an older lady dealing with amnesia



Last Section Update: 08/2013

Contributor(s): Shayna Sandhaus, PhD

1 Overview

Summary and Quick Facts for Amnesia

  • Amnesia, or memory loss, occurs when there is a problem with the way the brain stores or retrieves memories. Amnesia can result from a medical condition or physical trauma (organic amnesia) and/or emotional trauma (functional amnesia) that causes memories to be improperly stored or lost.
  • This protocol will provide an overview of the neurological processes underlying memory and how alteration of neural signaling in the brain can lead to amnesia. Various possible causes of amnesia will be outlined, as will several novel therapeutic avenues currently being explored.
  • A number of scientifically studied natural interventions may help support memory storage and retrieval. Natural interventions such as choline and phosphatidylserine may help improve memory and aid cognition.

What is Amnesia?

Amnesia, or memory loss, occurs when there is a problem with the way the brain stores or retrieves memories. Amnesia can result from a medical condition or physical trauma (organic amnesia), and/or emotional trauma (functional amnesia) that causes memories to be improperly stored or lost.

Anterograde amnesia is when the ability to recall information presented after the onset of amnesia is severely impaired; retrograde amnesia is when information acquired before the onset of amnesia is impaired. Both types of amnesia can be present at once.

Natural interventions such as choline and phosphatidylserine may help improve memory and aid cognition.

What Can Cause Amnesia?

  • Brain tumors
  • Stroke
  • Radiotherapy
  • Traumatic brain injury
  • Migraine headaches
  • Certain drugs such as benzodiazepines
  • Epilepsy
  • Infections such as Lyme disease, HIV/AIDS, or syphilis
  • Deficiencies of vitamins and other nutrients, such as vitamin B12 or thiamine
  • Alzheimer’s disease and other forms of dementia
  • Excessive alcohol consumption
  • Psychological trauma, and others

What are the Signs and Symptoms of Amnesia?

  • Asking the same questions repeatedly
  • Forgetting appointments
  • Misplacing objects
  • Inability to recall events or previously acquired information

What are Conventional Medical Treatments for Amnesia?

  • If there is an underlying medical condition, treating that may relieve the amnesia (eg, cholinesterase inhibitors and NMDA receptor agonists to treat Alzheimer’s; thiamine supplementation to treat a thiamin deficiency)
  • Psychotherapy

What are Emerging Therapies for Amnesia?

  • Guanfacine, an ADHD medication, may improve memory problems.
  • Piracetam, a synthetic derivative of the neurotransmitter GABA, has gained interest for treating memory problems.
  • Electrical stimulation, such as transcranial direct current stimulation, may improve working memory and recognition.
  • Hormone therapy with pregnenolone and/or dehydroepiandrosterone (DHEA) may have implications for memory disorders.

What Natural Interventions May Be Beneficial for Memory?

  • Choline. Choline is a lipid component that supports the structure and function of neurons. A form of choline, alpha-glycerylphosphorylcholine, has been shown to improve memory, attention, concentration, and cognition in many clinical studies.
  • Phosphatidylserine. Phosphatidylserine, another lipid component of neurons, has been shown to improve cognition, memory, neuron health, and more in multiple clinical studies.
  • B vitamins. The B vitamins (folate, thiamine, B6, and B12) are essential for brain and overall health. High levels of homocysteine, which is associated with B vitamin insufficiency, can damage neurons. Supplementation with B vitamins may slow cognitive decline.
  • Acetyl-L-carnitine. Acetyl-L-carnitine may have various neuroprotective effects. It has been shown in animal models to improve neurodegenerative dysfunction in Alzheimer’s, stroke, head trauma, and others.
  • Coenzyme Q10 (CoQ10). CoQ10 may have neuroprotective action. CoQ10 can protect parts of the brain from ischemic damage (such as from a stroke) and reduced behavioral effects of amnesia in animal models.
  • Pyrroloquinoline quinone (PQQ). Another potentially neuroprotective compound, PQQ, may improve cognitive function and prevent neuronal death associated with amnesia.
  • Omega-3 fatty acids. Supplementation with omega-3 fatty acids is good for brain health and can improve working memory. Animal studies have shown omega-3’s protect the brain from amnesia caused by ischemia, medications, and lead poisoning.
  • Magnesium. Magnesium plays an important role in the central nervous system. Patients with Alzheimer’s may have low levels of magnesium, and supplementation has prevented memory loss in animal models.
  • Ginkgo biloba. Ginkgo biloba is an extensively researched medicinal plant that can improve memory and slow cognitive decline.
  • Other natural interventions that may help cognition and memory include ashwagandha, huperzine A, vinpocetine, and blueberry.

