1 Overview

Summary and Quick Facts

  • 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 Targeted Natural Interventions

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).

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.


Abdel-Wahab BA and El-Aziz SMA. Ginkgo biloba protects against intermittent hypoxia-induced memory deficits and hippocampal DNA damage in rats. Phytomedicine 2012; 19: 444-450.

Addante RJ, Ranganath C et al. Neurophysiological evidence for a recollection impairment in amnesia patients that leaves familiarity intact. Neuropsychologia 50(2012)3004–3014.

Aggleton JP. Understanding anterograde amnesia: Disconnections and hidden lesions. The Quarterly Journal of Experimental Psychology 2008; 61(10): 1441-1471.

Ahmad A, Ramakrishna S, Meara J, Doran M. Autoimmune limbic encephalitis: a reversible form of rapidly progressive amnesia and seizures. The Journal of the Royal College of Physicians of Edinburgh 2010;40(2):123-125.

Ajami M, Eghtesadi S et al. Effect of Short and Long-Term Treatment with Omega-3 Fatty Acids on Scopolamine-Induced Amnesia. Iranian Journal of Pharmaceutical Research (2012);11 (2):533-540.

Alhaj HA, Massey AE, McAllister-Williams RH. Effects of DHEA administration on episodic memory, cortisol and mood in healthy young men: a double-blind, placebo-controlled study. Psychopharmacology (Berl). 2006;188(4):541-551.

Ally BA. Using pictures and words to understand recognition memory deterioration in amnestic mild cognitive impairment and Alzheimer's disease: a review. Current Neurology and Neuroscience Reports 2012;12(6):687-694.

Alzoubi KH, Khabour OF et al. The neuroprotective effect of vitamin E on chronic sleep deprivation-induced memory impairment: The role of oxidative stress. Behavioral Brain Research, 2012; 226: 205-210.

Amieva H, Meillon C et al. Ginkgo Biloba Extract and Long-Term Cognitive Decline: A 20-Year Follow-Up Population-Based Study. PLOS One. 2013;8(1): e52755.

Andres-Lacueva C, Shukitt-Hale B et al. Anthocyanins in aged blueberry-fed rats are found centrally and may enhance memory. Nutritional Neuroscience, 2005;8(2):111-120.

Annweiler C, Allali G et al. Vitamin D and cognitive performance in adults: a systematic review. European Journal of Neurology, 2009;16:1083-1089.

Annweiler C, Rolland Y et al. Higher Vitamin D Dietary Intake Is Associated With Lower Risk of Alzheimer’s Disease: A 7-Year Follow-up. Journal of Gerontology, 2012; 67(11):1205-11.

Arnsten AF, Cai JX, Goldman-Rakic PS. The alpha-2 adrenergic agonist guanfacine improves memory in aged monkeys without sedative or hypotensive side effects: evidence for alpha-2 receptor subtypes. The Journal of Neuroscience 1988;8(11):4287-4298.

Baddeley A. Working memory. Science 1992;255(5044):556-559.

Baitharu I, Jain V, Deep SN, Hota KB, Hota SK, Prasad D, Ilavazhagan G. Withania somnifera root extract ameliorates hypobaric hypoxia induced memory impairment in rats. J Ethnopharmacology 2013;145(2):431-41.

Balu M, Sangeetha P et al. Age-related oxidative protein damages in central nervous system of rats: modulatory role of grape seed extract. International Journal of Developmental Neuroscience, 2005; 23: 501-507.

Barbagallo M, Belvedere M et al. Altered ionized magnesium levels in mild-to-moderate Alzheimer's disease. Magnesium Research, 2011; 24(3): 115-121.

Barbagallo Sangiorgi GB, Barbagallo M et al. Alpa-Glycerophophocholine in the Mental Recovery of Cerebral Ischemic Attacks. Annals of the New York Academy of Sciences, 1994: 253-269.

Bartsch T and Deuschi G. Transient global amnesia: functional anatomy and clinical implications. Lancet neurology, 2010; 9: 205-214.

Barwhal K, Hota SK et al. Acetyl-L-Carnitine (ALCAR) Prevents Hypobaric Hypoxia0Induced Spatial Memory Impairment Through Extracellular Related Kinase-Mediated Nuclear Factor Erythroid 2-Related Factor 2 Phosphorylation. Neuroscience, 2009; 161: 501-514.

Bazin M-A, Kihel LE et al. The effects of DHEA, 3-hydroxy-5-androstane-6,17-dione, and 7-amino-DHEA analogues on short term and long term memory in the mouse. Steroids, 2009; 74: 931-937.

Benke T, Köylü B, Delazer M, Trinka E, Kemmler G. Cholinergic treatment of amnesia following basal forebrain lesion due to aneurysm rupture--an open-label pilot study. European Journal of Neurology 2005;12(10):791-796.

Bilo L, Meo R et al. Transient epileptic amnesia: An emerging late-onset epileptic syndrome. Epilepsia, 2009; 50: 58-61.

Blake MG, Boccia MM et al. Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation. Neurobiology of Learning and Memory, 2012; 98: 112-121.

Blecharz-Klin K, Piechal A et al. Pharmacological and biochemical effects of Ginkgo biloba extract on learning, memory consolidation and motor activity in old rats. Acta Neurobiol Exp 2009, 69: 217–231.

Brady D and Copp S. GPC (Glycerophosphocholine). Designs for Health, 2011.

Brand B and Lowenstein RJ. Dissociative Disorders: An Overview of Assessment, Phenomenology and Treatment. Psychiatric Times, 2010: 62-69.

Brandt J and Van Gorp WG. Functional (‘‘Psychogenic’’) Amnesia. Seminars in Neurology, 2006; 26(3): 331-340.

Cantrell DT, Levin HS, Capruso DX, Eisenberg HM. Reversible amnesia associated with a left temporal hematoma in a case of right temporal complex partial seizures. Epilepsia 1994;35(6):1321-1327.

