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Is Cognitive Functioning Impaired in Methamphetamine Users? A Critical Review

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Influence of Drugs on Cerebral Functions

Claudia Juárez-Portilla, Tania Molina-Jiménez, Jean-Pascal Morin, Gabriel Roldán-Roldán and Rossana Citlali Zepeda

Submitted: August tertiary, 2017 Reviewed: Oct 21st, 2017 Published: December 20th, 2017

DOI: 10.5772/intechopen.71842

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Abstract

Disorders related to the misuse of sure drugs represent not only a worldwide public health problem, simply likewise an economic and social consequence. Adolescents and children stand for the most vulnerable population for drug consumption and addiction. At this early on phase in life, a crucial phase of the neurodevelopmental process, substance abuse tin can induce brain plasticity mechanisms that may produce long-lasting changes in neural circuitry and ultimately beliefs. One of the consequences of these changes is the damage of cerebral functions, with bookish negative touch in the acquisition of new knowledge. In this affiliate, we volition depict the effects of illicit substances of abuse, both stimulants and depressants as well every bit prescription drug misuse and its influence of on learning and memory processes. Contempo prove on the new then-called smart drugs is also discussed.

Keywords

  • abuse
  • cognition
  • functioning
  • nootropic
  • smart
  • stimulants
  • depressant
  • retentiveness
  • impairment
  • adolescent

i. Introduction

Co-ordinate to United Nations Role on drugs and Offense, in 2015, around a quarter of a billion people used drugs, and approximately 29.5 million showed drug use disorders, including dependence [1]. Drug abuse produces health disruption. Disorders related to the utilise of certain drugs are associated with an important worldwide rate of morbidity. A wide range of drug-induced neurobiological modifications have been described; some of which tin can affect learning and memory functions. Stimulant drugs, like nicotine and amphetamine, better cognitive role at lower doses but impair retentivity operation at college doses. Depressant drugs, like booze, tin can cause long-term effects on prefrontal cortex function, disrupting cognitive abilities.

Several studies accept suggested that the influence of psychoactive drugs on learning and memory might be explained, at least in part, considering of the shared neurobiological mechanisms involved in learning and retention processes and the drug-induced structural and functional changes in the encephalon. Anatomically, there is an important overlap between the neural substrates of learning and memory and those of addiction. Some of the areas that show overlap include the cerebral cortex, hippocampus, amygdala and striatum [2]; all of them are components of the mesolimbic dopaminergic system.

Adolescence is a sensitive period in brain development characterized by a subtract in gray matter and an increase in white thing. The diminution of gray matter is thought to be due, at least in part, to the process of synaptic pruning, which is the developmental refinement of brain circuits past removal of superfluous synapses [three]. Early drug exposure is associated with frontal lobe damage, depression cognitive operation and emotional learning, every bit well as other behaviors. Moreover, it has been demonstrated that adolescent exposure to both prescription and social drugs impairs cognition, likewise every bit other behaviors, in the adulthood [4].

There is a clear bidirectional relationship betwixt abuse of drugs and poor academic achievement. Information technology has been suggested that cerebral deficits could make adolescents more vulnerable to substance abuse than others; conversely, other proposals debate that substance abuse is the source of cerebral impairments [five, 6, 7]. Of course the two possibilities are non mutually sectional; teenagers with poor academic performance may be more prone to abusing illicit drugs, which may impair their results at schoolhouse even farther. While the several social science theories have been proposed to try to explicate each of these phenomena [6], in the following text, we will focus on the cognitive consequences of adolescent substance abuse on the functioning of the nervous system that may accept a deleterious touch on cerebral abilities, academic achievement and long-term satisfaction with life in general.

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2. Stimulant drugs

Memory is the natural counterpart of learning; both are necessary for behavioral change that precedes survival of species. Substance abuse has been demonstrated to exert detrimental impact upon learning and memory. According to the United Nations Part on Drugs and Crime through Earth Drug Report 2017, 29.v million people globally suffer from drug use disorders [eight]. Cerebral harm is a well-established effect of long-term substance corruption, with stimulants every bit nicotine, methamphetamine (MA) and cocaine leading deficits in the area of executive part. Stimulants are a class of illicit drugs that tin have negative impact on individuals who use them, although this affect might exist masked by the believed benefits (Table ane) [9].