2 Introduction

Formation and recall of memories involve complex neurological processes across multiple parts of the brain (Hassabis 2007; Kwon 2012). Amnesia, or memory loss, occurs when there is a problem with the way the brain stores or retrieves memories (Hardt 2009).

Brain damage, such as occurs in Alzheimer’s and Parkinson’s disease, stroke, or traumatic brain injury, may lead to amnesia, but it can also be caused by traumatic psychological or emotional experiences (Hankey 1988; Sellal 2002; Addante 2012; Zeman 2010; Ally 2012; PubMed Health 2012; Mormino 2009). Memory loss may also arise as a consequence of alcohol or illegal drug use, and some prescription sedative medications such as benzodiazepines can cause amnesia (Jones 2000; PubMed Health 2012; Markowitsch 2013; Erickson 2003; Hirai 2001; Mormino 2009). For many patients amnesia resolves on its own; however, it can be permanent in some cases (Brandt 2006).

Although amnesia can be a symptom of Alzheimer’s disease or vascular dementia, amnesia and dementia are different phenomena (Mohs 1988; Hirai 2001). Dementias are usually associated with more pronounced cognitive deficits that impair activities of daily living. In contrast, amnesia typically affects only memory and, in many cases, patients can function relatively well with some assistance. In addition, dementias typically worsen over time, but amnesia not caused by an underlying progressive pathology is often stable over time (Mohs 1988; Roger 2008; Gerstein 2013; Hirai 2001).

Unfortunately, pharmacological treatments that restore lost memories have yet to be developed. This is because understanding of the neurological framework that underlies memory is still largely incomplete. However, in some forms of amnesia, psychological therapy may help patients recall bits and pieces of lost information and better cope with their condition (Brandt 2006). This protocol will provide an overview of the neurological processes underlying memory and how alteration of neural signaling in the brain can lead to amnesia. Various possible causes of amnesia will be outlined, as will several novel therapeutic avenues currently being explored. A number of scientifically-studied natural interventions that may modulate memory storage and retrieval will also be presented. In addition, readers are encouraged to review the Age-Related Cognitive Decline protocol, which discusses maintenance of overall brain health.

3 Understanding Memory

On a cellular level, memories involve interconnected nerve cells that develop strong connections via a process called long-term potentiation (Morris 2003). Memories are made using several structures in the brain including the amygdala (which processes emotions), limbic cortex (which coordinates sensory input with emotions), and thalamus (which regulates sensory information and alertness) (Rajmohan 2007; Petrovich 2011). However, the hippocampus, located near the middle of the brain, is one of the most important structures for memory (Staniloiu 2012). The hippocampus is thought to serve as a temporary storage space for memories until they can be transferred to other parts of the brain for permanent storage (Nadel 1997; Gräff 2012). Damage to any of these structures can cause amnesia (Deng 2010).

Memory is divided into different categories based upon timeframe:

‘Short-term’ memory allows remembrance of a small amount of information for anywhere from several seconds to a few minutes (Staniloiu 2012).

‘Long-term’ memory facilitates storage and retrieval of memories over a much longer timeframe (Dudai 2002). Long-term memory has been categorized as:

  • Non-declarative or procedural memory, which refers to unconscious memories such as knowing how to ride a bicycle (Ullman 2004).
  • Declarative memory, which refers to memories that can be consciously recalled such as the name of the Capital of the United States. Declarative memory has been categorized based on the type of information that is stored and recalled.
    • Semantic memory involves recalling pieces of information, such as the name of the president or a person’s birthday.
    • Episodic-autobiographical memory allows a person to recall certain events they experienced and to mentally re-experience them (Ullman 2004; Renoult 2012; Staniloiu 2012).

The bridge between short- and long-term memory is termed ‘working memory’; it allows for retention of new information with simultaneous retrieval of older memories (Baddeley 1992; Staniliou 2012).

4 Understanding Amnesia

Amnesia is categorized as organic when it occurs as a result of damage to brain structures due to processes such as infection, degenerative diseases, or stroke. It is categorized as functional when it occurs as a result of a traumatic psychological experience. Typically, organic amnesia allows for retention of older memories, but gives rise to difficulties in acquiring new memories (Moscovitch 2004). Functional amnesia is often characterized by the loss of personal identity (Kritchevsky 2004; Staniloiu 2012). Amnesia can also be classified into different types depending on which aspect of memory is affected; this is often determined by the areas in the brain that are damaged. 