Casadesus G, Barbara S-H et al. Modulation of Hippocampal Plasticity and Cognitive Behavior by Short-term Blueberry Supplementation in Aged Rats. Nutritional Neuroscience, 2004; 7: 309-316.

Cavaco S, Feinstein JS et al. Musical memory in a patient with severe anterograde amnesia. Journal of Clinical abd Experimental Neuropsychology, 2012; 34(10): 1089-1100.

Cermak LS, Verfaellie M, et al. Effect of spaced repetitions on amnesia patients’ recall and recognition performance. Neuropsychology 1996;10(2):219-227.

Cha SY, Kang TH, Kim SJ, Lee HY, Kim HJ, Jung DS, Kim EJ. Selective anterograde amnesia associated with hippocampal and splenial damage after heat stroke. Clinical Neurology and Neurosurgery 2013 Apr 18;PubMed PMID: 23602221.

Chan A, Remington R et al. A Vitamin/Nutriceutical Formulation Improves Memory and Cognitive Performance in Community-Dwelling Adults Without Dementia. The Journal of Nutrition, Health and Aging, 2010; 14(3): 224-230.

Chen L, Cai W et al. Modulatory Metaplasticity Induced by Pregnenolone Sulfate in the Rat Hippocampus: A Leftward Shift in LTP/LTD-Frequency Curve. Hippocampus, 2010; 20: 499-512.

Cheng JJ and Anderson WS. Deep Brain Stimulation of Entorhinal Cortex Shows Early Promise for Enhancement of Memory Function. Neurosurgery, 2012; 71(2): N24-N25.

Christianson SA, Neppe V, Hoffman H. Amnesia and vegetative abnormalities after irradiation treatment: a case study. Acta Neurologica Scandinavica 1994;90(5):360-366.

Claro FT, Patti CL, Abilio VC, Frussa-Filho R, Silva RH. Bovine brain phosphatidylserine attenuates scopolamine induced amnesia in mice. Progress in neuro-psychopharmacology & biological psychiatry. Jul 2006;30(5):881-886.

ClinicalKey. Piracetam. Available at: Accessed 7/29/2013.

Coultrap SJ, Bickford PC, Browning MD. Blueberry-enriched diet ameliorates age-related declines in NMDA receptor-dependent LTP. Age (Dordr) 2008;30(4):263-272.

Cullen B, Coen RF, Lynch CA, Cunningham CJ, Coakley D, Robertson IH, Lawlor BA. Repetitive behaviour in Alzheimer's disease: description, correlates and functions. International Journal of Geriatric Psychiatry 2005;20(7):686-693.

de Jager CA, Oulhaj A et al. Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment: a randomized controlled trial. International Journal of Geriatric Psychiatry, 2012; 27: 592-600.

Decamp E, Clark K et al. Effects of the alpha-2 adrenoceptor agonist guanfacine on attention and working memory in aged non-human primates. European Journal of Neuroscience, 2011; 34: 1018-1022.

Deng W, Aimone JB, Gage FH. New neurons and new memories: how does adult hippocampal neurogenesis affect learning and memory?. Nature Reviews Neuroscience 2010;11(5):339-350.

Deshmukh R, Sharma V et al. Amelioration of intracerebroventricular streptozotocin induced cognitive dysfunction and oxidative stress by vinpocetine — a PDE1 inhibitor. European Journal of Pharmacology, 2009; 620: 49-56.

Devi SA, Jolitha AB et al. Grape Seed Proanthocyanidin Extract (GSPE) and Antioxidant Defense in the Brain of Afult Rats. Med Sci Monit, 2006; 12(4): BR124-129

Dewar M, Salas SD et al. Profound Retroactive Interference in Anterograde Amnesia: What interferes? Neuropsychology, 2010; 24(3): 357-367.

Ducharme N, Banks WA et al. Brain distribution and behavioral effects of progesterone and pregnenolone after intranasal or intravenous administration. European Journal of Pharmacology, 2010; 641: 128-134.

Dudai Y. Molecular bases of long-term memories: a question of persistence. Current Opinion in Neurobiology 2002;12(2):211-216.

Durham JL, Jordan KA et al. Estradiol protects against hippocampal damage and impairments in fear conditioning resulting from transient global ischemia in mice. Brain Research, 2012; 1443: 64-74.

Erickson CA and Barnes CA. The neurobiology of memory changes in normal aging. Experimental Georntology, 2003; 61-69.

Fernandes JS, Mori MA et al. Long-term treatment with fish oil prevents memory impairments but not hippocampal damage in rats subjected to transient, global cerebral ischemia. Nutrition Research, 2008; 28: 798-808.

Ferrucci R, Manelli F et al. Transcranial direct current stimulation improves recognition memory in Alzheimer disease. Neurology, 2008; 71(7): 493-498.

Filgueiras CC, Krahe TE, Medina AE. Phosphodiesterase type 1 inhibition improves learning in rats exposed to alcohol during the third trimester equivalent of human gestation. Neuroscience Letters 2010;473(3):202-207.

Flight MH. Rescuing age-related memory loss. Nature Reviews Neurosciences, 2011; 12(9):490-1.

Fredericks S. Memory loss following coronary artery bypass graft surgery: a discussion of the implications for nursing. Canadian Journal of Cardiovascular Nursing 2012 Spring;22(2):33-6.

Fujiwara E, Brand M et al. Functional retrograde amnesia: A multiple case study. Cortex, 2008; 44: 29-45.

George O, Vallee M et al. Low Brain Allopregnanolone Levels Mediate Flattened Circadian Activity Associated with Memory Impairments in Aged Rats. Biological Psychiatry, 2010; 68: 956-963.

Gerstein, Paul S. "Delirium, Dementia, and Amnesia in Emergency Medicine ." Medscape. WebMD, 2013. Web. 19 May 2013. <>.