Drug Cognitive process Effect Model Reference
Stimulant drugs Attention
Vigilance
Memory		 Acute :
Improving selective visuospatial attention, spatial working memory and associative memory		 Monkey
Rat
Mice
Zebrafish
Human		 [10, 11]
Chronic :
Tolerance
Withdrawal syndrome
Mild deficits in memory and inhibition response
Disruption in prospective and visual retention, exact ability, reasoning and decision making		 Human
Rat		 [xiii, 25, 26, 27, 29]
Depressant drugs Attention
Retention		 Astute/depression doses :
Facilitation in working memory, verbal fluency and executive functions
Impaired working retentiveness, verbal fluency and executive functions		 Homo [37, 38, 41, 55, 56, 57]
Chronic/high doses :
Disruption in working and episodic retentivity, consolidation retention, attention and memory Also, presence of blackouts		 Human [39, 61, 62, 63, 64, 65, 66, 67]

Table 1.

Furnishings of the stimulants and depressant drugs in cerebral functions.

2.1. Nicotine

Nicotine is the main psychoactive component of tobacco and the responsible agent of tobacco dependency. According to the World Health Arrangement, despite its severe health consequences, about one billion people fume worldwide.

When nicotine is administered acutely, it produces positive effects improving cognitive functions, including sustained attention, vigilance, visuospatial selective attention, spatial working retentivity and associative retentivity, both in animal models [ten] and in humans [11]. Conversely, a vast amount of literature has showed that chronic nicotine utilise leads to tolerance, and 1 h afterward cessation of nicotine exposure, nicotine withdrawal syndrome emerges and it is characterized by mild cognitive deficits. In other words, nicotine tends to improve cognitive role at lower doses and impair performance at higher doses [12]. Furthermore, heavy smokers under astute abstinence from smoking feel decreased neurocognitive functions, including impairments in sustained attention, working memory and response inhibition [xiii]. Strong activation of memory-related brain regions that include the dorsolateral prefrontal cortex and hippocampus has been correlated with smoking-related cues in adult heavy smokers [fourteen]. These areas are involved in emotional learning and reward-related learning.

Some reports have shown that nicotine and nicotinic agonists, as mecamylamine, evoked cognitive enhancement past potentiating the release of dopamine [12, xv]. Working memory is critically reliant on dopaminergic neurotransmission. In add-on, rodent studies have revealed a straight human relationship between dopamine release in the prefrontal cortex and on memory job accuracy [16]. Moreover, cholinergic systems and nicotinic receptors are essential for cognitive processes and accept been implicated in diseases associated with cerebral impairment [17].

two.2. Methamphetamine (MA)

MA abuse represents a serious public wellness issue associated with a loftier likelihood of relapse. By 2008, nearly 25 million people worldwide were estimated to accept used MA, with abuse being amid younger age groups [xviii]. MA used is mainly for recreational purposes and it is known to induce a variety of desirable effects, including increased energy levels, positive mood, euphoria, reduced appetite, weight loss, enhanced mental acuity and social and sexual disinhibition [19]. In addition, MA-dependent individuals oftentimes claimed enhancement of cerebral function and ability to focus following drug assistants. However, this drug induces long-term changes in the brain structure and function, changes in synaptic plasticity, jail cell decease via apoptosis and neurotoxicity, and consequently, it causes dependence and withdrawal syndrome [20].

Anatomically, MA has a preferential neurotoxic upshot on the frontostriatal systems that contributes to both emotion dysregulation and neurocognitive damage [21]. For instance, MA addicts showed impaired performance on tests of cognitive flexibility, which measures the ability to alter behavior when presented with new information or irresolute outcomes. These deficits may impair MA addicts from altering their habitual drug abuse behavior, leading to an disability to initiate abstinence or resist relapse [22]. Cellular mechanism of this MA impairment has been associated with long-term downregulation of dopamine transporters, suggesting that there are structural changes in some of the dopamine nerve terminals [23]. Other findings suggest that MA employ causes changes in the metabolism of the insula and striatum [24]. In a written report in humans, MA-dependent participants had significantly lower results than control participants on memory tasks, including prospective memory and visual retentivity [25]. Appropriately, studies in immature developed MA abusers accept shown impaired verbal power, deficits in psychomotor processing [26], reasoning deficits reflecting problematic decision-making abilities as well every bit retrospective memory task impairment [27].