Anterograde Amnesia

Anterograde amnesia refers to the situation wherein people are unable to recall events or information presented to them just a few minutes previously (Dewar 2010). People with anterograde amnesia may have normal memory for anything that happened prior to the onset of amnesia. However, their ability to recall information presented to them after the onset of amnesia is severely impaired (Paller 2009; McLeod 2011). Short-term memory allows people with anterograde amnesia to temporarily retain information, but distraction causes the new information to be lost (Mayes 2010).

Anterograde amnesia is usually caused by damage to the hippocampus or other regions of the brain that work with the hippocampus in making new memories (Gilboa 2006; Aggleton 2008). Additional causes of anterograde amnesia include damage to the temporal lobe and Alzheimer’s disease (Cavaco 2012). Anterograde amnesia sometimes occurs in people treated with benzodiazepines; it can also occur in association with a form of thiamine deficiency called Korsakoff’s syndrome, which is often a complication of chronic alcoholism (Moscovitch 2004; Uzun 2010; Staniloiu 2012).

One interesting feature of anterograde amnesia is that it can specifically affect recognition but not “familiarity” based recall; as a result, people presented with a new object several times may feel as if they have seen the object before but fail to remember when (Gilboa 2006; Aggleton 2008). People with anterograde amnesia may also be able to learn and retain new habits or acquire new perceptual and motor skills, such as reading text from a reflection in a mirror or swinging a golf club (Cavaco 2012).

Retrograde Amnesia

Retrograde amnesia is a deficit in recalling information or memories stored before the onset of the amnesia. One characteristic of retrograde amnesia is that information stored close to the time of brain damage is affected more than the remote memories (Paller 2009). However, this is not always true, especially in the case of extensive brain damage. Retrograde amnesia usually occurs along with anterograde amnesia (Squire 1995). Retrograde amnesia has been associated with damage to the hippocampus or related structures (Winocur 2001; Winocur 2013).

One of the more commonly accepted theories about retrograde amnesia is that damage to the hippocampus impairs a process called memory consolidation. During memory consolidation, memories are first stored in the hippocampus, and then gradually transferred to other parts of the brain so the hippocampus is no longer needed to retain and access them. Retrograde amnesia affects memories made close to the time of injury, but usually does not impact older memories, which have already been consolidated (Squire 2007; Winocur 2013). Retrograde amnesia can result from head injury or can occur along with anterograde amnesia as part of Korsakoff’s syndrome (Paller 2009). Retrograde amnesia can also occur after electroconvulsive therapy (Meeter 2011), a type of infection known as encephalitis (Yoneda 1992), and after epileptic seizures (Hornberger 2010). Another form of retrograde amnesia, called functional retrograde amnesia, is characterized by memory deficits that occur in the absence of identifiable brain injury (Fujiwara 2008). In these cases, it is thought that psychological trauma can induce memory loss.

Transient Global Amnesia

Transient global amnesia is a temporary form of amnesia in which short-term memory is affected (Kirshner 2011; Rison 2012). This condition results in a period of anterograde and retrograde amnesia lasting for less than 24 hours (Kirshner 2011; Bartsch 2010; Megevand 2011). People with transient global amnesia generally are able to recognize family members, preserve intellectual abilities, and maintain remote memories; repetitive questioning is a characteristic sign of transient global amnesia. Anterograde memory is typically the first to be recovered, followed by a “shrinking” of the retrograde amnesia until only a short period of memory loss remains (Kirshner 2011). Transient global amnesia typically affects middle-aged individuals and may be triggered by emotional or physical stress, but the exact cause is unknown (Hunter 2011). Since this form of amnesia is only temporary, no treatment is necessary (Rison 2012).

5 Causes

Many different factors can trigger memory loss:

  • Brain tumors (PubMed Health 2012)
  • Stroke (Novitzke 2008)
  • Radiotherapy (Parkin 1991; Christianson 1994; Warrington 2012)
  • Traumatic brain damage (PubMed Health 2012)
  • Migraine headaches (PubMed Health 2012)
  • Heat stroke (Cha 2013)
  • Medications, such as benzodiazepines (Uzun 2010)
  • Epilepsy (Bilo 2009)
  • Infections (especially of the nervous system) including Lyme disease, HIV/AIDS, or syphilis (PubMed Health 2012)
  • Deficiencies of vitamins and other nutrients, such as vitamin B12 or thiamine (PubMed Health 2012)
  • Alzheimer’s disease and other forms of dementia (Hirai 2001; Ally 2012)
  • Excessive alcohol consumption (Nespor 2004)
  • Coronary artery bypass surgery (Fredericks 2012)
  • General anesthesia (though this is often the desired effect) (Perouansky 2011)
  • Psychological trauma