Gibbs RB, Chipman AM et al. Donepezil plus estradiol treatment enhances learning and delay-dependent memory performance by young ovariectomized rats with partial loss of septal cholinergic neurons. Hormones and Behavior, 2011; 59: 503-511.

Gilboa A, Winocur G et al. Hippocampal Contributions to Recollection in Retrograde and Anterograde Amnesia. Hippocampus, 2006; 16: 966-980

Gold PE. The many faces of amnesia. Learn. Mem. 2006 13: 506-514.

Goo M-J, Choi SM et al. Protective Effects of Acetyl-L-Carnitine on Neurodegenarative Changes In Chronic Cerebral Ischemia Models and Learning-Memory Impairment in Aged Rats. Archives of Pharmacal Research, 2012; 35(1): 145-154.

Goyarzu P, Malin DH et al. Blueberry Supplemented Diet: Effects on Object Recognition Memory and Nuclear Factor-kappa B Levels in Aged Rats. Nutritional Neuroscience, 2004; 7(2): 75-83.

Gräff J, Woldemichael BT, Berchtold D, Dewarrat G, Mansuy IM. Dynamic histone marks in the hippocampus and cortex facilitate memory consolidation. Nature Communications 2012;3:991.

Groó D, Pálosi E, Szporny L. Effects of vinpocetine in scopolamine-induced learning and memory impairments. Drug Development Research 1987;11:29-36.

Grossman L, Stewart A et al. Effects of piracetam on behavior and memory in adult zebrafish. Brain Research Bulletin, 2011; 85: 58-63.

Hamani C, McAndrews MP et al. Memory Enhancement Induced by Hypothalamic/Fornix Deep Brain Stimulation. Annals of Neurology, 2008; 63: 119-123.

Hamilton L, Fay S, Rockwood K. Misplacing objects in mild to moderate Alzheimer's disease: a descriptive analysis from the VISTA clinical trial. Journal of Neurology, Neurosurgery and Psychiatry 2009;80(9):960-965.

Hankey GJ, Stewart-Wynne EG. Amnesia following thalamic hemorrhage Another stroke syndrome. Stroke 1988;19(6):776-778.

Hansen N. Action mechanisms of transcranial direct current stimulation in Alzheimer’s disease and memory loss. Frontiers in Psychiatry, 2012; 3.

Hardt O Wang S-H et al. Storage or retrieval deficit: The yin and yang of amnesia. Learning and Memory, 2009; 16: 224-230

Harrison FE and May JM. Vitamin C function in the brain: vital role of the ascorbate transporter SVCT2. Free Radical Biology and Medicine, 2009; 46: 719-730.

Hasanein P and Shahidi S. Effects of combined treatment with vitamins C and E on passive avoidance learning and memory in diabetic rats. Neurobilogy of Learning and Memory, 2010; 93: 472-478

Hassabis D, Kumaran D et al. Patients with hippocampal amnesia cannot imagine new experiences. Protocols of the National Academy of Science, 2007; 104(5): 1726-1731.

Hassanshahi J, Hassanshahi GH et al. Comparison of Therapeutic Effects of Vvitamin C and CoQ10 in Reducing of Damaged Cells in Mice Hippocampus Following Ischemia-Reperfusion. Journal of MAssand University Medical Science, 2012; 22(94): 2-13.

Hassanshahi J, Zamani M et al. An Assay of bax and bcl2 Expression in Mice Hippocampus Following Ischemia-Reperfusion Treatment with CoQ10. Zahedan Journal of Research and Medical Science, 2013.

Henderson VW. Aging, estrogens, and episodic memory in women. Cognitive and Behavioral Neurology 2009;22(4):205-214.

Hirai S. Distinction between Dementia and Memory Decline. Journal of the Medical Association of Japan, 2001; 44(60: 274-278.

Hirayama S., Terasawa K. et al.  The effect of phosphatidylserine administration on memory and symptoms of attention-deficit hyperactivity disorder: a randomised, double-blind, placebo-controlled clinical trial. J Hum Nutr Diet, 2013.

Hoane MR, Gilbert DR et al. Magnesium dietary manipulation and recovery of function following controlled cortical damage in the rat. Magnesium Research 2008; 21 (1): 29-37.

Holemans X, Dupuis M, Misson N, Vanderijst JF. Reversible amnesia in a Type 1 diabetic patient and bilateral hippocampal lesions on magnetic resonance imaging (MRI). Diabetic Medicine 2001;18(9):761-763.

Hornberger M, Mohamed A et al. Focal retrograde amnesia: Extending the clinical syndrome of transient epileptic amnesia. Journal of Clinical Neuroscience, 2010; 17: 1319-1321.

Hunter G. Tranient Global Amnesia. Neurologic the Clinics 2011; 29: 1045-1054.

Imperato A, Ramacci MT, Angelucci L. Acetyl-L-carnitine enhances acetylcholine release in the striatum and hippocampus of awake freely moving rats. Neuroscience Letters 1989;107(1-3):251-255.

Ishrat T, Khan MB et al. Coenzyme Q10 modulates cognitive impairment against intracerebroventricular injection of streptozotocin in rats. Behavioural Brain Research, 2006; 171: 9-16.

Jakala P, Riekkinen M et al. Guanfacine, But Not Clonidine, Improves Planning and Working Memory Performance in Humans. Neuropsychopharmacology, 1999; 20: 460-470.

Jia N, Han K, Kong JJ, Zhang XM, Sha S, Ren GR, Cao YP. (-)-Epigallocatechin-3-gallate alleviates spatial memory impairment in APP/PS1 mice by restoring IRS-1 signaling defects in the hippocampus. Molecular and Cellular Biochemistry 2013 May 10. [Epub ahead of print] PubMed PMID: 23660953.

Jiang X, tian Q et al. Acetyl-L-Carnitine Ameliorates Spatial Memory Deficits Induced by Inhibition of Phosphoinositol-3 Kinase and Protein Kinase C. Journal of Neurochemistry, 2011; 118: 864-878.

