Effects of alcohol on memory

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Ethanol Ethanol-structure.svg
Ethanol
Alcoholic beverages Alcoholic beverages.jpg
Alcoholic beverages

Effects of alcohol on memory include disruption of various memory processes, affecting both formation and recall of information.

Contents

Mode of actions

Effects on the hippocampus

Alcohol acts as a general central nervous system depressant, but it also affects some specific areas of the brain to a greater extent than others. Memory impairment caused by alcohol has been linked to the disruption of hippocampal function—particularly affecting gamma-Aminobutyric acid (GABA) and N-methyl-D-aspartate (NMDA) neurotransmission which negatively impacts long-term potentiation (LTP). [1] The molecular basis of LTP is associated with learning and memory. [2] Particularly, damage to hippocampal CA1 cells adversely affects memory formation, [3] and this disruption has been linked to dose-dependent levels of alcohol consumption. [4] At higher doses, alcohol significantly inhibits neuronal activity in both the CA1 and CA3 pyramidal cell layers of the hippocampus. [5] [6] [7] This impairs memory encoding, [8] since the hippocampus plays an important role in the formations of new memories.

A hippocampal pyramidal cell Hippocampal-pyramidal-cell.png
A hippocampal pyramidal cell

Molecular effects on GABA and NMDA receptors

A GABAA receptor GABAA receptor schematic.png
A GABAA receptor

Alcohol also acts as a positive allosteric modulator of GABA receptors, specifically type GABAA. [9] Upon activation, these GABA receptors conduct Cl-, resulting in neuronal hyperpolarization. This hyperpolarization decreases the chance of an action potential occurring and thus, it has an inhibitory effect on neurotransmission in the central nervous system. GABAA receptor subtypes vary in their sensitivities to dosage of alcohol consumed. Furthermore, acute alcohol intake promotes GABAergic neurotransmission via the presynaptic release of GABA, the dephosphorylation of GABAA receptors (increasing GABA sensitivity), and the elevation of endogenous GABAergic neuroactive steroids. [10] Protein kinase C (PKC) has been implicated in differentially modulating the response of the GABAA receptor to alcohol, with effects depending on the PKC isozyme. [11] Alcohol effects have also implicated protein kinase A in affecting GABAA receptor function, such as promoting sensitivity. [12] Enhancement of GABAergic transmission due to alcohol consumption can also be brought about by neuroactive steroids, such as allopregnanolone, which act as GABAA receptor agonists. [10] [13] Both chronic alcohol consumption and alcohol dependence are correlated with the altered expression, properties, and functions of the GABAA receptor that may contribute to alcohol tolerance. [10] There is still much yet to be discovered about alcohol's specific and varying effects on both the GABAA receptor and its subtypes.

At higher doses, ethanol also affects NMDA receptors (NMDARs) by inhibiting the ion current induced by NMDA, a glutamate receptor agonist. [14] This inhibition of synaptic excitation by alcohol has been shown to be dose-dependent (up to a certain point, after which it did not differ by much). [15] Alcohol appears to produce this inhibition by using a site of the NMDAR that is accessible from the extracellular environment. [16] Therefore, this inhibition of an ion current usually produced by NMDAR activation leads to decreased LTP in hippocampal areas. [17] Alcohol negatively affects LTP to a greater degree in immature versus mature animals. [18] In adolescents, alcohol decreases the expression of both the NMDAR NR2A subunit in the hippocampus and the NR1 subunit in the prefrontal cortex. [19] Studies have also found that a decrease in phosphorylation of 2B subunit in the prefrontal cortex, the hippocampus, the nucleus accumbens, and the striatum. [20] NMDARS may be affected by PKA regulation due to the actions of alcohol. [21] Alcohol's effects on GABAA neurotransmission may indirectly inhibit the activity of the NMDAR, and they may contribute to its blockade of LTP induction; however, alcohol's direct effects on NMDAR alone are sufficient for the inhibition of LTP. [22] The varying dose-dependent response to alcohol relies on the combined interactions and responses of the GABAA receptors, NMDARs, and metabotropic glutamate receptors subtype 5 (mGluR5). [23] [24] [25] These changes prevent excitatory synaptic transmissions from occurring, affecting synaptic plasticity and, in turn, memory and learning. However, there is still much yet to be elucidated concerning specific molecular mechanisms of how alcohol affects memory formation.

