptic neuron.

4. There is another type of receptor on the postsynaptic cell membrane. the N-methyl-D-aspartate (NMDA) receptor. The NMDA receptor is not normally open to allow an influx of molecules from the postsynaptic cleft. Instead, it is occupied by a Magnesium (Mg2+) molecule which acts as a barrier, not allowing molecules in or out through the NMDA receptor.

5. When the Na+ concentration becomes high enough inside the postsynaptic cell, it causes a depolarization event in the postsynaptic cell. This, in turn, repulses the Magnesium (Mg2+) which is then followed by calcium influx through the cell membrane.

6. Calcium (Ca2+) now enters the postsynaptic cell acting as an important secondary messenger activating many intracellular cascades.

7. Ca2+ binds to respective binding proteins causing insertion of new α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors on the postsynaptic cell membrane.

8. Prolonged increase of calcium results in gene expression which cause more AMPA receptor insertion into the postsynaptic cell membrane.

9. Late Phase LTP increases neurotrophic factors including nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF) through gene activation. These proteins help to strengthen the connection between the two neurons as well as ensure general maintenance as to prevent apoptosis (programmed cell death) of these neurons.

How do Nootropics contribute to LTP?

Acetylcholine and encoding new memories

Acetylcholine has been found to have a major role in the encoding of new memories. One method which acetylcholine works is by suppressing excitatory signaling of other neuronal connections that are on the neural network where the new memory is being encoded[11] If Acetylcholine did not prevent this blurring effect other assumptions, previously learned material, and memories on that neural network would be partially combined into the newly encoded memory. To state this simply, the neuromodulatory effects of acetylcholine allow for a very clear memory of what was learned to be created.

This concept is easy to illustrate by displaying how alcohol consumption impacts acetylcholine receptors. Of course, when you consume alcohol, depending on how much, it may cause blurred memories or even a complete lack of memory.

Complex diagram showing how Long term potentiation contributes to memory formation

This, of course, is an extreme example. But the blurring of memory is not limited to cases involving alcohol. If acetylcholine is at a surplus it can result in strong clear memories and if it is at a deficit it can result in blurred memories. Have you ever remembered something a certain way and asked yourself or even out loud: I wonder why I remember it that way? Ir may have been as a result of inadequate levels of acetylcholine when your brain encoded the memory.  Cerebral Key is formulated with Citicoline, a high-quality choline source which allows for increased production of acetylcholine. Noopept has been found to stimulate acetylcholine processes as well as acetylcholine delivery.[10] This leads to enhanced results of all acetylcholine functions.

Bacopa Monnieri also increases the level of encoding new memories. This is thought to be a result of the dendritic growth effects of Bacopa Monnieri supplementation which we will examine in another section.

MEMORY CONSOLIDATION

How can nootropics help memory consolidation?

Glycogenolysis, the process of breaking down glycogen into glucose, is necessary for memory consolidation. Serotonin is critical in the process of glycogenolysis[12][13], therefore a serotonin deficit could lead to impairment of memory consolidation.

Nootropics impact memory consolidation by ensuring adequate levels of serotonin are available for use. Both ingredients in the formula, Vitamin D3 and Bacopa Monnieri have serotonin based benefits from supplementation. Vitamin D3, through activation of tryptophan hydroxylase 2(TPH2), allows for as much serotonin production as possible given the available biomolecular resources in the body.[4]This is because TPH2 is the rate-limiting enzyme of serotonin synthesis. The concept of the rate-limiting step is very important to understand when approximating the effectiveness of a process, and is, therefore, a focus of those who are trying to optimize the process. With the rate-limiting enzyme TPH2 being activated in abundance, the body will produce more serotonin in a shorter time with the same amount of precursor materials. Bacopa Monnieri has also been shown to increase the amount of the enzyme TPH2, providing benefits of the same nature.[14] In addition, Bacopa Monnieri has also been found to heighten expression of the serotonin transporter (SERT)[14], leading to increased delivery of serotonin where it is in demand.

ENERGY

Upgrade mitochondrial function

Energy is created in the mitochondria

Energy is created through the Citric acid cycle ( aka Krebs cycle )

What other factors influence glucose delivery?

How does the body produce energy?