Jones C, Griffiths RD, Humphris G. Disturbed memory and amnesia related to intensive care. Memory 2000;8(2):79-94.

Joseph JA, Arendash G et al. Blueberry Supplementation Enhances Signaling and Prevents Behavioral Deficits in an Alzheimer Disease Model. Nutritional Neuroscience, 2003; 6(3): 153-162.

Kaschel R. Specific memory effects of Ginkgo biloba extract EGb 761 in middle-aged healthy  volunteers. Phytomedicine, 2011; 18:1202-1207.

Kato-Kataoka A, Sakai M et al. Soybean-Derived Phosphatidylserine Improves Memory Function of the Elderly Japanese Subjects with Memory Complaints. Journal of Clinical Biochemical Nutrition, 2010; 47: 246-255.

Kennedy DO, Haskell CF et al. Acute cognitive effects of standardised Ginkgo biloba extract complexed with phosphatidylserine. Hum. Psychopharmacol Clin Exp 2007; 22: 199–210.

Kidd P and Copp S. GPC: Optimizing Mental Focus, Memory, and Brain Repair. Crayhon Research, 2005.

Kirshner HS. Transient Global Amnesia: A Brief Review and Update. Current Neurological and Neuroscience Reports, 2011; 11: 578-582.

Kobayashi S, Iwamoto M et al. Acetyl-L-carnitine improves aged brain functioning. Geriatrics Gerontology International, 2010; 10: S99-S106.

Konar A, Shah N et al. Protective Role of Ashwagandha Leaf Extract and Its Component Withanone on Scopolamine-Induced Changes in the Brain and Brain-Derived Cells. PLOS One, 2011; 6(11): e227265-e27276.

Kopelman MD, Bright P, Buckman J, Fradera A, Yoshimasu H, Jacobson C, Colchester AC. Recall and recognition memory in amnesia: patients with hippocampal, medial temporal, temporal lobe or frontal pathology. Neuropsychologia 2007;45(6):1232-1246.

Krikorian R, Shidler MD et al. Blueberry Supplementation Improves Memory in Older Adults. J. Agric. Food Chem. 2010, 58, 3996–4000.

Kritchevsky M, Chang J, Squire LR. Functional amnesia: clinical description and neuropsychological profile of 10 cases. Learning & Memory 2004;11(2):213-226.

Krupp LB, Christodoulou C, Melville P, Scherl WF, MacAllister WS, Elkins LE. Donepezil improved memory in multiple sclerosis in a randomized clinical trial. Neurology 2004;63(9):1579-1585.

Kullenberg D, Taylor LA et al. Health Effects of Dietary Phospholipids. Lipids in Health and Disease, 2012; 11:3.

Kwon JT, Jhang J, Kim HS, Lee S, Han JH. Brain region-specific activity patterns after recent or remote memory retrieval of auditory conditioned fear. Learning & Memory 2012;19(10):487-494.

Liu G. Prevention of cognitive deficits in Alzheimer’s mouse model by elevating brain magnesium. Molecular Neurodegeneration 2012, 7(Suppl 1):L24

Lockrow J, Praksam A et al. Cholinergic degeneration and memory loss delayed by vitamin E in a Down syndrome mouse model. Experimental Neurology, 2009; 216(2): 278-289.

Luine V and Frankfurt M. Interactions between estradiol, BDNF and dendritic spines in promoting memory. Neuroscience, 2013; 239: 34-45.

Ma J, Huang S et al. Progesterone for acute traumatic brain injury. The Cochrane Collaboration, 2012.

Ma T, Gong K et al. Huperzine A promotes hippocampal neurogenesis in vitro and in vivo. Brain Research, 2013; 1506: 35-43.

Malaguarnera M, Vacante M et al. Acetyl-L-carnitine improves cognitive functions in severe hepatic encephalopathy: a randomized and controlled clinical trial. Metabolism and Brain Diseases, 2011; 26: 281-289.

Malkova L, Kozikowski AP et al. The effects of huperzine A and IDRA 21 on visual recognition memory in young macaques. Neuropharmacology, 2011; 60: 1263-1268.

Mannella P and Simonciti T. Sex steroids and their receptors: Molecular actions on brain cells. Gynecological Endocrinology, 2012; 28(S1): 2-4.

Markowitsch HJ and Staniloiu A. The impairment of recollection in functional amnesic states. Cortex. 2013;49(6):1494-510.

Massaad CA and Klann E. Reactive Oxygen Species in the Regulation of Synaptic Plasticity and Memory. Antioxidants and Redox Signaling, 2011; 14(10): 2013-2054.

Mayes A. Theories of Hippocampal Function in Anterograde Amnesia. Journal of Neurology, Neurosurgery and Psychiatry, 2010; 81(10). E1-2.

Mayo Clinic Staff. Amnesia. Last updated 11 Oct. 2011a. Accessed 19 May 2013. <>.

Mayo Clinic Staff. Alzheimer’s Disease. Last updated 18 Aug. 2011b. Accessed 7 Aug. 2013. <>.

Mayo W, Le Moal M, Abrous DN. Pregnenolone sulfate and aging of cognitive functions: behavioral, neurochemical, and morphological investigations. Hormones and Behavior 2001;40(2):215-217.

McAllister TW, McDonald BC et al. Alpha-2 adrenergic challenge with guanfacine one month after mild traumatic brain injury: Altered working memory and BOLD response. International Journal of Psychophysiology, 2011; 112: 107-114.

McKay GCM, Kopelman MD. Psychogenic amnesia: when memory complaints are medically unexplained. Advances in psychiatric treatment 2009;15:125-128.

McLeod, Saul. "Anterograde Amnesia." Anterograde Amnesia. Simply Psychology, 2011. Web. 23 Apr. 2013. <>.

Meeter M, Murre JMJ et al. Retrograde amnesia after electroconvulsive therapy: A temporary effect?. Journal of Affective Disorders, 2011; 132: 216-222.