Effects on other brain regions

Alcohol also impairs and alters the functioning in the cerebellum, which affects both motor function and coordination. [26] It has a notable inhibitory effect on the neurons of the cerebral cortex, affecting and altering thought processes, decreasing inhibition, and increasing the pain threshold. It also decreases sexual performance by depressing nerve centers in the hypothalamus. [27] [28] Alcohol also has an effect on urine excretion via inhibition of anti-diuretic hormone (ADH) secretion of the pituitary gland. Lastly, it depresses breathing and heart rate by inhibiting neuronal functioning of the medulla. [29]

Long-term memory

Long-term memory (LTM) has both a long duration and a large capacity. [30] Memories that are stored in LTM can last from a few days to a lifetime. [30] LTM consists of both explicit memory (requiring conscious awareness) and implicit memory (unconscious awareness). [30] Information selected for LTM goes through three processes. First of all, in the encoding stage, information from the senses is incorporated into mental activity in the form of a memory. [30] Secondly, storage involves taking this information and holding it indefinitely in memory. [30] Lastly, retrieval is the ability to recall information from the long-term memory storage. Each of these processes can be affected by alcohol. [30]

Animation: Hippocampus (red) Hippocampus.gif
Animation: Hippocampus (red)

Explicit memory

Explicit memory requires conscious and intentional effort for recall. [30] It includes both episodic memory (for specific events, such as a party) and semantic memory (for general information, such as one's name). [30]

Alcohol impairs episodic encoding, specifically for cued recall, recognition of completed word fragments, and free recall. [31] A blackout is an example of a difficulty in encoding episodic memories due to alcohol. Blackouts are caused by a rapid increase in blood alcohol concentration (BAC) which in turn distorts the neurons in the hippocampus. [32] This distortion impairs a person's ability to form new episodic memories. [32]

High doses of alcohol severely disrupt the storage process of semantic memories. [33] Alcohol was found to impair the storage of novel stimuli but not that of previously learned information. [33] Since alcohol affects the central nervous system, it hinders semantic storage functioning by restricting the consolidation of the information from encoding. [33]

Retrieval of explicit memory is significantly impaired by alcohol. When compared to sober participants, intoxicated participants performed quite poorly on a recall task for everyday events (i.e., episodic memory). [34] Intoxicated participants are also slower to respond in reaction time tasks. [35] Alcohol also impairs retrieval in word recognition tasks. [31] When both encoding and retrieval take place during intoxication, there are surprisingly more impairments for cued recall than for free recall. [31] In terms of gender differences in retrieval processes, females tend to score lower than males on recall tasks when intoxicated. [35]

Implicit memory

Implicit memory does not require conscious effort or intention for recall. [30] It occurs when previous experience influences performance on a certain task. [30] This is evident in priming experiments. Implicit memory includes procedural memory, which influences our everyday behaviours, such as riding a bike or tying shoes. [30] People can perform these abilities without even thinking about them, which means procedural memory functions automatically. While retrieval of explicit memory is severely impaired by alcohol, retrieval of implicit memory is not. [34] Intoxicated subjects score higher on recognition tasks (involving implicit memory) than they can on recall tasks (involving explicit memory). [34]

Short-term memory

Short-term memory refers to the temporary storage of small amounts of information over short delays. [30] Digit span refers to the proposed number of pieces of information (5-9) that can be held in short-term memory. This is also referred to as the magic number seven—plus or minus two. Any more pieces of information than this, and newer items replace previous items. [36] Alcohol intoxication has been found to have dissociative effects on both short-term memory and cognitive functioning. [37] [38]