The evidences pointed that astute assistants of MA improves cerebral functions, while chronic consumption of MA deteriorates them.

2.three. Cocaine

Cocaine has long been 1 of the most common recreational stimulants, especially for adolescents. A recent judge indicates that half a million of United States habitants use this drug weekly; in this sense, cocaine addiction represents a substantial brunt for societies worldwide, linked to agin outcomes such equally violence, suicide and disability, as well as loftier rates of chronic relapse [28]. In the brain, crack cocaine use has been shown to crusade toxic effects, particularly in the prefrontal cortex. These abnormalities are associated with neuropsychological impairments.

Abundant evidence has shown that cocaine withdrawal induces memory decline after its chronic utilise. It has been reported that chronic cocaine users showed significant harm on verbal memory and fluency also as deficits in cerebral flexibility, just not in spatial memory, after acute withdrawal. Further, Briand and colleagues observed that object recognition was disturbed after withdrawal from chronic exposure to cocaine by an object recognition chore in 2-calendar week abstinent rats [29]. Several reports accept shown that the insular and prefrontal cortices, involved in cognitive control, show reduced activity on selective attention and inhibitory control tasks in cocaine addicts [xxx]. These brain areas may be involved in the maintenance and relapse of drug apply [31]. Individuals with cocaine abuse and dependence testify college insula, frontal and/or striatum activation in response to cocaine-related cues, reflecting heightened attending in response to this drug [32, 33]. Furthermore, imaging data have revealed that grayness affair volume loss over time is twice as fast among cocaine addicts as in healthy individuals. Given that gray matter book in prefrontal cortex has been related to working retentivity performance, these findings are in keeping with the idea that long-term cocaine use may cause sustained deleterious effect on working memory.

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3. Depressant drugs

Adolescence is the critical period for initiation of alcoholic beverage consumption. Epidemiologic studies reveal that alcohol use is remarkably common among teenagers, with increasing rates of alcohol abuse in the US including heavy episodic drinking [33]. Later alcohol and tobacco, marijuana is the social drug most frequently consumed by this accomplice. Additionally, a high percentage of alcohol abusers also consume marijuana [34]. Several studies have shown that both booze and marijuana tend to alter the construction and part of the brain and are associated with impaired decision-making, retentiveness and impulsivity in immature adults and adolescents (Table i).

3.ane. Ethanol

Evidence shows a direct correlation betwixt early onset of alcohol intake and alcohol-related problems in adulthood, suggesting that adolescent exposure to the reinforcing properties of this drug increases the probability of its abuse later [35]. Yet, as for other addictive substances, the effect of exposure to alcohol depends to a great extent on how much and for how long it is consumed.

Acute booze intake has a biphasic upshot on brain activity, causing excitation and euphoria at depression claret concentration and depression equally information technology increases [36]. However, regarding cognitive functions, experimental data have been inconsistent using a variety of cognitive tests. Thus, low or moderate doses of alcohol, relative to placebo, produced facilitation [37, 38], deficits [39] or no change [40] in retention performance at subtoxic amounts (<65 mg/dl). Moreover, it plainly does non produce adverse furnishings and may even slightly improve working memory in nonproblem drinkers, regardless of sexual practice [41]. Nevertheless, as the dose of alcohol increases, confusion, loss of awareness and selective attention begin to occur, significantly diminishing the execution of working memory and its long-term consolidation. The effect of alcohol on long-term memory formation is much greater than its touch on the capacity to recall previously consolidated memories or to retrieve brusk-term retention. It is well known that if subjects are asked to echo newly acquired information following short delays (seconds) later on its presentation while intoxicated, they often do fine [42]. Likewise, they are able to recall data acquired earlier astute intoxication. On the reverse, subjects perform very poorly using delays longer than 20 min, specially if they are distracted between the stimulus presentation and testing [43].

