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Sharpen Your Memory With These Nootropics

Sharpen Your Memory With These Nootropics

How many times have you heard someone say “Oh, what was the name of...?”. This is a prime example of a lagging memory and sub-optimal memory performance. You see, the modern lifestyle is fast-paced. We are constantly being exposed to new information, which is often-times, completely irrelevant, and does not serve us in any way. This places great stress on the brain to filter out which information is required for storage or clearance. Memory can be defined as a multifaceted learning process that allows us to store new information and access stored information (1). At its core, the word memory comes from the Latin memoria, meaning "mindful "and memor, "remembering." But this definition is deceptively simple. Like other cognitive functions, memory isn't just a single thing.

However, one must also understand the many aspects of memory. These can be further classified into various sub-types.

  1. Long-Term Memory. 
  2. Short-Term Memory.
  3. Explicit Memory. 
  4. Implicit Memory. 
  5. Declarative
  6. Procedural
  7. Episodic 
  8. Semantic.
  9. Retrospective
  10. Prospective.

So apart from maintaining a healthy diet, proper sleep, correcting nutrient deficiencies, adequate movement/exercise and stress management - which nootropics can specifically help one to achieve optimal memory performance?
In this article, an explanation regarding the mechanisms involved in learning and memory will be explored. In addition, an analysis of the critical roles certain neurotransmitters play on memory performance will be explored. Furthermore, an understanding of the key pathophysiological states whereby memory performance is compromised will be presented. Finally, a clear description of the most well-researched nootropics to support memory performance will be analysed. 

How Memory Is Formed In The Human Brain

Packed into a kilogram or so of neural wetware between the ears is everything we think we know: A compendium of useful and trivial facts about the world, the history of our lives, plus every skill we’ve ever learned, from riding a bike to persuading a loved one to take out the trash. Memories make each of us unique, and they give continuity to our lives. Understanding how memories are stored in the brain is an essential step toward understanding ourselves (2). 

We must aim to classify and clarify, from a neuroanatomical, neurophysiological, and psychological perspective, different memory models that are currently widespread in the literature as well as to describe their origins (3).

Memory is precisely the capacity that allows us to connect experiences, learn and make sense of our lives. In short, it allows us to build our story (3).  It’s important to first have an understanding regarding the breakdown of the 3 phases of memory. 

The encoding phase, storage phase and retrieval phase.

The first phase, is known as the encoding phase. This is where information comes into our memory system (from sensory input), and needs to be changed into a form that the system can cope with, so that it can be stored.

Think of this as similar to changing your money into a different currency when you travel from one country to another. For example, a word which is seen (in a book) may be stored if it is changed (encoded) into a sound or a meaning (i.e. semantic processing) (4). 

There are three main ways in which information can be encoded (changed):

  1. Visual (picture)
  2. Acoustic (sound)
  3. Semantic (meaning)

The second phase is the "Storage" phase

This in regards to the nature of memory stores, i.e., where the information is stored, how long the memory lasts for (duration), how much can be stored at any time (capacity) and what kind of information is held.
The way we store information impacts the way we retrieve it. There has been a significant amount of research regarding the differences between short term memory (STM) and long term memory (LTM).
Information can only be stored for a brief duration in STM (0-30 seconds), but LTM can last a lifetime (5). 

The final phase is the “Memory” retrieval phase.

This refers to the access of information from storage. If we can’t remember something, it may be because we are unable to retrieve it. When we are asked to retrieve something from memory, the differences between STM and LTM become apparent.

STM is stored and retrieved sequentially. For example, if a group of participants are given a list of words to remember, and then asked to recall the fourth word on the list, participants go through the list in the order they heard it in order to retrieve the information.

LTM is stored and retrieved by association. This is why you can remember what you went upstairs for if you go back to the room where you first thought about it.

Organizing information can help aid retrieval. You can organize information in sequences (such as alphabetically, by size or by time). Imagine a patient being discharged from hospital whose treatment involved taking various pills at various times, changing their dressing and doing exercises. If the doctor gives these instructions in the order which they must be carried out throughout the day (i.e., in the sequence of time), this will help the patient remember them (6). 

Neurotransmitters That Impact Memory Performance

Several neurotransmitters including acetylcholine (ACh), glutamate, ?-amino-butyric acid (GABA), and catecholamines have been investigated in a variety of memory models, with considerable evidence of extracellular level variations that correlated with changes in neuronal activity during memory formation (7).

As is the case for most of the brain, the major excitatory neurotransmitter for the prefrontal cortex is glutamate and the major inhibitory neurotransmitter is GABA. While these neurotransmitters are necessary for prefrontal neuronal activity and are involved in the focal specificity of this activity, modulatory neurotransmission in the PFC has been shown to play a prominent role in working memory. Prefrontal dopamine neurotransmission, in particular, has been shown to be important for working memory in animals and in humans. Previous findings have demonstrated the involvement of catecholamines (dopamine and norepinephrine) in working memory (8).