Anterior cingulate cortex (yellow) Gray727 anterior cingulate cortex.png
Anterior cingulate cortex (yellow)
Animation: Parietal lobe (red) Parietal lobe animation small.gif
Animation: Parietal lobe (red)

Brain areas affected by alcohol

Alcohol affects the functioning of the brain. Neurochemical changes occurring in the anterior cingulate are correlated with altered short-term memory functions in the brains of young alcoholic men. [39] fMRIs of alcohol-dependent women displayed significantly less blood oxygen in the frontal and parietal regions, especially in the right hemisphere. [40] This is supported by findings of short-term memory impairment by lesions of both the parietal lobe [41] and the prefrontal cortex. [42] Associations between third ventricle volume and cognitive performance on memory tests have been found in alcoholics. [43] Specifically, increases in third ventricular volume correlate with a decline in memory performance. [43]

Tasks and intoxication findings

Short-term memory is commonly tested with visual tasks. Short-term memory, especially for non-verbal and spatial material, are impaired by intoxication. [43] Alcohol decreases iconic memory (a type of visual short-term memory). [44] With BACs between 80 and 84 mg/dL, more intrusion errors occur in a delayed recall task compared to a control group. [45] Intrusion errors, which represent reflective cognitive functioning, occur when irrelevant information is produced. Alcoholics have less control of inhibiting intrusions. [45] Acute alcohol intoxication in social drinkers caused more intrusion errors in delayed recall tasks than in immediate free recall tasks. [45] Acute alcohol intoxication increases the susceptibility to interference, which allows for more intrusion errors when there is a short delay. [45] Free recall (given list of words then asked to recall list) is significantly lower and therefore impaired by alcohol intoxication. [46] [47] Encoding deficits were found in verbal free recall and recognition tasks under the influence of alcohol. [48] A discrimination task found significant alcohol-related impairments both in depth perception and in visual short-term memory. [49] State-dependent learning and relearning studies in male heavy drinkers demonstrate that the condition of intoxication while learning and sobriety when tested caused a performance deficit in free recall tasks. [50] These findings are supportive of alcohol-induced storage deficits (not retrieval deficits). [50] The effects of acute alcohol consumption on visual short-term memory, stereoscopic depth perception, and attention were all studied. A 33% alcohol condition showed significant impairments both in depth perception and in visual short-term memory (assessed by the vernier discrimination task). [51]

Working Memory Model. Alcohol intoxication can disrupt rehearsal strategies which may involve the phonological loop and/or the visuospatial sketchpad. Working memory model.svg
Working Memory Model. Alcohol intoxication can disrupt rehearsal strategies which may involve the phonological loop and/or the visuospatial sketchpad.

Effects on working memory

Working memory allows one to keep things in mind while simultaneously performing complex tasks. [30] It involves a system for both the temporary storage and the manipulation of information, subsequently forming a crucial link between perception and controlled action. [52] Evidence suggests that working memory involves three components: the central executive which controls attention, the visuo-spatial sketchpad which holds and manipulates spatial information, and the phonological loop which performs a similar function for auditory and speech-based information. [52]