As studies indicate that the extent of alcohol-induced retentiveness deficits increases with the dose simply maintains the same design (i.e., greater difficulty at forming new long-term memories than recalling the existing ones), it appears that this drug mostly affects memory consolidation.

Unfortunately, during adolescent life, repeated intoxication with high doses of alcohol becomes more frequent and memory impairments are more profound, commonly resulting in blackouts, that is, a complete incapability to remember all or part of a drinking event [44]. Heavy alcohol drinking associated with blackouts [45] does not necessarily involve loss of consciousness, but rather a failure to transfer information from brusk- to long-term retentivity [46]. Individuals with a history of blackouts evidence episodic retention impairments while intoxicated [47], especially at retrieving the spatiotemporal context of events [48]. Moreover, long-term (3 years) heavy alcohol intake in adolescents between fifteen and xix years of age induced memory deficits [49] likewise as volume reduction in subcortical and temporal regions [50].

The mechanisms underlying alcohol-induced memory disruption are still elusive. Throughout several decades, it was supposed that booze produces a nonspecific general depression of brain activity. Later, enquiry led to supposition that alcohol depressed the activity of neurons past altering the fluidity of the neuronal membrane and consequently the activity of proteins, including ion channels that might, in turn, produce synaptic dysfunctions [51].

It was not until recently that new pharmacological data regarding the effects of booze on neural cells revealed that this drug has actually very selective effects on various neurotransmitter systems, both excitatory, east.k., glutamatergic and cholinergic, and inhibitory, such equally GABAergic, glycinergic and serotonergic amidst others. Alcohol could modify the activeness of specific receptor subtypes besides [52]. All these neurotransmission mechanisms have a deep bear on on cerebral functions. Paradoxically, repeated booze exposure might promote the germination of a particular drug-advantage–associated implicit retentiveness that could underlay its habit [53].

The primary risk of booze ingestion early in life is that the adolescent brain is still in a maturation catamenia and drug intoxication profoundly affects its development and the private's futurity life.

3.2. Cannabis

Recently, endocannabinoids, endogenous ligands that bind to and activate the same receptors as ix-delta-tetrahydrocannabinol (THC), the psychoactive component of cannabis, were found to play an important function in the diminution of grayness affair [three]. Cannabis is the third most prevalent drug of abuse amid teenagers, behind alcohol and tobacco [54]. Many studies in humans have shown that chronic cannabis consumption, especially when initiated early in life, correlates with a range of cognitive impairments in adulthood, including learning and retention deficits. Meanwhile, the evidence remained equivocal, partly due to the myriad of confounding factors, characteristic of human being studies, too equally different methodology employed by the distinct studies, some unveiling clear effects, while others finding marginal or no furnishings [55]. However, in recent years, a clearer picture is emerging, which seems to propose that teenage cannabis consumption may indeed have long-term detrimental furnishings on cerebral processes, including memory. The present section surveys the testify linking boyish cannabis consumption and prevailing memory deficits. We will further discuss the present state of cognition on such questions as how is it that cannabis consumption can touch retentivity? Is memory homogenously affected or are there certain types of memory more impaired? Also, if cannabis intake during adolescence affects brain function in the long-term, are such sequelae reversible?

Starting time, as for the acute effects of marijuana consumption, impaired working memory during the astute phase of cannabis intoxication has been observed in several studies [55, 56]. For example, randomized clinical trials with dronabinol, a constructed derivate of THC, revealed impaired verbal fluency, working memory and executive functions in healthy subjects during and in the hours following intoxication [57]. On the other hand, other works on healthy subjects plant that performance on exact working retention was left unaffected but that the tasks elicited a higher activation of parahippocampal areas, which may bespeak either "neurophysiological inefficiency" or alternate/compensatory neural mechanisms in these subjects [58]. This is consequent with another fMRI study that was conducted on otherwise good for you adults that were current marijuana users and that showed hyperactivation during a verbal working retention challenge, which the authors propose may be related to suboptimal efficiency during cerebral challenge in this group [59]. Finally, another study by the same group showed that the frequency of cannabis use is positively correlated to blood oxygenation level–dependent signal in the left parahippocampal gyrus during a visual associative memory task, regardless of the historic period of onset (early on vs. late adolescence) [60].