TCA / CAC / KREBS CYCLE

The body uses energy in the form of ATP. ATP is the energy currency of life. ATP is produced by the body in several ways including through Glycolysis, the Krebs Cycle, and the electron transport chain. Glycolysis is an oxygen independent process and occurs outside of the mitochondria. The Krebs cycle and electron transport chain requires oxygen and the pyruvic acid produced from glycolysis. They both take place inside mitochondria of cells and generate the bulk of ATP. The Electron Transport chain is a series of complexes that host biochemical reactions yielding 32 ATP as the end result. This process is driven by enzymes which are made up of many different proteins.

Diagram explaining various biological processes responsible for producing ATP

How do Nootropics help optimize energy production?

ALCAR is able to increase the levels of proteins used inside the mitochondria resulting in greater energy output.[15]More specifically, it increases the levels of proteins levels which are increased are used to produce mitochondrial cristae. Cristae are especially important as they host the process of the electron transport chain which generates ATP.  The cristae increase the surface area of the inner membrane, allowing for the faster production of ATP because there are more places to perform the process. If we think of the mitochondria as the energy factory, these proteins represent the workers and the cristae represent the equipment inside the factory. In this way, ALCAR is capable of increasing the biological hardware used to create energy. Additionally, ALCAR contributes its acetyl group to form more acetyl-CoA. Acetyl-CoA is necessary for the production of energy through the Krebs Cycle, which generates 90 percent of the body’s energy. Finally, ALCAR facilitates the transportation of fats into cells for use as energy. [16]

The Vitamin B5 in Cerebral Key is required to synthesize Coenzyme A (CoA).  Since CoA is required for the Krebs Cycle, it is clear how supplementing with Vitamin B5 is beneficial to energy production.

Caffeine has several mechanisms of action including inhibiting adenosine from binding to adenosine receptors. Adenosine, a chemical used by the central nervous system, is responsible for regulating the sleep cycle. As adenosine accumulates in the brain, it will activate responses which lead to feeling tired and wanting to sleep. Caffeine is able to bind to adenosine receptor sites in the brain, effectively preventing the sleep symptoms associated with adenosine build up for a period of time. Caffeine increases neural activity by blocking the molecule adenosine from binding to adenosine receptors. This increased neural activity triggers an increase in adrenaline and also raises energy levels[17][18] An increase in adrenaline causes the liver to release more sugar into the bloodstream.  Caffeine and ALCAR have been proven to be a synergistic combination for sustained energy.[19] ALCAR optimizes the energy production process in the mitochondria while caffeine causes the body to release more energy for use.

Vitamin B12 helps to synthesize succinyl-CoA, which is very impactful on the Krebs Cycle. Vitamin B12 also optimizes blood sugar metabolism[20] B12 plays a critical role in the creation of new red blood cells which transport oxygen to the brain.

Increased Concentration

What breaks our concentration?

1. Low energy levels

2. Low Acetylcholine levels

3. Most obviously, distractions.

It is important to maintain a healthy diet. This is simply to ensure that there is a source of subsistence that the body can use to produce energy. Low energy levels are correlated with a poor diet or deficiency in essential vitamins.

The ability to focus can be attributed to adequate levels of acetylcholine and levels of energy available in the body. First is to ensure sufficient levels of acetylcholine are available for use in the brain, as acetylcholine has been found to be a neuromodulator which is active during periods of sustained concentration[21] A neuromodulator is a neuron which through the use of neurotransmitters, such as acetylcholine, controls a diverse set of other neurons.  

L-Theanine is another nootropic in Cerebral Key that improves concentration. L-Theanine raises levels of the neurotransmitter GABA in the brain.[22] GABA is the primary inhibitory neurochemical in the brain. This means it suppresses unnecessary neurological activity, resulting in a calm state of mind. This excess neural transmission which is suppressed by L-Theanine is often in the form of distracting stimuli. For instance, when you have caffeine and seem to be more productive, but get distracted by whatever comes up in the moment. This is caused by a raised level of dopamine which results in one being more receptive to stimuli in their environment. This is a benefit of the neurotransmitter dopamine, however, it can often work against us distracting us from the priority task. This is where L-Theanine steps in to balance the distracting stimuli that can occur by a caffeine induced dopamine spike. It has been scientifically proven that the combination of Caffeine and L-Theanine results in improvements of sustained attention, reaction time, and task switching.[23] Furthermore, L-Theanine has also been found to raise levels of alpha brain waves which are associated with relaxation, creativity, selective attention mechanisms, and mental alertness.[24]

Longevity / Health Maintenance

Nootropics and neuroprotection

How does oxidative damage harm the brain?