In the short term

Alcohol consumption has substantial, measurable effects on working memory, although these effects vary greatly between individual responses. Not much is really known about the neural mechanisms that underlie these individual differences. [53] It is also found that alcohol impairs working memory by affecting mnemonic strategies and executive processes rather than by shrinking the basic holding capacity of working memory. Isolated acute-moderate levels of alcohol intoxication do not physically alter the structures that are critical for working memory function, such as the frontal cortex, the parietal cortex, the anterior cingulate, and parts of the basal ganglia. [37] One finding regarding the effects of alcohol on working memory points out that alcohol reduces working memory only in individuals with a high baseline working memory capacity, [54] which suggests that alcohol might not uniformly affect working memory in many different individuals. Alcohol appears to impair the capacity of working memory to modulate response inhibition. [54] Alcohol disinhibits behaviour, but it only does so in individuals with a low baseline working memory capacity. [54] An interesting finding is that the incentive to perform well with working memory measurement tasks while under the influence of alcohol 'does, in fact, have some effect on working memory, as it boosts scores in the rate of mental scanning and reaction time to stimulus; however, it did not reduce the number of errors as opposed to subjects with no incentive to perform well. [55] Even acute alcohol intoxication (a blood alcohol concentration of 0.08-0.09%) produces a substantial impairment of working memory processes that require mnemonic rehearsal strategies. [37] It is less likely for alcohol to impair a working memory task that does not rely on memory rehearsal or associated mnemonic strategies. [37] Because of this, working memory is very susceptible to falter when an individual participates in tasks involving retention concerning both auditory and visual sequences. [37]

An interesting example of this is the failure of guitarists or other musicians performing concerts to cue in on auditory patterns and make it known that their performance is hindered by intoxication, whereas professional basketball (a less sequence-heavy activity for working memory) standout Ron Artest admitted in an interview with Sporting News to drinking heavily during half-time early in his career and the fact that it had little—if not any recognizable—effect on his working memory. His former coach Fran Fraschilla has gone on record saying: [56]

It's a surprise because every day at practice, he came out in a mood to play. He came out in a basketball rage. He was fully committed; he wanted to let our upperclassmen know that he was the alpha male. It never came up that he had any sort of a problem with alcohol. This is the first I've heard of it.

In the long term

Alcohol has been shown to have just some long-term effects on working memory. Findings have shown that in order for working memory to be substantially affected, long-term heavy drinking must be sustained over a long period of time, as up to one drink per day does not impair any cognitive function and may actually decrease the risk of a cognitive decline. [57] Furthermore, chronic alcoholism is associated with the impairment in both sustained attention and visual working memory. As a result, alcoholics have reduced ability, but not necessarily inability, to perform these executive tasks. This is assumed to be subserved by regions of the prefrontal cortex. [58] While it may not serve as a surprise that chronic alcoholism is linked to any decreased cognitive function such as working memory, one surprising finding is not only that even moderate levels of alcohol consumption during pregnancy were shown to have an adverse effect on the child's working memory when tested at 7.5 years of age, but also that working memory may be the most important aspect of attention that is adversely affected by prenatal alcohol exposure. [59]

Prospective memory

Prospective memory involves remembering to carry out an intended action in the future without an explicit reminder. [30] Alcohol has been found to impair this ability. Chronic heavy alcohol users report significantly more prospective forgetting compared to low-dose and alcohol-free controls. [60] The Prospective Memory Questionnaire assesses short-term habitual prospective memory, long-term episodic prospective memory, and internally cued prospective memory. [60] Chronic heavy alcohol users reported significantly greater deficits for all three aspects of prospective memory. [60] Individuals that report heavy alcohol use report 24% more difficulties with prospective memory than those who report that they are light drinkers and 30% more difficulties than those who report that they never drink. [61] The effects of alcohol on prospective memory can also be assessed in the laboratory by simulating prospective memory tasks that individuals face in everyday life. Individuals who are given 0.6 g/kg alcohol prior to performing prospective memory tasks do significantly poorer than a placebo group. [62] Alcohol can damage the prefrontal and frontal areas of the brain, and this may be responsible for prospective memory impairments since prospective memory performance is highly correlated with frontal executive functions. [60]

The memory inhibiting effects of alcohol are often a prominent topic in popular culture. It appears in movies, books, and television shows. Several movies show characters drinking alcohol to the point of memory loss and awakening the next morning with a host of problems due to actions they performed while intoxicated.