But beyond the acute intoxication stage, i obvious question is whether cannabis consumption produces long-term sequelae on cognition. Working retention functioning appears to exist especially sensitive to cannabis consumption in the early teenage years (before the age of xvi–17). Testing 122 long-term heavy cannabis users on a corroborated 28-solar day abstinence period and 87 control subjects, Pope and collaborators showed that although adult-onset cannabis users inappreciably differed from controls, those that started before the age of 17 were impaired in a series of cerebral tests, most especially in exact retentiveness [61]. Further research has shown that the observed cannabis-induced deficits may prevail fifty-fifty after 6 weeks of discontinuation; although after 3 months of complete discontinuation, no divergence was observed between previous heavy users and controls [62]. Notwithstanding, a more recent study in adolescents 18–20 years old with a history of chronic, heavy cannabis use, while functioning in a verbal memory test was comparable to that of age-matched controls, a significant bilateral atrophy was observed, even after 6 months of supervised drug abstinence [63]. The putative detrimental effects of cannabis use appear to be dose-dependent. For example, performance in the Rey Auditory Verbal Learning Test correlated negatively with the number of years of cannabis misuse [64].

Nonetheless, these results did not allow to make up one's mind whether cannabis had long-term detrimental effects on the cognitive abilities and encephalon functioning of these youths in one case they reached adulthood or whether a preexisting set of slight cognitive deficiencies such as lower exact retentiveness somewhat predisposed these youths to maladaptive behaviors including early-onset cannabis consumption. More to the point, as the authors pointed out, fifty-fifty if the toxic effects of cannabis were the culprit, it was impossible to determine in the light of these results, whether the observed differences were due to long-term effects of cannabis on these subjects or more brusk-term effects during adolescence that made them perform poorly at schoolhouse and therefore made them less prone to develop these cognitive skills through machismo.

In this regard, a recent widely reaching assay from the Cannabis Cohorts Research Consortium using data from iii distinct longitudinal studies started to shed light on this issue [57]. The study found that young adults that were cannabis users as teenagers were more likely to experience adverse outcomes as diverse as cannabis habit, suicide attempt and high-school dropout. Importantly, the authors study that controlling for the potential confounding factors present, both before and during boyhood and spanning private, parental and peer factors, failed to abolish virtually of the associations observed. Along with the fact that they likewise observed a dose-response relation, heavy users having the poorest outcomes as adults, the findings support the hypothesis that teenage marijuana consumption has long-term detrimental furnishings on cognition, retentivity and general well-existence. Finally, preclinical research brought farther support for a causal relationship between teenage cannabis consumption and adult cerebral impairments; chronic consumption of cannabis in rats during adolescence, but not adulthood, dumb spatial working memory when tested as adults [65, 66].

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4. Prescription drugs

According to the Anxiety and Depression Clan of America, mental disorders are common among children in the United States. Feet and major depression disorders are ordinarily diagnosed in children between 8 and 15 years of historic period (National Wellness and Nutrition Examination Survey). The handling of metal disorders in children and adolescents depends on the damage degree. Yet, these treatments usually include drugs that affect cerebral functions. On the other manus, during childhood and adolescence, sports activities, especially at college levels, are often a crusade of painful injuries that requires acute or chronic treatment of anti-inflammatory and/or analgesic drugs. All these treatments that are administered to school students could have an impact on cerebral functions and therefore on academic achievement. In this section, nosotros will discuss the effects of nonsteroidal anti-inflammatory, anxiolytic and antidepressant drugs (Tabular array 2).