6 Symptoms and Diagnosis

Symptoms of memory loss depend on the type of memory affected. Patients may have anterograde amnesia, retrograde amnesia, and in some cases a combination of the two (McKay 2009; Mayo Clinic 2011a). Anterograde amnesia, which can be seen in Alzheimer’s disease and age-related cognitive decline, or transient global amnesia can cause people to ask the same questions repeatedly, forget important appointments, misplace objects, or leave appliances on (Cullen 2005; Owen 2007; Hamilton 2009; Kirshner 2011). Memories of recent events are the most likely to be impaired, while older memories may remain intact. Retrograde amnesia, on the other hand, causes people to be unable to recall events or information acquired previously (Mayo Clinic 2011a).

Diagnosing amnesia can be difficult; a comprehensive evaluation is often necessary. The first step usually involves careful examination of the patient’s medical history to determine what type(s) of memory are affected and when the amnesia began. Identification of any underlying health problems that may be causing the amnesia, such as Alzheimer’s disease, tumors, infections, epilepsy, vitamin deficiencies, medications, or brain damage, is also important (Mayo Clinic 2011a). Blood tests such as a chemistry panel and complete blood count, which may reveal underlying conditions or nutritional deficiencies, and radiological imaging of the brain, may help further identify the cause of the amnesia (Sucholeiki 2012). To precisely characterize the memory loss, specialists may administer several tests that help measure concentration, short- and long-term memory, item recall and recognition, and other mental tasks that require an intact memory (Cermak 1996; Kopelman 2007). Identifying possible causes of amnesia as well as the exact way that memory is affected can help direct treatment and coping strategies.

7 Conventional Treatment

Currently, little is available in the way of treatment options for amnesia; no drugs exist for most types of amnesia, and the focus is trying to help compensate for the memory deficit. If a particular cause of the memory loss can be identified, such as an infection, tumor, or side effect of a medication, addressing these conditions may also relieve the amnesia. Because Korsakoff’s syndrome is caused by thiamine deficiency, thiamine supplementation, proper diet, and avoidance of alcohol can help prevent further memory loss and lead to recovery of some lost memory in people with this condition (Mayo Clinic 2011a).

Psychotherapy has also been useful in the treatment of amnesia, especially for people whose amnesia has been caused by emotional or psychological trauma, including post-traumatic stress disorder (PTSD). Psychotherapy, sometimes with the aid of sedating medications, can help people suffering from functional or psychogenic amnesia (amnesia with a psychological cause) regain access to the lost memories (Brandt 2006). When successful, psychotherapy can also reduce the additional emotional strain and anxiety caused by memory loss (Brand 2010). People with other forms of amnesia may also benefit from psychiatric treatment and support groups to help cope with their disorder and develop tools to minimize the impact of the memory loss on their quality of life.

One cause of memory loss that can be treated using conventional medicine is Alzheimer’s disease. There are two classes of medications that can be used to treat amnesia and other cognitive problems caused by Alzheimer’s disease. The first class, cholinesterase inhibitors, increase the amount of acetylcholine, a neurotransmitter that is decreased in the brain of patients with Alzheimer’s disease. Donepezil (Aricept®) is approved to treat all stages of Alzheimer’s disease, and in some patients it temporarily delayed the progression of mild cognitive impairment. Rivastigmine (Exelon®) and galantamine (Razadyne®) are approved to treat mild to moderate disease. The other class of drugs that may help amnesia in Alzheimer’s disease modulates signaling by another important neurotransmitter in the brain called glutamate, which is important for learning and memory. This class of drugs is known as NMDA receptor antagonists, and the only approved medication in this class, memantime (Namenda®), is used for moderate and severe cases of the Alzheimer’s. However, these medications have significant side effects. Cholinesterase inhibitors may cause nausea, diarrhea, and vomiting. Memantine, on the other hand, may cause headache, confusion, agitation, and dizziness (Mayo Clinic 2011b).

8 Novel and Emerging Treatments


Guanfacine is a drug approved by the Food and Drug Administration for treating attention deficit hyperactivity disorder (ADHD), and it has gained interest as a treatment for memory problems (Flight 2011). Guanfacine works by stimulating parts of the brain that respond to the hormone epinephrine (Decamp 2011). This drug was found to improve working memory and attention in animal models (Arnsten 1988; Decamp 2011; McAllister 2011). It has also been shown to improve working memory in humans (Jakala 1999; Swartz 2008). Although this drug has not yet been approved for the treatment of memory disorders in humans, its potential for helping to slow or reverse memory decline remains intriguing, especially as it has already been approved for use in other conditions (Flight 2011).