One example is The Hangover, where three groomsmen lose the groom during a bachelor party in Las Vegas, so they retrace their steps to find him. [63] The characters still had functioning implicit/procedural memory, which allowed them to carry out the many acts they performed that night, but their episodic memory was impaired and thus they had no recollection of the events occurring. In addition to alcohol the characters were also under the influence of flunitrazepam.

Another movie is What Happens in Vegas. After an intoxicated night in "Sin City," two people wake-up to find they got married. [64]

Songs such as Waking Up in Vegas by Katy Perry [65] and Last Name by Carrie Underwood [66] also depict characters waking up and not remembering the night before due to alcohol consumption.

By some accounts, popular culture makes light of the memory problems that can result from alcohol consumption.

The court case R. v. Daviault [1994] concerned the viability of a legal defense based on intoxication.

See also

Related Research Articles

Long-term memory (LTM) is the stage of the Atkinson–Shiffrin memory model in which informative knowledge is held indefinitely. It is defined in contrast to sensory memory, the initial stage, and short-term or working memory, the second stage, which persists for about 18 to 30 seconds. LTM is grouped into two categories known as explicit memory and implicit memory. Explicit memory is broken down into episodic and semantic memory, while implicit memory includes procedural memory and emotional conditioning.

<span class="mw-page-title-main">Hippocampus</span> Vertebrate brain region involved in memory consolidation

The hippocampus is a major component of the brain of humans and other vertebrates. Humans and other mammals have two hippocampi, one in each side of the brain. The hippocampus is part of the limbic system, and plays important roles in the consolidation of information from short-term memory to long-term memory, and in spatial memory that enables navigation. The hippocampus is located in the allocortex, with neural projections into the neocortex, in humans as well as other primates. The hippocampus, as the medial pallium, is a structure found in all vertebrates. In humans, it contains two main interlocking parts: the hippocampus proper, and the dentate gyrus.

In neurology, anterograde amnesia is the inability to create new memories after an event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions of the brain involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

<span class="mw-page-title-main">Fornix (neuroanatomy)</span> Bundle of nerve fibers in the brain

The fornix is a C-shaped bundle of nerve fibers in the brain that acts as the major output tract of the hippocampus. The fornix also carries some afferent fibers to the hippocampus from structures in the diencephalon and basal forebrain. The fornix is part of the limbic system. While its exact function and importance in the physiology of the brain are still not entirely clear, it has been demonstrated in humans that surgical transection—the cutting of the fornix along its body—can cause memory loss. There is some debate over what type of memory is affected by this damage, but it has been found to most closely correlate with recall memory rather than recognition memory. This means that damage to the fornix can cause difficulty in recalling long-term information such as details of past events, but it has little effect on the ability to recognize objects or familiar situations.

<span class="mw-page-title-main">Spatial memory</span> Memory about ones environment and spatial orientation

In cognitive psychology and neuroscience, spatial memory is a form of memory responsible for the recording and recovery of information needed to plan a course to a location and to recall the location of an object or the occurrence of an event. Spatial memory is necessary for orientation in space. Spatial memory can also be divided into egocentric and allocentric spatial memory. A person's spatial memory is required to navigate in a familiar city. A rat's spatial memory is needed to learn the location of food at the end of a maze. In both humans and animals, spatial memories are summarized as a cognitive map.

In neurology, retrograde amnesia (RA) is the inability to access memories or information from before an injury or disease occurred. RA differs from a similar condition called anterograde amnesia (AA), which is the inability to form new memories following injury or disease onset. Although an individual can have both RA and AA at the same time, RA can also occur on its own; this 'pure' form of RA can be further divided into three types: focal, isolated, and pure RA. RA negatively affects an individual's episodic, autobiographical, and declarative memory, but they can still form new memories because RA leaves procedural memory intact. Depending on its severity, RA can result in either temporally graded or more permanent memory loss. However, memory loss usually follows Ribot's law, which states that individuals are more likely to lose recent memories than older memories. Diagnosing RA generally requires using an Autobiographical Memory Interview (AMI) and observing brain structure through magnetic resonance imaging (MRI), a computed tomography scan (CT), or electroencephalography (EEG).