Reactive oxygen species (ROS) are an unavoidable byproduct of aerobic metabolism. Superoxide is a form of reactive oxygen species which causes damage to cells, specifically DNA and RNA.[25]This could result in the development of a variety of cancers.Oxidative stress is highest when we are physically or emotionally stressed. Oxidative stress damages many parts of a cell including lipids, proteins, DNA and RNA. This damage causes many diseases including cancer, diabetes, rheumatoid arthritis, Alzheimer’s disease, and Parkinson’s disease.[26]

How does beta amyloid plaques harm the brain?

Beta amyloid is a type of plaque like substance that builds up in neurons over time. If enough of this is allowed to build up, it can result in the blocking of cell to cell signaling at synapses. Worse yet, it can result in the activation of immune system cells which trigger inflammation just before destroying disabled cells. This inflammation in some cases starts a chain reaction of cell death and is an underlying mechanism in some neurodegenerative diseases[27]

How do nootropics combat these problems?

 1. Superoxide Dismutase detoxifies superoxide.  This significantly reduces the amount of oxidative damage. Nootropics that increase superoxide dismutase include Bacopa Monnieri and ALCAR. [28][29]

2. Glutathione is one of the most powerful antioxidants made by the body. Production of glutathione has shown to be increased by several nootropics including Bacopa Monnieri and citicoline.[28][30]

3. Vitamin B12, playing a hand in many intracellular processes, contributes to the repair of damaged DNA.[31]

4. Noopept has been shown to attenuate the buildup of beta amyloid plaques. This implies major neuroprotective benefits which could prevent neurodegenerative diseases.[32] Bacopa Monnieri also carries the benefit of preventing beta amyloid plaque build-up.[33]

Regenerate Brain Networks

The D1 dopamine receptor site is in part responsible for neuronal growth. Sulbutiamine increased D1 receptor site density which is commonly depleted through the use of drugs or alcohol. Receptor site density can also be understood as the number of receptors available for neurotransmitters to bind to on a given neuron. The lower the amount of receptors, the less the neurotransmitter will have an impact. In the case of dopamine, a lack of receptors may result in lack of motivation and increased irritability. In this way, by restoring dopamine receptors, sulbutiamine is said to have a regenerative effect on neural networks.[34]

How can nootropics decrease stress?

There is a class of nootropics called adaptogens. Adaptogens are capable of modulating the biological response to stress in a number of ways. We are going to explain how one of these adaptogens works to produce such an incredible benefit. Bacopa Monnieri is a powerful adaptogen which is a key ingredient of the Cerebral Key formula.

Bacopa Monnieri is a natural cognitive enhancer that has been used all over the world for thousands of years. Bacopa Monnieri induces expression of stress response genes, which prepares one for perceived stress and minimizes its impact.[36] Through working in the “background” causing the body at a cellular level to experience stress, the effects of Bacopa Monnieri essentially raise the threshold of stress that the body can process without negative results. It is important to understand that Bacopa Monnieri acclimates the body to stress, but doesn’t cause any stress itself. Additionally, Bacopa Monnieri has been found to prevent reductions in the levels of the neurotransmitters dopamine and serotonin during times of stress. This is significant if we examine what the implications are of low dopamine and serotonin levels.[37] The result of low dopamine and serotonin would appear in the form of feeling tired, unmotivated, and irritable. Does that sound familiar? Bacopa Monnieri reverses this, allowing for a better response to stressful experiences.

Reduce Anxiety

What is anxiety in the brain?

Anxiety is a fear or worries about an event one will experience in the near future. Anxiety is not necessarily always a bad thing. It can serve as a utility to indicate that maybe one should become more prepared to successfully handle that experience. The actual feeling of anxiety is a complex interaction of many neurotransmitters resulting in the activation of the amygdala. The amygdala is the fear center of the brain, and in the case of anxiety, there is some research which supports the theory that the amygdala draws on deep seated emotional memories stored in the hippocampus.[38] These memories could be, in theory, the root cause of the specific anxiety experienced.

How do nootropics reduce anxiety?

L-Theanine promotes the chief inhibitory neuro chemical GABA.[39] GABA is able to suppress neural activity which is unnecessary which can lead to a more calm state of mind. So if we assume that the “unnecessary neural activity” is, in fact, all negative thoughts that are related to the specific anxiety experienced, then suppression of these thoughts is anxiety reducing in function.

Noopept is another nootropic which has noted benefits of reducing anxiety.