Drug Cognitive procedure Effect Model Reference
Prescription drugs Spatial memory impairment Acute administration: Neuroprotection
Subchronic administration: improving cognitive functions
Chronic administration: better spatial memory impairment		 Rat
Mouse		 [70, 71, 72, 73, 74, 75]
Cognitive and emotional alterations Reestablishment of the deterioration in memory and spatial learning
Diminish despair and memory damage
Chronic assistants: increase jail cell proliferation in hippocampus
Increment of BDNF levels		 Human Rat [78, 81, 82, 83, 84, 85, 86]
Memory and learning impairment Restore cognitive impairment
Better executive role
Increment spatial memory		 Mouse [88, 89, xc]
Knowledge-enhancing drugs Formation of memories and performing tasks Enhancing cognitive functioning in Alzheimer's illness patients
Amend cognitive functions as: verbal memory, attention memory, data processing, executive function and memory mood		 Human [95, 96]
Alertness and enhance cognition Improves attending, retention and executive function in slumber-deprived individuals
Express effects in nonsleep deprived
Mental performance of subjects with low baseline performance		 Man [101, 102, 103, 104, 105]
Attention deficit/hyperactivity disorder Improve knowledge processes as: working retentiveness, speed of processing, verbal learning and retentivity and attention Human
Rat		 [107, 108, 109, 111]

Table 2.

Furnishings of the prescription and cognition-enhancing drugs in cognitive functions.

4.1. Nonsteroidal anti-inflammatory drugs (NSAIDs)

NSAIDs are therapeutic agents commonly used in clinical practice for their analgesic, anti-inflammatory and antipyretic activity [67]. Although these chemical compounds are structurally different, they all inhibit both isoforms of the cyclooxygenase enzyme, COX-1 and COX-ii, an enzyme responsible for inflammation and hurting, which is necessary for prostaglandins and prostanoid synthesis [68]. Unremarkably, COX-two is expressed in dendritic spines of hippocampal and cortex neurons and has been implicated in synaptic modification, because its expression increases during long-term potentiation [69]. Moreover, astrocytes express prostaglandin E2 receptors (EP) and prostaglandin E2 (PGE2), which regulate membrane excitability, synaptic transmission and synaptic plasticity implicated in learning and memory processes [lxx]. Also, the administration of misoprostol, an agonist of PGE2 receptors, ameliorates the long-term deficits observed in Huntington illness R6/1 mice by increasing the branching in hippocampal neurons and stimulating the synthesis of brain-derived neurotrophic factor (BDNF) [71]. Furthermore, subchronic administration of acetylsalicylic and ascorbic acids increases expression of receptors related with cognitive function such as learning and memory, while chronic treatment of acetylsalicylic acid lessens the spatial retentiveness damage observed in an experimental model of Alzheimer's disease [72]. Several reports bespeak that celecoxib, a selective COX-ii inhibitor, reduces oxidative stress in a model of hypoxia reoxygenation, reducing the activation of microglia and astrocytes in the neonatal rat brain and improving cerebral function, suggesting that celecoxib may have neuroprotective actions [73]. In improver, multiple exposures to sevoflurane, a model that mimics the neurotoxicity induced by anesthesia, produces an increment in proinflammatory cytokines and deterioration in cognitive office in young mice, effects that were attenuated past the administration of ketorolac [74]. Another written report showed that meloxicam ameliorated the depressive-like behavior, cognitive impairment and neuroinflammation in hippocampus caused by chronic unpredictable balmy stress [75]. Then, NSAIDs indirectly could disrupt cognitive functions.