Explicit memory is one of the two main types of long-term human memory, the other of which is implicit memory. Explicit memory is the conscious, intentional recollection of factual information, previous experiences, and concepts. This type of memory is dependent upon three processes: acquisition, consolidation, and retrieval.

<span class="mw-page-title-main">Acamprosate</span> Medication

Acamprosate, sold under the brand name Campral, is a medication which reduces alcoholism cravings. It is thought to stabilize chemical signaling in the brain that would otherwise be disrupted by alcohol withdrawal. When used alone, acamprosate is not an effective therapy for alcohol use disorder in most individuals, as it only addresses withdrawal symptoms and not psychological dependence. It facilitates a reduction in alcohol consumption as well as full abstinence when used in combination with psychosocial support or other drugs that address the addictive behavior.

A drug-related blackout is a phenomenon caused by the intake of any substance or medication in which short-term and long-term memory creation is impaired, therefore causing a complete inability to recall the past. Blackouts are frequently described as having effects similar to that of anterograde amnesia, in which the subject cannot recall any events after the event that caused amnesia.

<span class="mw-page-title-main">Ro15-4513</span> Chemical compound

Ro15-4513 is a weak partial inverse agonist of the benzodiazepine class of drugs, developed by Hoffmann–La Roche in the 1980s. It acts as an inverse agonist, and can therefore be an antidote to the acute impairment caused by alcohols, including ethanol, isopropanol, tert-butyl alcohol, tert-amyl alcohol, 3-methyl-3-pentanol, methylpentynol, and ethchlorvynol.

Memory and trauma is the deleterious effects that physical or psychological trauma has on memory.

<span class="mw-page-title-main">Alcohol withdrawal syndrome</span> Medical condition

Alcohol withdrawal syndrome (AWS) is a set of symptoms that can occur following a reduction in alcohol use after a period of excessive use. Symptoms typically include anxiety, shakiness, sweating, vomiting, fast heart rate, and a mild fever. More severe symptoms may include seizures, and delirium tremens (DTs); which can be fatal in untreated patients. Symptoms start at around 6 hours after last drink. Peak incidence of seizures occurs at 24-36 hours and peak incidence of delirium tremens is at 48-72 hours.

<span class="mw-page-title-main">Short-term effects of alcohol consumption</span> Overview of the short-term effects of the consumption of alcoholic beverages

The short-term effects of alcohol consumption range from a decrease in anxiety and motor skills and euphoria at lower doses to intoxication (drunkenness), to stupor, unconsciousness, anterograde amnesia, and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once it is in the bloodstream, it can diffuse into nearly every cell in the body.

Memory consolidation is a category of processes that stabilize a memory trace after its initial acquisition. A memory trace is a change in the nervous system caused by memorizing something. Consolidation is distinguished into two specific processes. The first, synaptic consolidation, which is thought to correspond to late-phase long-term potentiation, occurs on a small scale in the synaptic connections and neural circuits within the first few hours after learning. The second process is systems consolidation, occurring on a much larger scale in the brain, rendering hippocampus-dependent memories independent of the hippocampus over a period of weeks to years. Recently, a third process has become the focus of research, reconsolidation, in which previously consolidated memories can be made labile again through reactivation of the memory trace.

Kindling due to substance withdrawal is the neurological condition which results from repeated withdrawal episodes from sedative–hypnotic drugs such as alcohol and benzodiazepines.

<span class="mw-page-title-main">Memory improvement</span> Act of improving ones memory

Memory improvement is the act of enhancing one's memory. Factors motivating research on improving memory include conditions such as amnesia, age-related memory loss, people’s desire to enhance their memory, and the search to determine factors that impact memory and cognition. There are different techniques to improve memory, some of which include cognitive training, psychopharmacology, diet, stress management, and exercise. Each technique can improve memory in different ways.