Piracetam is a synthetic derivative of the inhibitory neurotransmitter gamma-amino butyrate (GABA). There are several piracetam analogues, known as the “racetams,” and these compounds have been studied for their neurological and vascular effects in conditions ranging from ischemic stroke to Alzheimer’s disease since the 1960’s (ClinicalKey 2013). Piracetam has gained interest as researchers work to find treatments for memory problems (Waegemans 2002; Samartgis 2012). Although the exact mechanism by which piracetam works is not fully understood (Rao 2012), it appears to improve cell membrane fluidity (an important aspect of neuronal health), and modulate the flow of ions in and out of neurons (ions are integral components of neuronal signal transduction). Piracetam has been shown to reduce neuron damage associated with oxygen deprivation and reoxygenation in cell culture studies (Solanki 2011) and to improve memory and anxiety in animal models of amnesia (Grossman 2011; Samartgis 2012). Case reports also show that it may be useful in treating amnesia in humans, though there are some concerns in patients with psychiatric disease, as evidence suggests the possibility that piracetam could worsen conditions such as psychosis (Rao 2012). Although more studies are needed to determine if piracetam exerts a meaningful benefit in amnesia, its long history of safe use and its ability to modulate neuronal properties make it a candidate for future research in this area.

Electrical Stimulation

Applying electrical currents to the brain may also treat amnesia. Two different techniques for supplying these currents have been studied. The least invasive is transcranial direct current stimulation, which uses saline-soaked sponge electrodes applied to the surface of the head to deliver mild electrical currents (Hansen 2012). It appears that these mild electrical currents can modulate the way that neurons work (Zaehle 2011; Hansen 2012). Studies have found that transcranial direct current stimulation improves working memory and recognition memory (Ferrucci 2008; Ohn 2008; Tseng 2012; Zaehle 2011). Another method of delivering electrical currents is called deep brain stimulation, in which electrodes are surgically placed inside the brain to deliver mild electrical currents to specific brain regions. One of the first journal articles to describe this possibility was a case report of a man who was receiving deep brain stimulation as a treatment for obesity and, unexpectedly, noticed improved memory (Hamani 2008). Since then, scientists have performed a small study using deep brain stimulation on patients with epilepsy who did not respond to drugs, and have found that these currents could improve the formation of memories of spatial information (Cheng 2012; Suthana 2012).

Hormones and Hormone Replacement Therapy

Changes in hormone levels may also play a role in amnesia. A class of hormones called neurosteroids are synthesized within the nervous system and modulate several aspects of brain function. Two neurosteroids in particular have been implicated in memory disorders: pregnenolone and dehydroepiandrosterone (DHEA) (George 2010). In animals, increasing age has been associated with lower pregnenolone levels. Moreover, memory impairment was associated with low pregnenolone levels, and several animal models revealed that pregnenolone administration into the nervous system improved memory (Mayo 2001; Vallée 1997; Chen 2010; Petit 2011).

In addition to its direct effects on the brain, pregnenolone also serves as a precursor for DHEA. Much like pregnenolone, DHEA levels drop dramatically (by as much as 80%) in old age. This decrease in DHEA may play a role in the gradual decline of memory and cognitive function in the elderly as well as in patients with Alzheimer’s disease (Sorwell 2010). Animal studies found that DHEA supplementation improves memory (Bazin 2009; Ducharme 2010). Although human studies on the effects of DHEA are limited, DHEA also may improve memory in young healthy males (Alhaj 2006).

Other hormones, including estrogen, have also been found to play a role in preventing amnesia in animal models (Gibbs 2011; Durham 2012). In humans, verbal declarative memory was found to be increased in the postmenstrual period of the menstrual cycle, when estrogen levels are high as compared to in the premenstrual period, and verbal memory appears to improve after the administration of estrogens in women who surgically enter menopause (Protopopescu 2008; Henderson 2009). Estrogen supplementation is an especially intriguing target as estrogen has been found to increase the levels of a compound called brain-derived neurotrophic factor (BDNF), which increases the connections between neurons and aids in making memories (Sanchez 2006; Luine 2013).