Noopept’s major metabolite appears to induce an anxiolytic effect.[40] The underlying mechanism that results in the anxiety reducing properties is not completely understood, but it is hypothesized that there is an endogenous system which co regulates memory and anxiety. Noopept has been found to possess an inhibitory characteristic on postsynaptic currents in the hippocampus. In theory, this could be where the past memory which is the source of a specific anxiety is blocked. Again the details are unknown, but noopept supplementation has been shown to produce Anxiety reducing effects. [41]

How do nootropics increase creativity?

  1.    Increase Spatial memory ( relational/visual thinking )
  2.    Increase Alpha Waves associated with higher creativity.
  3.    Increased inspiration through enhanced sensory experiences.
  4.    Increased communication between the 2 hemispheres of the brain

Noopept has been shown to sensitize the acetylcholine processes and stimulate delivery of acetylcholine to neurons.[10] Acetylcholine enhances sensory experiences, the senses being what one sees, hears, and feels. This can be very rewarding for creative work and will likely become one’s preferred state.

Noopept also results in improvements of spatial memory.[42][43] Spatial memory is often explained as the source of how one is able to remember how to navigate to work or school, however, this explanation is limiting. Spatial memory is also known as relational thinking or visual thinking. Relational thinking may be used to understand the cause and effect relationships of elements of one’s work. This is a skill that is used by scientists and artists alike to push the boundaries of their work. To creatively design something that has been inspired by the relational thinking. Relational thinking is a major source of innovation when used effectively. Visual thinking is more of a synthesis of knowledge and experience. To visualize something that does not yet exist is the essence of creation. It is the first creation. In this way nootropics, such as noopept can sharpen the tools in the creative work shed of the mind.

Alpha brain waves have been associated with higher creativity and creative thinking.[44] Noopept and L-Theanine have both been proven to increase Alpha brain waves when supplemented.[24][45] The experience of being in an alpha brainwave state is often described as a meditative state, where insights frequently occur.

Noopept is hypothesized to increase communication between the 2 hemispheres of the brain resulting in increased creativity.This is achieved by increased synaptic growth between the 2 hemispheres.  Let us explore the natural state of the brain regarding the differences between the 2 hemispheres. The Left brain is responsible for consistent habit / or staying the same. It is also wired to check if ideas are aligned with accepted societal views. While the right brain is more receptive to new ideas, adapting and changing behavior to achieve better results, as well as producing creative solutions. Changing habits, assumptions about the world, and behavior is not the default state of thinking for people, but with increased communication between the 2 hemispheres of the brain, the result is literally a more open mind. This result allows for a greater source of creative insight to be drawn from.

 