Megevand P and Landis T. Recognition Memory without Awareness during Transient Global Amnesia. European Neurology, 2011; 66: 294-295.

Mohs RC. Memory impairment in amnesia and dementia: implications for the use of animal models. Neurobiology of Aging 1988;9(5-6):465-468.

Mondon K, Bléchet C, Gochard A, Elaroussi D, Fetissof F, Autret A, de Toffol B, Hommet C. Transient global amnesia caused by painless aortic dissection. BMJ Case Reports 2009; pii: bcr09.2008.0935.

Mormino EC, Kluth JT et al. Episodic memory loss is related to hippocampal-mediated b-amyloid deposition in elderly subjects. Brain, 2009; 132: 1310-1323.

Morris MC, Evans DA et al. Dietary Folate and Vitamin B12 Intake and Cognitive Decline Among Community-Dwelling Older Persons. Archives of Neurology, 2005; 62:641-645.

Morris RGM, Moser EI et al. Elements of a Neurobiological Theory of the Hippocampus: the Role of Activity-Dependent Synaptic Plasticity in Memory. Philosophical Transactions of the Royal Society, 2003; 358: 773-786.

Moscovitch M. 2004. Amnesia. International Encyclopedia of the Social & Behavioral Sciences. Copyright © 2001 Elsevier Sciences Ltd.

Myers TM, Sun W et al. Systemic administration of the potential countermeasure huperzine reversibly inhibits central and peripheral acetylcholinesterase activity without adverse cognitive–behavioral effects. Pharmacology, Biochemistry and Behavior, 2010; 96: 477-481.

Nadel L and Moscovitch M. Memory consolidation, retrograde amnesia and the hippocampal complex. Current Opinion in Neurobiology, 1997; 7: 217-227.

Narendran R, Frankle WG et al. Improved Working Memory but No Effect on Striatal Vesicular Monoamine Transporter Type 2 after Omega-3 Polyunsaturated Fatty Acid Supplementation. PLOS One, 2012; 7(10).

Nespor K. Alcohol-related amnesia ("blackout") in broader perspective. Cas Lek Cesk. 2004;143(12):861-2.

Novitzke J. Privation of Memory: What can be done to help stroke patients remember?. Journal of Vascular and Interventional Neurology 2008;1(4):122-123.

Nyakas C, Felszeghy K et al. Neuroprotective Effects of Vinpocetine and its Major Metabolite Cis-apovincaminic Acid on NMDA-Induced Neurotoxicity in a Rat Entorhinal Cortex Lesion Model. CNS Neuroscience and Therapeutics, 2009; 16: 89-99.

Ohn SH, Park C-I et al. Time-dependent effect of transcranial direct current stimulation on the enhancement of working memory. Cognitive Neuroscience and Neuropsychology 2008; 19(1): 43-47.

Ohwada K, Takeda H et al. Pyrroloquinolone (PQQ) Prevents Cognitive Deficit Caused by Oxidative Stress in Rats. Journal of Clinical Biochemical Nutrition, 2008; 42: 29-34.

Oudshoorn C, Mattace-Raso FUS et al. Higher Serum Vitamin D 3 Levels Are Associated with Better Cognitive Test Performance in Patients with Alzheimer’s Disease. Dementia and Geriatric Cognitive Disorders, 2009; 25: 539-543.

Owen D, Paranandi B, Sivakumar R, Seevaratnam M. Classical diseases revisited: transient global amnesia. Postgraduate Medical Journal 2007;83(978):236-239.

Paller KA. Memory Consolidation: Systems. Encyclopedia of Neuroscience, 2009: 741-749.

Parkin AJ, Hunkin NM. Memory loss following radiotherapy for nasal pharyngeal carcinoma--an unusual presentation of amnesia. British Journal of Clinical Psychology 1991;30 ( Pt 4):349-357.

Parletta N, Milte CM et al. Nutritional modulation of cognitive function and mental health. Journal of Nutritional Biochemistry, 2013.

Parnetti L, Amenta F et al. Choline alphoscerate in cognitive decline and in acute cerebrovascular disease: an analysis of published clinical data. Mechanisms of Aging and Development, 2001; 122: 2041-2055.

Pasinetti GM and Ho L. Role of grape seed polyphenols in Alzheimer’s disease neuropathology. Nutrition and Dietary Supplements, 2010; 2: 97-103.

Pauly-Takacs K, Moulin CJA et al. SenseCam as a rehabilitation tool in a child with anterograde amnesia. Memory, 2010; 19(7): 705-712

Perouansky M and Pearce RA. How we recall (or don’t): the hippocampal memory machine and anesthetic amnesia. Canadian Journal of Anesthesia, 2011; 58: 157-166.

Petit GH, Tobin C et al. Pregnenolone sulfate and its enantiomer: Differential modulation of memory in a spatial discrimination task using forebrain NMDA receptor deficient mice. European Neuropsychopharmacology, 2011; 21: 211-215.

Petrovich GD. Learning and the motivation to eat: forebrain circuitry. Physiology & behavior. Sep 26 2011;104(4):582-589.

Poly C, Massaro JM et al. The relation of dietary choline to cognitive performance and white-matter hyperintensity in the Framingham Offspring Cohort. The American Journal of Clinical Nutrition, 2011; 94: 1584-1591.

Protopopescu X, Butler T, Pan H, Root J, Altemus M, Polanecsky M, McEwen B, Silbersweig D, Stern E. Hippocampal structural changes across the menstrual cycle. Hippocampus 2008;18(10):985-988.

Przybelski RJ and Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Archives of Biochemistry and Biophysics, 2009; 480: 202-205.

PubMed Health. Memory loss. Forgetfulness; Amnesia; Impaired memory; Loss of memory; Amnestic syndrome. 2012. Available at: Last accessed: June 1, 2013.