Acetylcholine could also enhances encoding by enhancing long-term potentiation (LTP). Acetylcholine enhances LTP in many areas, including the hippocampus, entorhinal cortex and piriform cortex. Recent studies also demonstrate nicotinic enhancement of long-term potentiation.
In summary, there is increasing convergence of research on the role of acetylcholine in learning and memory. Top-down behavioral approaches have become more focused in using anatomically localized manipulations of cholinergic modulation. Bottom up cellular data from brain slice physiology can be linked to behavior by use of detailed computational models. In the section below, you will have a greater understanding of how we can influence acetylcholine production and efficiency (9).

Glutamate is the most abundant excitatory neurotransmitter in the brain. Excitatory has a very specific meaning in neuroscience, in general terms, an excitatory neurotransmitter increases the likelihood that the neuron it acts upon will have an action potential (also called a nerve impulse). When an action potential occurs the nerve is said to fire, with fire, in this case, being somewhat akin to the completion of an electric circuit that occurs when a light switch is turned on. The result of neurons firing is that a message can be spread throughout the neural circuit. It is estimated that well over half of all synapses in the brain release glutamate, making it a critical  neurotransmitter for neural circuit communication and memory (10). 

Disease States And Factors That Contribute To Impaired Memory Performance:

Alcohol and smoking use: Excessive alcohol intake kills brain cells and impairs cognitive function, including memory, over time. Alcohol abuse may even increase the risk of dementia. Because of alcohol's brain toxicity, experts recommend limiting your alcohol intake to one or two drinks per week. Alcohol primarily interferes with the ability to form new long-term memories, leaving intact previously established long-term memories and the ability to keep new information active in memory for brief periods. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments (11).

Chronic Stress: Exams, tight deadlines and interpersonal conflicts are just a few examples of the many events that may result in high levels of stress in both students and teachers. Research over the past two decades identified stress and the hormones and neurotransmitters released during and after a stressful event as major modulators of human learning and memory processes, with critical implications for educational contexts. While stress around the time of learning is thought to enhance memory formation, thus leading to robust memories, stress markedly impairs memory retrieval (12). There are many mechanisms by which stress can impair memory, but the main factor appears to be related to impaired hippocampal and hypothalamic functioning.

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Dehydration: Severe dehydration can cause temporary cognitive impairment, including memory loss, confusion, and other symptoms of dementia.

No matter how mild, dehydration is not a desirable condition because there is an imbalance in the homeostatic function of the internal environment. This can adversely affect cognitive performance, not only in groups more vulnerable to dehydration, such as children and the elderly, but also in young adults. However, few studies have examined the impact of mild or moderate dehydration on cognitive performance. This paper reviews the principal findings from studies published to date examining cognitive skills. Being dehydrated by just 2% impairs performance in tasks that require attention, psychomotor, and immediate memory skills, as well as assessment of the subjective state (13).

Nutrient deficiencies:

Selenium: The major function of selenium, is it’s antioxidant role, played through selenoprotein P (SePP) and the enzymes glutathione peroxidase (GPx), thus aiding with total body antioxidant defences. Some studies suggest that cognitive decline is associated with a decrease in GPx activity, therefore low selenium intake can adversely affect memory performance (14)

Choline: This nutrient is used by the body to produce acetylcholine, an important neurotransmitter essential for brain and nervous system functions including memory (15).

B-Vitamins: Recent research has highlighted the potential impact of nutritional factors and individual micronutrients on the brain and on cognitive performance, especially in older adults. The B vitamins, folate, B12, and B6, are of particular interest because even subclinical deficiencies in these vitamins are thought to be relatively common in the general population and in older adults in particular (16).

Depression: Objective assessments of cognitive performance suggest that patients with melancholic depression have significantly greater impairment in memory and executive function, compared with patients with non-melancholic depression. In addition, severity of symptoms,17–19 cumulative duration of depressive episodes and presence of comorbidities,  were all independently and negatively correlated with cognitive function (17).

Traumatic Brain Injury (TBI): The studies on memory deficit following TBI’s can be clinically driven using standard memory tests or theoretically driven using measures of specific aspects of memory within well-controlled experimental paradigms. In clinical practice, the results of memory assessments are used to monitor progress during treatment with, for example, medication and cognitive remediation programs (18). There are many nootropics that can help restore damage from TBI’s, which will be explored below.

Sleep Deprivation:  Today, prolonged wakefulness is a widespread phenomenon. Nevertheless, in the field of sleep and wakefulness, several unanswered questions remain. Prolonged wakefulness can be due to acute total sleep deprivation (SD) or to chronic partial sleep restriction. 

According to the well-controlled studies, the less sleep obtained due to sleep restriction, the more cognitive performance is impaired. The negative effect of both acute total and chronic partial SD on attention and working memory is supported by existing literature. Total SD impairs a range of other cognitive functions as well (19). 

Diabetes: The long-term risk of dementia increases in patients with diabetes by a factor of two (20).