Progesterone, another important hormone that has neurological functions, may be useful for treating amnesia. Like other neurosteroids, progesterone also affects the growth and development of neurons (Mannella 2012). In animal models, progesterone has been shown to affect the number of connections between nerve cells (Woolley 1993). Progesterone has also been found to reduce chemically induced amnesia in animal models (Tanabe 2004). In addition, post-menopausal women who receive early hormone replacement therapy, including progesterone, have more brain activity in the hippocampus (Smith 2011). Progesterone supplementation has also shown promise in improving the neurological function, and it improved the outcome in patients who suffered traumatic brain injury (Ma 2012; Wright 2007).

Individuals interested in learning more about the benefits of hormone restoration therapy and how to move forward with hormone supplementation are encouraged to review Life Extension’s Male Hormone Restoration or Female Hormone Restoration protocol.

9 Nutrients

The natural interventions outlined in this protocol are limited to those supported by evidence for memory modulation. Since overall brain health can significantly impact the acquisition, consolidation, and recall of memories, readers are encouraged to review the Age-Related Cognitive Decline protocol for additional suggestions.

Choline and Phosphatidylserine

Choline and phosphatidylserine are lipid components that support the structure and function of neurons involved in memory acquisition and recall. Choline plays an important role in the neuronal processes underlying memory via two different mechanisms. First, choline serves as a precursor for the neurotransmitter acetylcholine, which is important for neuronal signaling involved in memory (Poly 2011). Consequently, drugs that increase acetylcholine levels are an important part of treatment for Alzheimer’s disease. Second, the neurons in the brain have high levels of phosphatidylcholine, a lipid found in cell membranes. It is thought that diminished levels of phosphatidylcholine in neurons may contribute to memory loss and other forms of cognitive decline (Kullenberg 2012).

In animal models of memory loss, choline supplementation relieved memory impairment by improving the process of memory consolidation (Blake 2012). Trials in humans have also yielded promising results. Supplementation with alpha-glycerylphosphorylcholine (also known as alpha-GPC), a form of choline, has been found to improve memory and concentration. In young, healthy individuals, alpha-GPC has been shown to prevent drug-induced amnesia (Kidd 2005). Over 23 clinical trials on alpha-GPC have been performed. Some of the benefits observed include improved attention, memory, concentration, and cognition (Brady 2011). This compound has also been found to reduce memory loss and other signs of neurological damage due to stroke (Parnetti 2001; Barbagallo 1994). Another study found that individuals with higher choline intake performed better on memory tests, such as those that measured visual and verbal memory, and other measures of cognitive function (Poly 2011).

Phosphatidylserine, another lipid important for neuron health, is one of the most extensively studied compounds for memory impairment (Kullenberg 2012). Animal studies have found that phosphatidylserine lessened drug-induced amnesia (Vaisman 2009; Claro 2006). In addition, multiple studies show that supplementation with phosphatidylserine, either on its own or complexed with other fats, improves memory in elderly individuals with memory problems (Richter 2010; Kato-Kataoka 2010; Vakhapova 2010). Specifically, phosphatidylserine improves verbal recall of information and may improve cognitive deficits in elderly individuals with memory complaints but without signs of dementia (Richter 2010; Vakhapova 2010). Phosphatidylserine may also improve memory in people with attention deficit hyperactive disorder (Hirayama 2013). In addition to preserving neuron health, phosphatidylserine may be able to improve memory by increasing the levels of both glucose (aiding in the energy consumption of neurons) and acetylcholine in the brain (Kullenberg 2012). Another clinical study found that phosphatidylserine may enhance the effects of Ginkgo biloba, a plant well known for its benefits on brain health (Kennedy 2007).

Life Extension Study: Nutrient Complex May Positively Impact Cognitive Performance

A 2012 study conducted by Life Extension Clinical Research, Inc. assessed the impact of daily dosing of a dietary supplement containing alpha-glycerylphosphorylcholine (alpha-GPC), phosphatidylserine, vinpocetine, grape seed extract, wild blueberry extract, ashwagandha extract, and uridine-5’-monophosphate on cognitive performance in forty middle-aged to elderly subjects with subjective memory complaints.

An online cognitive assessment tool (Computerized Neuropsychological Test) was used to assess the change in cognitive performance from baseline to day 30 and day 60; the Global Impression Improvement (CGI-I) scale provided an overall clinically determined summary measure.

Twenty-nine subjects completed the study with no significant adverse events being reported. This study found a statistically significant improvement in three tests: working memory, inspection time, and executive function. Based on the CGI-I scale, improvement was noted after 30 and 60 days of product dosing.

The study was presented at the Experimental Biology 2012 multidisciplinary scientific conference in San Diego, California April 21-25, 2012.