<span class="mw-page-title-main">Effects of stress on memory</span> Overview of the effects of stress on memory

The effects of stress on memory include interference with a person's capacity to encode memory and the ability to retrieve information. Stimuli, like stress, improved memory when it was related to learning the subject. During times of stress, the body reacts by secreting stress hormones into the bloodstream. Stress can cause acute and chronic changes in certain brain areas which can cause long-term damage. Over-secretion of stress hormones most frequently impairs long-term delayed recall memory, but can enhance short-term, immediate recall memory. This enhancement is particularly relative in emotional memory. In particular, the hippocampus, prefrontal cortex and the amygdala are affected. One class of stress hormone responsible for negatively affecting long-term, delayed recall memory is the glucocorticoids (GCs), the most notable of which is cortisol. Glucocorticoids facilitate and impair the actions of stress in the brain memory process. Cortisol is a known biomarker for stress. Under normal circumstances, the hippocampus regulates the production of cortisol through negative feedback because it has many receptors that are sensitive to these stress hormones. However, an excess of cortisol can impair the ability of the hippocampus to both encode and recall memories. These stress hormones are also hindering the hippocampus from receiving enough energy by diverting glucose levels to surrounding muscles.

<span class="mw-page-title-main">Memory</span> Faculty of mind to store and retrieve data

Memory is the faculty of the mind by which data or information is encoded, stored, and retrieved when needed. It is the retention of information over time for the purpose of influencing future action. If past events could not be remembered, it would be impossible for language, relationships, or personal identity to develop. Memory loss is usually described as forgetfulness or amnesia.

The long-term impact of alcohol on the brain has become a growing area of research focus. While researchers have found that moderate alcohol consumption in older adults is associated with better cognition and well-being than abstinence, excessive alcohol consumption is associated with widespread and significant brain lesions. Other data – including investigated brain-scans of 36,678 UK Biobank participants – suggest that even "light" or "moderate" consumption of alcohol by itself harms the brain, such as by reducing brain grey matter volume. This may imply that alternatives and generally aiming for lowest possible consumption could usually be the advisable approach.

The hippocampus participates in the encoding, consolidation, and retrieval of memories. The hippocampus is located in the medial temporal lobe (subcortical), and is an infolding of the medial temporal cortex. The hippocampus plays an important role in the transfer of information from short-term memory to long-term memory during encoding and retrieval stages. These stages do not need to occur successively, but are, as studies seem to indicate, and they are broadly divided in the neuronal mechanisms that they require or even in the hippocampal areas that they seem to activate. According to Gazzaniga, "encoding is the processing of incoming information that creates memory traces to be stored." There are two steps to the encoding process: "acquisition" and "consolidation". During the acquisition process, stimuli are committed to short term memory. Then, consolidation is where the hippocampus along with other cortical structures stabilize an object within long term memory, which strengthens over time, and is a process for which a number of theories have arisen to explain the underlying mechanism. After encoding, the hippocampus is capable of going through the retrieval process. The retrieval process consists of accessing stored information; this allows learned behaviors to experience conscious depiction and execution. Encoding and retrieval are both affected by neurodegenerative and anxiety disorders and epilepsy.

References

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  63. ↑ "The Hangover" (2009). Retrieved from https://www.imdb.com/title/tt1119646/.
  64. ↑ "What Happens in Vegas" (2008). Retrieved from https://www.imdb.com/title/tt1033643/plotsummary.
  65. ↑ "YouTube – Waking Up in Vegas Lyrics – Katy Perry" (2009). Retrieved from https://www.youtube.com/watch?v=06Qf7GdAF70
  66. ↑ "YouTube – Carrie Underwood – Last Name" (2009). Retrieved from https://www.youtube.com/watch?v=f27zNlmRMWU
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