PubMed Health. Wernicke-Korsakoff syndrome. Korsakoff psychosis; Alcoholic encephalopathy; Encephalopathy – alcoholic; Wernicke’s disease. 2013. Available at: Accessed 7/1/13.

Rafii MS, Walsh S, Little JT, Behan K, Reynolds B, Ward C, Jin S, Thomas R, Aisen PS, Alzheimer's Disease Cooperative Study. A phase II trial of huperzine A in mild to moderate Alzheimer disease. Neurology 2011;76(16):1389-1394.

Rajmohan V, Mohandas E. The limbic system. Indian Journal of Psychiatry 2007;49(2):132-139.

Ramirez MR, Izquierdo I, do Carmo Bassols Raseira M, Zuanazzi JA, Barros D, Henriques AT. Effect of lyophilised Vaccinium berries on memory, anxiety and locomotion in adult rats. Pharmacological Research 2005;52(6):457-462.

Rao MG, Holla B et al. Piracetam treatment in patients with cognitive impairment. General Hospital Psychiatry, 2012.

Ratra M, Sharma PL et al. Neuroprotective effect of Vinpocetine against 3- NP Induced reduction of body weight and oxidative stress in Rats. International Journal of Phytomedicine, 2011; 3: 362-369.

Renoult L, Davidson PS, Palombo DJ, Moscovitch M, Levine B. Personal semantics: at the crossroads of semantic and episodic memory. Trends in Cognitive Sciences 2012;16(11):550-558.

Richter Y, Herzog Y et al. The effect of phosphatidylserine-containing omega-3 fatty acids on memory abilities in subjects with subjective memory complaints: a pilot study. Clinical Interventions in Aging, 2010: 313-316.

Rison RA and Rosenheck RE. Transient Global Amnesia: A Case Report. Case Rep Neurol 2012;4:126–130.

Roger KS. Priorities for people living with dementia: education, counseling, research. Journal of Clinical Interventions in Aging 2008;3(3):573-579.

Sachdeva D and Burns A. Dimebolin in Dementia. CNS Neuroscience and Therapeutics, 2011;17:199-205.

Samartgis JR, Schachte L et al. Piracetam, an AMPAkine drug, facilitates memory consolidation in the day-old chick. Pharmacology, Biochemistry and Behavior, 2012; 103: 253-258.

Sanchez AL, Matthews BJ, Meynard MM, Hu B, Javed S, Cohen Cory S. BDNF increases synapse density in dendrites of developing tectal neurons in vivo. Development 2006;133(13):2477-2486.

Sandhu JS, Shah B, Shenoy S, Chauhan S, Lavekar GS, Padhi MM. Effects of Withania somnifera (Ashwagandha) and Terminalia arjuna (Arjuna) on physical performance and cardiorespiratory endurance in healthy young adults. International Journal of Ayurveda Research 2010;1(3):144-149.

Sarreshtehdari M, Gheibi N et al. Effect of Magnesium Administration on Passive Avoidance Memory and Formalin-Induced Nociception in Diabetic Rats. Tropical Journal of Pharmaceutical Research December 2012; 11 (6): 947-954

Scafidi S, Racz J et al. Neuroprotection by Acetyl- L –Carnitine after Traumatic Injury to the Immature Rat Brain. Dev Neurosci 2010;32:480–487.

Scanlon JM, Aizenman E et al. Effects of pyrroloquinoline quinone on glutamate-induced production of reactive oxygen species in neurons. European Journal of Pharmacology, 1997; 326: 67-74.

Schaevitz LR, Nicolai R, Lopez CM, D'Iddio S, Iannoni E, Berger-Sweeney JE. Acetyl-L-carnitine improves behavior and dendritic morphology in a mouse model of Rett syndrome. PLoS One 2012;7(12):e51586.

Schaffhauser H, Mathiasen JR et al. Dimebolin is a 5-HT6 antagonist with acute cognition enhancing activities. Biochemical Pharmacology, 2009; 78: 1035-1042.

Sellal F, Manning L, Seegmuller C, Scheiber C, Schoenfelder F. Pure retrograde amnesia following a mild head trauma: a neuropsychological and metabolic study. Cortex 2002;38(4):499-509.

Seshadri S, Beiser A, Selhub J, Jacques PF, Rosenberg IH, D'Agostino RB, Wilson PW, Wolf PA. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. New England Journal of Medicine 2002;346(7):476-483.

Sharma V and Yadav S. Cognitive Enhancing Activity of Docosahexaenoic Acid and Gamma-Linolenic Acid in Lead Induced Amnesia. Bulletin of Pharmaceutical Research 2012;2(2):109-11.

Shen YX, Xu SY, Wei W, Sun XX, Yang J, Liu LH, Dong C. Melatonin reduces memory changes and neural oxidative damage in mice treated with D-galactose. Journal of Pineal Research 2002;32(3):173-178.

Shi Q, Pu J et al. Huperzine A Ameliorates Cognitive Deficits and Oxidative Stress in the Hippocampus of Rats Exposed to Acute Hypobaric Hypoxia. Neurochemical Research, 2012; 37: 2042-2052.

Silberstein RB, Pipingas A et al. Examining Brain-Cognition Effects of Ginkgo Biloba Extract: Brain Activation in the Left Temporal and Left Prefrontal Cortex in an Object Working Memory Task. Evidence-Based Complementary and Alternative Medicine, 2011.

Singh N, Bhalla M et al. An Overview of Ashwagandha: A Rasayana (Rejuvenator) of Ayurveda. African Journal of Traditional, Complementary and Alternative Medicine, 2011; 8(S): 208-213.

Slinin Y, Paudel M et al. Association Between Serum 25(OH) Vitamin D and the Risk of Cognitive Decline in Older Women. Journal of Gerontology, 2012; 67(10): 1092-1098.

Slutsky I, Abumaria N et al. Enhancement of Learning and Memory by Elevating Brain Magnesium. Neuron. 2010; 65: 165-177.