Cognitive deficits may occur at the very earliest stages of diabetes and are further exacerbated by the metabolic syndrome. The duration of diabetes and glycemic control may have an impact on the type and severity of cognitive impairment, but as yet we cannot predict who is at greatest risk of developing cognitive impairment. The patho-physiology of cognitive impairment is multifactorial, although dysfunction in each interconnecting pathway ultimately leads to discordance in metabolic signaling. The pathophysiology includes defects in insulin signaling, autonomic function, neuroinflammatory pathways, mitochondrial (Mt) metabolism, the sirtuin-peroxisome proliferator-activated receptor-gamma co-activator 1? (SIRT-PGC-1?) axis, and Tau signaling (20).

Researched Nootropics To Support Memory Performance 

Rhodiola Rosea

Rhodiola rosea L. (R. rosea L.) is widely used to stimulate the nervous system, extenuate anxiety, enhance work performance, relieve fatigue, and prevent high altitude sickness.

The possible mechanisms of R. rosea L. for learning and/or memory function are through antioxidant, cholinergic regulation, anti-apoptosis activities, anti-inflammatory, improving coronary blood flow, and cerebral metabolism. One major article provides the first-ever comprehensive preclinical systematic review of Rhodiola Rosea for cognitive behavior in animal studies and the findings indicated that Rhodiola Rosea improves learning and memory function in experimental models and in some preclinical studies in humans (21). 

Curcumin

Mice fed a curcumin diet had better working and long-term memory in a dose-dependent manner. These mice also had a reduction in the amyloid beta 42 (A?42) aggregates and better clearance of the dissolved aggregates. There was a significantly higher number of autophagosomes in the CA1 region of the curcumin groups along with an increased expression of Beclin 1 and downregulation of the PI3K/Akt/mTOR signaling pathway; these are biomarkers of autophagy - AKA, cell death (22).

Due to various effects of curcumin, such as decreased Beta-amyloid plaques, delayed degradation of neurons, metal-chelation, anti-inflammatory, antioxidant and decreased microglia formation, the overall memory in patients with Alzheimer's disease has improved (23).

Based on the main findings detailed above, curcumin will lead to a promising treatment for Alzheimer's disease.

Panax Ginseng

Numerous preclinical studies have confirmed that ginseng and its active components such as ginsenosides, gintonin, and compound K are pharmacologically efficacious in different models of and are linked to cognitive impairment. Among their several roles, they act as an anti-neuroinflammatory and help fight against oxidative stress and modulate the acetylcholine signaling.

Ginsenosides Rd has the potential for treating cognitive impairment in several model studies. In an amyloid ?-protein precursor (APP) transgenic (Tg) mice model, Rd improved learning and memory probably via inhibiting the transcription activity of NF-?B. Suppression of the transcription activity of the NF-?B pathway might have led to the reduction of proinflammatory cytokines, and the generation of protective factors eventually increased (24).

In addition, one study found that ginseng administration (50 mg/kg) led to increased dopamine and norepinephrine in the brainstem and increased serotonin in the cortex (25), which may influence memory function. 

Bacopa Monnieri:

The major compounds present in this herb, that have been subject to rigorous research over the years are the bacosides. These have the potential to regenerate other antioxidants, including brain-protective enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx). Bacopa Monnieri’s antioxidant activity has also been suggested to counter irregular protein clusters in the brain that are associated with degeneration.

Bacopa Monnieri is considered an adaptogen herb that helps to strengthen the body’s resistance to stress. Some animal research seems to support this possibility, with one finding that Bacopa Monnieri supplementation appears to modulate certain stress hormones and markers in the brain. Researchers interpreted these results as preparing the brain for clear, quick thinking in stressful situations.

Animal research suggests that this nootropics may increase cerebral blood flow by 25% in rats, a bioactivity described by researchers as a “pro-cognitive” effect.

Bacopa Monnieri also supports the production of acetylcholine, a key neurotransmitter for memory, sharp mental performance and long-range brain health. In animal research, Bacopa’s acetylcholine support has been suggested to help learning and memory (26). 


References

1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5491610/ 
2. https://www.ncbi.nlm.nih.gov/pubmed/15994538 
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5491610/ 
4. https://www.ncbi.nlm.nih.gov/pubmed/19847359 
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246028/ 
6. https://www.simplypsychology.org/memory.html 
7. https://www.ncbi.nlm.nih.gov/books/NBK3921/ 
8. http://learnmem.cshlp.org/content/14/8/554.full.html 
9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659740/ 
10. https://www.ncbi.nlm.nih.gov/pubmed/12644276 
11. https://www.ncbi.nlm.nih.gov/pubmed/15303630 
12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6380371/ 
13. https://www.ncbi.nlm.nih.gov/pubmed/22855911 
14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3656646/ 
15. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5579609/ 
16. https://academic.oup.com/psychsocgerontology/article/56/6/P327/610645 
17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304584/
18. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796352/
19. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2656292/
20. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5528145/
21. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288277/
22. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5964053/ 
23. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781139/
24. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6173364/
25. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659585/
26. https://www.ncbi.nlm.nih.gov/pubmed/23772955