4.2. Antidepressant drugs

Major depression is a common mental disorder affecting adolescents in the United States. According to the National Institute of Mental Health, in 2015, an estimated of three million adolescents aged 12–17 in the United States had, at least, one major depressive episode. Major depressive disorder is a long-term disabling condition occurring with relapse and recurrences, which could become a chronic status [76]. Amidst all the symptoms presented in this psychopathology, memory and attention deficits are considered an important clinical manifestation of major depressive disorder [77]. Furthermore, cognitive and emotional alterations observed in depressive patients take been associated with changes in neuronal activity of prefrontal cortex, cingulate cortex and hippocampus. In major depressive disorder, orbitofrontal, ventromedial and prefrontal cortices are hypoactive, and postmortem evidence indicates histopathological changes in orbitofrontal and prefrontal cortex [78]. Additionally, significant hyperactivity in anterior cingulated cortex, inferior frontal gyrus and occipitoparietal regions has been observed in adolescents with major depressive disorder [79]. Besides, a reduction in the volume of the hippocampus was reported, which is related to the severity and the elapsing of the major depressive disorder [eighty]. All these alterations were shown to contribute to changes in cerebral and emotional processing in depressive patients. Nevertheless, antidepressant handling contributed to reestablish mood and cognitive functions. For example, the chronic assistants of deprenyl, a monoamine-oxidase-B inhibitor, reestablished the deterioration in retentiveness and spatial learning and also macerated the lipid peroxidation and the neuronal loss in prefrontal cortex, striatum and hippocampus [81]. Moreover, treatment with desipramine, a norepinephrine reuptake inhibitor, caused reestablished long-term potentiation and diminished despair and memory impairment, through activation of CREB in the hippocampus [82]. Similar furnishings were observed with fluoxetine (serotonin reuptake inhibitor); rats receiving a chronic treatment of fluoxetine increased cell proliferation and BDNF in hippocampus associated to a retentivity and learning improvement [83]. These studies suggest that antidepressants revert retentiveness and learning deterioration observed in fauna models of depression.

Regarding clinical studies, patients with major depressive disorder showed lower levels of BDNF in plasma, which correlates with retention function deficits; hence, BDNF levels increased after the antidepressant handling [84]. Nevertheless, the impairment in psychomotor and memory processes observed in depressed treated patients has no significance for clinical purposes [85]. Moreover, some evidence has shown that conventional antidepressant treatment selectively diminishes cognitive dysfunction [86].

The involvement of antidepressant drugs in cognitive functions is non clear; all the same, animal model studies have shown that synaptic plasticity is increased in neuronal regions involved in mood and retention processing [81, 82, 83, 84].

4.3. Anxiolytics

Cognitive impairments have been consistently reported in feet disorders. Benzodiazepine, which acts in a specific site of the GABA A receptor, has been, for many years, the first-line therapy for the treatment of anxiety disorders. Although benzodiazepines are attractive for their rapid therapeutic outcome, these drugs take undesirable side effects both in the short term (e.thousand., sedation) and in the long-term (e.g., dependence and retention impairment [87]). Some reports have indicated that GABAergic neurotransmission in the hippocampus is involved in the modulation of learning and retention functions [88]. Also, the administration of an inverse agonist of α5 subtype GABA A receptors (RO4938581) enhances long-term potentiation in hippocampus, restores the cognitive harm caused by the scopolamine treatment and improves the executive part in monkeys without affecting emotional state [89]. Furthermore, a partial inverse agonist of α5 subtype GABA A receptors increased spatial retentiveness [ninety]. These studies signal that GABAergic neurotransmission regulates memory and learning processes, which opens the possibility of designing new selective molecules with clinical utility, not just for treating anxiety disorders, merely also for improving cognitive functions.

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5. Cognition-enhancing drugs

The search for drugs that ameliorate cognitive functions to treat several diseases, including Alzheimer affliction (AD), attention arrears disorder (ADD), attending deficit hyperactivity disorder (ADHD), has derived a wide number of synthetic drugs that, in plough, increment learning, executive functions, or creativity in healthy people. These drugs, as well named "smart drugs" or "nootropics," have different chemical origins and mechanisms and in general take showed little or no effect in improving learning and retentiveness tasks. There is a growth in the consumption of these drugs past adolescents [91, 92], mainly due to academic demands and competitiveness [93]. According to the Federal Substance Abuse and Mental Health Services Administration, every year around 137,000 college students in the Us begin to use psychostimulants. Furthermore, consumption of stimulant drugs of corruption increases in key academic dates (Tabular array two) [94].

Nootropics have focused their targets on modulation of neurotransmission, hormones, transduction systems and neuron metabolism. However, nosotros will focus on legal stimulants commonly used by students to improve academic performance: acetylcholinesterase inhibitors, memantine, modafinil and methylphenidate.