 Logo of Cerebral Key

References
  1. Himmelheber, AM; Sarter, M; Bruno, JP et al “Increases in cortical acetylcholine release during sustained attention performance in rats”. Brain research. Cognitive brain research (2000) 9 (3): 313–25. doi:10.1016/S0926-6410(00)00012-4. PMID 10808142
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782876/
  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659740/
  4. RP Patrick, BN Ames et al “Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior.” FASEB J. 2015 Jun;29(6):2207-22. doi: 10.1096/fj.14-268342. Epub 2015 Feb 24.
  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4069480/
  6. Stough C, Lloyd J, Clarke J, Downey LA, Hutchison CW, Rodgers T… et al “The chronic effects of an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects” . Psychopharmacology (Berl). (2001) Jul;232(13):2427
  7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC41066/
  8. https://www.ncbi.nlm.nih.gov/pubmed/9331355/
  9. https://www.ncbi.nlm.nih.gov/pubmed/11520933
  10. https://www.ncbi.nlm.nih.gov/pubmed/19240853
  11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659740/
  12. https://www.ncbi.nlm.nih.gov/pubmed/26834586
  13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978258/
  14. Charles PD, Ambigapathy G, Geraldine P, Akbarsha MA, Rajan KE et al “Bacopa monniera leaf extract up-regulates tryptophan hydroxylase (TPH2) and serotonin transporter (SERT) expression: implications in memory formation” . J Ethnopharmacol. (2011) Mar 8;134(1):55-61. doi: 10.1016/j.jep.2010.11.045. Epub 2010 Dec 1
  15. Musicco C, Capelli V, Pesce V, Timperio AM, Calvani M, Mosconi L… et al “Rat liver mitochondrial proteome: changes associated with aging and acetyl-L-carnitine treatment”. 2011 Oct 19;74(11):2536-47. doi: 10.1016/j.jprot.2011.05.041. Epub 2011 Jun 6
  16. Mehta S et al “ Activation and transportation of fatty acids to the mitochondria via the carnitine shuttle”. (October 6, 2013) Retrieved from http://pharmaxchange.info/press/2013/10/activation-and-transportation-of-fatty-acids-to-the-mitochondria-via-the-carnitine-shuttle-with-animation/
  17. Huang ZL, Urade Y, Hayaishi O et al “The role of adenosine in the regulation of sleep” . Curr Top Med Chem. 2011;11(8):1047-57.
  18. Okada M, Kawata Y, Kiryu K, Mizuno K, Wada K, Tasaki H… et al Effects of adenosine receptor subtypes on hippocampal extracellular serotonin level and serotonin reuptake activity . J Neurochem. (1997)Dec;69(6):2581-8.
  19. Cha YS, Choi SK, Suh H, Lee SN, Cho D, Li K et al “Effects of carnitine coingested caffeine on carnitine metabolism and endurance capacity in athletes” . J Nutr Sci Vitaminol (Tokyo). (2001) Dec;47(6):378-84
  20. https://www.ncbi.nlm.nih.gov/pubmed/15476449
  21. https://www.ncbi.nlm.nih.gov/pubmed/10808142
  22. Kimura R, Murata T et al “Influence of alkylamides of glutamic acid and related compounds on the central nervous system. I. Central depressant effect of theanine” . Chem Pharm Bull (Tokyo). (1971) Jun;19(6):1257-61.
  23. Einöther SJ, Martens VE, Rycroft JA, De Bruin EA et al “L-theanine and caffeine improve task switching but not intersensory attention or subjective alertness” . Appetite. (2010) Apr;54(2):406-9. doi: 10.1016/j.appet.2010.01.003. Epub 2010 Jan 15.
  24. Song CH, Jung JH, Oh JS, Kim KS et al “Effects of Theanine on the Release of Brain Alpha Wave in Adult Males”. Korean J Nutr. 2003 Nov;36(9):918-923. Korean.
  25. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC19375/
  26. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3614697/
  27. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2813509/
  28. Bhattacharya SK, Bhattacharya A, Kumar A, Ghosal S et al “Antioxidant activity of Bacopa monniera in rat frontal cortex, striatum and hippocampus” . Phytother Res. (2000) May;14(3):174-9
  29. https://www.ncbi.nlm.nih.gov/pubmed/25776802
  30. https://www.ncbi.nlm.nih.gov/pubmed/11588329
  31. Banerjee RV, Matthews RG (1990). “Cobalamin-dependent methionine synthase”. The FASEB Journal 4 (5): 1450–9. PMID 2407589.
  32. https://www.ncbi.nlm.nih.gov/pubmed/17092975
  33. https://www.ncbi.nlm.nih.gov/pubmed/22074576
  34. Trovero F, Gobbi M, Weil-Fuggaza J, Besson MJ, Brochet D, Pirot S et al “Evidence for a modulatory effect of sulbutiamine on glutamatergic and dopaminergic cortical transmissions in the rat brain”. Neurosci Lett (2000) 292 (1):
  35. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2630359/
  36. Chowdhuri DK, Parmar D, Kakkar P, Shukla R, Seth PK, Srimal RC et al “Antistress effects of bacosides of Bacopa monnieri: modulation of Hsp70 expression, superoxide dismutase and cytochrome P450 activity in rat brain” . Phytother Res. (2002) Nov;16(7):639-45
  37. Sheikh N, Ahmad A, Siripurapu KB, Kuchibhotla VK, Singh S, Palit G et al “Effect of Bacopa monniera on stress induced changes in plasma corticosterone and brain monoamines in rats” . J Ethnopharmacol. (2007) May 22;111(3):671-6. Epub 2007 Jan 30
  38. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055419/
  39. Kimura R, Murata T et al “Influence of alkylamides of glutamic acid and related compounds on the central nervous system. I. Central depressant effect of theanine” . Chem Pharm Bull (Tokyo). (1971) Jun;19(6):1257-61.
  40. https://www.ncbi.nlm.nih.gov/pubmed/17369939
  41. https://www.ncbi.nlm.nih.gov/pubmed/11550054
  42. http://www.sciencedirect.com/science/article/pii/S0092867403001223
  43. https://www.ncbi.nlm.nih.gov/pubmed/18214292
  44. http://www.sciencedirect.com/science/article/pii/S0010945215001033
  45. https://www.ncbi.nlm.nih.gov/pubmed/21414388