B Vitamins

B vitamins, including folate, thiamine, pyridoxine (vitamin B6), and vitamin B12, may also have an important role in preventing amnesia. Vitamin B12’s role in maintaining the health of the nervous system is particularly well established, since a lack of vitamin B12 may cause damage to the peripheral nervous system (Tangney 2012). Along with vitamin B12, the importance of folate and vitamin B6 for cognitive function has also come into focus. All of these vitamins are needed to reduce the levels of homocysteine in the brain; homocysteine contributes to vascular dysfunction (Morris 2005; Parletta 2013). Homocysteine levels tend to rise as people age and are associated with an increased risk of Alzheimer’s disease (Seshadri 2002; Tangney 2012).

In addition to its role as a risk factor for stroke, homocysteine is directly toxic to neurons, both in people with Alzheimer’s disease and in healthy individuals. One of the ways in which B vitamins may help prevent amnesia and other forms of cognitive decline is by lowering the levels of homocysteine. They may also help in the synthesis of different neurotransmitters needed for the brain to function properly (Parletta 2013). Low levels of several vitamin B12-related markers are also associated with low brain volume and decreased cognitive function (Tangney 2011; Tangney 2012). A study reported that supplementation with folate, vitamin B12, and vitamin B6 for 2 years slows cognitive decline and improves the clinical status (de Jager 2011), while other studies reported that they can also slow brain atrophy (Tangney 2012; Smith 2010). Ensuring adequate intake of thiamine is an important consideration in the prevention of amnesia, since lack of thiamine can cause Korsakoff’s syndrome, a symptom of which is amnesia (PubMed Health 2013).


The death of neurons within the hippocampus and other regions of the brain is thought to play a role in the development of amnesia. Acetyl-L-carnitine is a substance naturally produced by the body that may have a variety of neuroprotective effects. One of its main roles is to help the mitochondria, colloquially referred to as “cellular powerhouses,” produce energy more efficiently (Goo 2012; Malaguarnera 2011; Barwhal 2009). Moreover, it may help increase the levels of acetylcholine within the brain (Imperato 1989; White 1990; Jiang 2011; Schaevitz 2012). Supplementation with acetyl-L-carnitine has improved neurodegenerative dysfunction in many different animal models, including Alzheimer’s disease (Jiang 2011; Zhou 2011), age-related learning and memory impairment (Kobayashi 2010), poor blood flow/stroke (Barwhal 2009; Goo 2012; Zhang R 2012), and head trauma (Scafidi 2010). Acetyl-L-carnitine also improved cognitive function, including memory, in people with hepatic encephalopathy, a disease caused by liver damage (Malaguarnera 2011).

Coenzyme Q10 and Pyrroloquinoline quinone

Coenzyme Q10 (CoQ10), a naturally occurring vitamin-like substance involved in the cellular production of energy, may have some neuroprotective properties (Massaad 2011; Ishrat 2006). A related compound, pyrroloquinoline quinone (PQQ), may have neuroprotective effects as well (Zhang 2002; Ohwada 2008; Scanlon 1997). Studies of neuron cell cultures and animal models of amnesia have found that both of these substances may improve cognitive function and prevent cell death leading to amnesia (Hassanshahi 2012; Zhang 2002; Hassanshahi 2013; Massaad 2011; Ishrat 2006; Scanlon 1997; Zhang L 2012; Ohwada 2008). One potential cause of amnesia is stroke, which damages the hippocampus and other parts of the brain by depriving them of oxygen (a form of damage known as ischemia). CoQ10 protects the hippocampus and other parts of the brain from ischemic damage, suggesting that it could help prevent amnesia due to stroke (Hassanshahi 2012; Hassanshahi 2013). In animal models, CoQ10 and PQQ have reduced the behavioral effects of amnesia due to traumatic brain injury and amnesia-inducing medications (Zhang L 2012; Ohwada 2008; Ishrat 2006).

Omega-3 Fatty Acids

Omega-3 fatty acids are a class of fats that include docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). In an animal model, these fats were shown to reverse ischemia-induced amnesia, and the improvement was maintained even after treatment was stopped (Fernandes 2008). Increasing intake of these fats, either by eating foods rich in omega-3 fatty acids (such as fatty fish) or taking fish oil supplements, may help protect the brain from amnesia. Studies on animal models of amnesia suggest that long-term treatment with omega-3 fatty acids can protect the brain from amnesia caused by low oxygen levels, medications, and lead poisoning (Fernandes 2008; Ajami 2012; Yadav 2012; Sharma 2012). Moreover, in humans, EPA and DHA supplementation has been shown to improve working memory (Narendran 2012).