Smith AD, Smith SM, de Jager CA, Whitbread P, Johnston C, Agacinski G, Oulhaj A, Bradley KM, Jacoby R, Refsum H. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial. PLoS One. 2010;5(9):e12244.

Smith YR, Bowen L et al. Early Initiation of Hormone Therapy in Menopausal Women Is Associated with Increased Hippocampal and Posterior Cingulate Cholinergic Activity. Journal of Clinical Endocrinology and Metabolism, 2011; 96(11): 1761-1770.

Solanki P, Prasad D et al. Preventive effect of Piracetam and Vinpocetine on hypoxia-reoxygenation induced injury in primary hippocampal culture. Food and Chemical Toxicology, 2011; 49: 917-922.

Soman S, Korah PK, Jayanarayanan S, Mathew J, Paulose CS. Oxidative stress induced NMDA receptor alteration leads to spatial memory deficits in temporal lobe epilepsy: ameliorative effects of Withania somnifera and Withanolide A. Neurochemical Research 2012;37(9):1915-1927.

Sorwell KG and Urlanksi HF. Dehydroepiandrosterone and age-related cognitive decline. Age, 2010; 32: 61-67.

Spencer JPE. The impact of fruit flavonoids on memory and cognition. British Journal of Nutrition, 2010; 104: S40-S47.

Squire LR, Alvarez P. Retrograde amnesia and memory consolidation: a neurobiological perspective. Current Opinion in Neurobiology 1995;5(2):169-177.

Squire LR, Bayley PJ. The neuroscience of remote memory. Current Opinion in Neurobiology 2007;17(2):185-196.

Staniloiu A and Markowitsch HJ. Towards solving the riddle of forgetting in functional amnesia: recent advances and current opinions. Froniters in Psychology, 2012; 3: 1-23.

Stone J, Campbell IW, Moran GD, Mumford CJ. A case of reversible amnesia. Postgraduate Medical Journal 2001;77(903):54-55, 59-60.

Sucholeiki R. Transient Global Amnesia Workup. Medscape Reference: Drugs, Diseases & Procedures. Workup page. Available at: Last updated 9/25/2012. Accessed 7/1/2013.

Sun QQ, Xu SS, Pan JL, Guo HM, Cao WQ. Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students. Zhongguo Yao Li Xue Bao. 1999;20(7):601-603.

Suthana N, Haneef Z, Stern J, Mukamel R, Behnke E, Knowlton B, Fried I. Memory enhancement and deep-brain stimulation of the entorhinal area. New England Journal of Medicine 2012;366(6):502-510.

Swartz BE, McDonald CR et al. The Effects of Guanfacine on Working Memory Performance in Patients With Localization-Related Epilepsy and Healthy Controls. Clinical Neuropharmacology, 2008; 31(5): 251-260.

Takatsu H, Owada K et al. Effect of Vitamin E on Learning and Memory Deficit in Aged Rats. Journal of Nutrition Science and Vitaminology, 2009; 55: 389-393.

Tanabe F, Miyasaka N et al. Early Initiation of Hormone Therapy in Menopausal Women Is Associated with Increased Hippocampal and Posterior Cingulate Cholinergic Activity. Journal of Medical and Dental Science, 2004; 51: 89-98.

Tangney CC, Aggarwal NT et al. Vitamin B12, cognition, and brain MRI measures. Neurology, 2011; 77: 1276-1283.

Tangney CC. Is there a link between vitamin B12 deficiency and cognitive decline in the elderly? Aging Health, 2012; 8(5): 441-443.

Tobinaga S, Hashimoto M et al. Chronic Administration of Cardanol (Ginkgol) Extracted from Ginkgo biloba Leaves and Cashew Nutshell Liquid Improves Working Memory-Related Learning in Rats. Biol. Pharm. Bull, 2012: 35(1): 127-129.

Tohda C, Komatsu K et al. Scientific Basis for the Anti-dementia Drugs of Constitutents from Ashwagandha (Withania somnifera). Journal of Traditional Medicine, 2005; 22: 176-182.

Tseng P, Hsu T-Y et al. Improving visual working memory performance with transcranial direct current stimulation. Journal of Vision, 2012; 12(9)

Tuzcu M and Baydas G. Effect of melatonin and vitamin E on diabetes-induced learning and memory impairment in rats. European Journal of Pharmacology, 2006; 537: 106-110.

Ullman MT. Contributions of memory circuits to language: the declarative/procedural model. Cognition 2004;92(1-2):231-270.

Uysal N, Baykara B et al. Combined Treatment with Progesterone and Magnesium Sulfate Positively Affects Traumatic Brain Injury in Immature Rats. Turkish Neurosurgery 2013, Vol: 23, No: 2, 129-137.

Uzun S, Kozumplik O, Jakovljević M, Sedić B. Side effects of treatment with benzodiazepines. Psychiatria Danubia 2010;22(1):90-93.

Vaisman N, Pelled D. n-3 phosphatidylserine attenuated scopolamine-induced amnesia in middle-aged rats. Progress in neuro-psychopharmacology & biological psychiatry. Aug 31 2009;33(6):952-959.

Vakhapova V, Cohen T et al. Phosphatidylserine Containing  –3 Fatty Acids May Improve Memory Abilities in Non-Demented Elderly with Memory Complaints: A Double-Blind Placebo-Controlled Trial. Dementia and Geriatric Cognitive Disorders, 2010; 29: 467-474.

Vallée M, Mayo W, Darnaudéry M, et al. Neurosteroids: deficient cognitive performance in aged rats depends on low pregnenolone sulfate levels in the hippocampus. Proc Natl Acad Sci U S A. 1997;94(26):14865-70.

Vislocky LM and Fernandez ML. Biomedical Effects of Grape Products. Nutrition Review, 2010; 68(11): 656-670.

Waegemans T, Wilsher CR, Danniau A, Ferris SH, Kurz A, Winblad B. Clinical efficacy of piracetam in cognitive impairment: a meta-analysis. Dementia and Geriatric Cognitive Disorders 2002;13(4):217-224.