Magnesium levels are higher in the fluid surrounding the brain and spine, called cerebrospinal fluid, than in the blood. This suggests magnesium plays an important role in the central nervous system (Slutsky 2010). In an animal model, a diet deficient in magnesium increased memory deficits after brain injury, and the administration of magnesium following acute brain injury significantly reduced tissue damage and improved behavioral outcome. In addition, a study showed that animals undergoing traumatic brain injury and receiving a diet with less magnesium had a higher mortality and worse neurological outcome (Hoane 2008). Evidence also suggests that people with mild-to-moderate Alzheimer’s disease often have diminished magnesium concentrations in their blood (Barbagallo 2011).

Magnesium supplementation also improves memory and reduces memory loss in many animal models of amnesia, suggesting that it could be an effective therapy for treating or preventing memory loss (Liu 2012; Slutsky 2010; Sarreshtehdari 2012; Uysal 2013). Although it is difficult for regular magnesium supplements to gain access to the brain, scientists have developed a modified form of magnesium, called magnesium-L-threonate, which is better able to get into the brain and may be more efficacious (Slutsky 2010).

Ginkgo Biloba

Ginkgo biloba is one of the most extensively researched medicinal plants. It contains two different types of compounds, called flavone glycosides and terpene lactones, which have a variety of health benefits (Blecharz-Klin 2009). Importantly, ginkgo biloba may be able to improve brain health in a variety of ways: by improving energy utilization, preventing neuron death, and modulating neurotransmission (Blecharz-Klin 2009; Tobinaga 2012; Walesiuk 2009; Abdel-Wahab 2012). Trials on humans have yielded promising results: this plant improved memory in healthy middle-aged volunteers and slowed cognitive decline in the elderly (Amieva 2013; Kaschel 2011; Wesnes 2000). Another study reported that ginkgo biloba caused, after 14 days of administration, specific brain activity changes that resulted in improved working memory (Silberstein 2011).


Ashwagandha, also known as Indian ginseng, has been used in Ayurvedic medicine for centuries (Sandhu 2010). Studies suggest it may promote the growth, repair, and regeneration of damaged neurons, especially those that were damaged by Alzheimer’s and Parkinson’s disease and other neurodegenerative conditions (Singh 2011; Konar 2011).

Huperzine A

Huperzine A is a compound derived from the Chinese plant Huperzia serrata. Its role in treating amnesia mainly stems from its ability to reversibly and selectively inhibit acetylcholinesterase. Inhibition of acetylcholinesterase leads to elevation of the neurotransmitter acetylcholine, which is important for memory; some Alzheimer’s disease medications also work by this mechanism (Ye 1999; Malkova 2011; Rafii 2011). In several animal models, huperzine A improved memory and cognitive function (Wang 2010; Shi 2012). It was also shown that, after oral administration for 8-24 weeks, 300-500 mcg of huperzine A daily improved the mental state of Alzheimer’s disease patients and was well tolerated (Wang 2009). It may also benefit people with cognitive deficiencies due to vascular disease (Xu 2012). In addition, huperzine A was shown in animal models to promote the growth of neurons within the hippocampus (Ma 2013).


Vinpocetine, a derivative of the periwinkle plant, may be useful in treating amnesia due to underlying neurological problems. In addition to having neuroprotective effects, vinpocetine may be able to enhance memory by improving the function of neurons in the hippocampus and other parts of the brain that control memory (Deshmukh 2009; Ratra 2011). Animal and cell culture studies have shown that vinpocetine can improve memory and protect neurons from a variety of different types of damage (Deshmukh 2009; Ratra 2011; Solanki 2011; Nyakas 2009; Groó 1987). Note: Women who are pregnant or could become pregnant should not use vinpocetine.


Blueberries are particularly rich in a class of compounds called flavonoids, which may also enhance blood flow to the brain and optimize nerve function (Spencer 2010). Many animal studies have found that supplementing the diet with blueberries enhanced memory (Joseph 2003; Andres-Lacueva 2005; Goyarzu 2004; Casadesus 2004; Coultrap 2008; Ramirez 2005). The effects of blueberry supplementation may modulate some of the biochemical signaling pathways in the hippocampus, which is intricately involved in memory (Williams 2008). A small study on the elderly also found that the daily consumption of blueberry juice for 12 weeks improved memory (Krikorian 2010).


  • Aug: Comprehensive update & review

Disclaimer and Safety Information

This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the therapies discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. Life Extension has not performed independent verification of the data contained in the referenced materials, and expressly disclaims responsibility for any error in the literature.


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