Walesiuk A, Braszko JJ. Preventive actionof Ginkgo biloba in stress-and corticosterone-induced impairment ofspatial memory in rats. Phytoedicine, 2009; 16: 40-46.

Wang B-S, Wang H et al. Efficacy and safety of natural acetylcholinesterase inhibitor huperzine A in the treatment of Alzheimer’s disease: an updated meta-analysis. Journal of Neurological Transmission, 2009; 116: 457-465.

Wang J, Zhang HY et al. Huperzine A Improves Chronic Inflammation and Cognitive Decline in Rats With Cerebral Hypoperfusion. Journal of Neuroscience Research, 2010; 88: 807-815.

Warrington JP, Csiszar A, Mitschelen M, Lee YW, Sonntag WE. Whole brain radiation-induced impairments in learning and memory are time-sensitive and reversible by systemic hypoxia. PLoS One 2012;7(1):e30444.

Webster SJ, Wilson CA et al. The acute effects of dimebolin, a potential Alzheimer’s disease treatment, on working memory in rhesus monkeys. British Journal of Pharmacology, 2011; 164: 970-978.

Werenica A, Chirstoff RR et al. Administration of the Phosphodiesterase type 4 Inhibitor Rolipram into the Amygdala at a Specific Time Interval after Learning Increases Recognition Memory Persistence. Learning and Memory, 2012; 19: 495-498.

Wesnes KA, Ward T et al. The memory enhancing effects of a Ginkgo biloba/Panax ginseng combination in healthy middle-aged volunteers. Psychopharmacology (2000) 152:353–361.

White HL, Scates PW. Acetyl-L-carnitine as a precursor of acetylcholine. Neurochemical Research 1990;15(6):597-601.

Wilkins CH, Birge SJ et al. Vitamin D Deficiency Is Associated With Worse Cognitive Performance and Lower Bone Density in Older African Americans. Journal of the National Medical Association , 2009; 101(4): 349-354.

Williams CM, Mogsen MAE et al. Blueberry-induced changes in spatial working memory correlate with changes in hippocampal CREB phosphorylation and brain-derived neurotrophic factor (BDNF) levels. Free Radical Biology and Medicine, 2008; 46: 295-305.

Winocur G, McDonald RM, Moscovitch M. Anterograde and retrograde amnesia in rats with large hippocampal lesions. Hippocampus 2001;11(1):18-26.

Winocur G, Sekeres MJ et al. Hippocampal Lesions Produce Both Nongraded and Temporally Graded Retrograde Amnesia in the Same Rat. Hippocampus, 2013; 23(5):330-341.

Woolley CS and McEwen BS. Roles of Estradiol and Progesterone in Regulation of Hippocampal Dendritic Spine Density During the Estrous Cycle in the Rat. The Journal of Comparative Neurology, 1993; 336: 293-306.

Wright DW, Kellermann AL et al. ProTECT: A Randomized Clinical Trial of Progesterone for Acute Traumatic Brain Injury. Annals of Emergency Medicine, 2007; 49(4): 391-404.

Wu A, Ying Z et al. Vitamin E Protects Against Oxidative Damage and Learning Disability After Mild Traumatic Brain Injury in Rats. Neurorehabilitation and Neural Repair, 2010; 24: 290-298.

Wu KJ, Hsieh MT, Wu CR, Wood WG, Chen YF. Green Tea Extract Ameliorates Learning and Memory Deficits in Ischemic Rats via Its Active Component Polyphenol Epigallocatechin-3-gallate by Modulation of Oxidative Stress and Neuroinflammation. Evidence-Based Complementary and Alternative Medicine 2012;2012:163106.

Xu ZQ, Liang X-M et al. Treatment with Huperzine A Improves Cognition in Vascular Dementia Patients. Cell Biochemistry and Biophysiology, 2012; 62: 55-68.

Yadav S and Sharma V. Neuroprotective Role and Anti-Amnesic Effect of Docosahexaenoic Acid and Hamm-Linilenic Acid in Lead Induced Neurological Deficit and Amnesia in Swiss Albino Mice. Bulletin of Pharmaceutical Research 2012;1(S):144.

Ye JW, Cai JX, Wang LM, Tang XC. Improving effects of huperzine A on spatial working memory in aged monkeys and young adult monkeys with experimental cognitive impairment. Journal of Pharmacology and Experimental Therapeutics 1999;288(2):814-819.

Yoneda Y, Yamadori A et al. Isolated Prolonged Retrograde Amnesia. European Journal of Neurology, 1992; 32: 340-342.

Zaehle T, Sandmann P et al. Transcranial direct current stimulation of the prefrontal cortex modulates working memory performance: combined behavioural and electrophysiological evidence. BMC Neuroscience, 2011; 12(2).

Zeman A, Butler C. Transient epileptic amnesia. Current Opinion in Neurology 2010;23(6):610-616.

Zhang L, Liu J et al. The Neuroprotective Effect of Pyrroloquinoline Quinone on Traumatic Brain Injury. Journal of Neurotrauma, 2012; 29: 851-864.

Zhang R, Zhang H, Zhang Z, Wang T, Niu J, Cui D, Xu S. Neuroprotective Effects of Pre-Treament with l-Carnitine and Acetyl-l-Carnitine on Ischemic Injury In Vivo and In Vitro. International Journal of Molecular Sciences 2012;13(2):2078-20790.

Zhang Y and Rosenberg PA. The essential nutrient pyrroloquinoline quinone may act as a neuroprotectant by suppressing peroxynitrite formation. European Journal of Neuroscience, 2002;16:1015-1024.

Zhou P, Chen Z et al. Acetyl-L-Carnitine Attenuates Homocysteine-Induced Alzheimer-Like Histopathological and Behavioral Abnormalities. Rejuvenation Research, 2011; 14(6): 669-680.