5.1. Antidementia drugs

5.one.1. Acetylcholinesterase inhibitors (AChEIs)

Near of the drugs that are used to heighten cognitive functions, both in patients and in healthy volunteers, piece of work through acetylcholine (ACh) neurotransmission. ACh is a neurotransmitter closely involved in synaptic transmission and also in the formation of memories and performing tasks. Donepezil, rivastigmine or galantamine had expert results enhancing cognitive performance in patients with mild to moderate AD, when compared with placebo [95]. However, diverse studies conducted in good for you volunteers have showed that AChEIs lightly improve verbal memory after semantic processing of words, attending retention, information processing, executive role and memory mood [96].

five.1.two. Memantine

Memantine is a psychostimulant used to care for moderate to severe AD. It acts on the glutamatergic system by antagonizing N-methyl-d-aspartate (NMDA) receptors. This drug has been showed to slightly improve cerebral functions as monotherapy of Ad [97]. There are few studies most the cognitive-enhancing capacity of memantine on good for you volunteers. The studies published were tested with astute single dose of memantine, finding that this drug does not increment mental performance significantly [96].

5.ii. Modafinil

Modafinil is a psychostimulant indicated in the treatment of narcolepsy, shift work sleep disorder and excessive daytime sleepiness [98]. Since approval by FDA, in 1998, modafinil has been widely used not simply to treat wakefulness disorders, but as well to increase alertness and enhance cognition. Modafinil exhibits advantages among other psychostimulants, including the lack of unwanted side effects (e.m., tolerance, corruption potential, sleep rebound and locomotor excitability) [99], and, in almost countries, it is not a controlled substance; therefore, it tin be easily purchased online. Modafinil exerts its deportment through an unknown mechanism. Still, it is recognized that modafinil inhibits dopamine and noradrenaline uptake, elevates catecholamine'due south levels, therefore raises extracellular serotonin, glutamate, histamine and orexin and reduces GABA's concentration [100]. Although the effects of modafinil as a wakefulness promoter have been proven [101], its properties as cognitive enhancer are still controversial. In sleep-deprived individuals, modafinil improves attention, retentiveness and executive function [102], while the effects of modafinil in non–sleep-deprived adolescents are express [103]. Other reports have constitute that modafinil actually improves several cerebral functions [104]. Interestingly, modafinil has showed to enhance mental functioning of subjects with low baseline performance or IQ on several tasks evaluated [105].

5.iii. Methylphenidate (MPH)

MPH (Ritalin©) is a psychostimulant approved for the treatment of attention deficit/hyperactivity disorder (Add together/ADHD) [106]. Additionally, MPH is ane of the most effective cognitive enhancers used past healthy people [107], considering it acts through a machinery coordinating to that of cocaine: increases the levels of the catecholamines, dopamine, norepinephrine and serotonin, by blocking their send [108]. This drug improves working retention, speed of processing, verbal learning and retention and attention [102]. Withal, MPH furnishings are non restricted to spatial problems, since information technology also improves digit span exam score [109]. Although MPH has demonstrated to be effective and condom in most of the patients when used in the curt term, several side furnishings have been reported: subtract of appetite, insomnia, headache, irritability, weight loss, sadness, abdominal hurting, nausea, somnolence, dizziness, among others. Several studies take reported that MPH handling during babyhood produces "permanent" changes in behavioral responses to other psychostimulants [110]. Moreover, a recent study made on rats has showed that acute and long-term exposure of adolescents to MHP has important effects on reward-dependent learning and decision [111].

v.4. Considerations virtually apply and misuse of cognition-enhancing drugs

There are some difficulties evaluating the efficacy of smart drugs, mainly due to the heterogeneity of subjects and the differences in the cognitive evaluation methods. Besides, the disparities in the pattern of the studies have been challenging the evaluation of smart drugs in healthy subjects. Yet, there are some studies that have used systematic methodology to analyze the literature published on healthy volunteers [96, 97]. According to these reviews, antidementia drugs, AChEIs and memantine enhance cognitive functions in patients with Advertising; yet, their effects on healthy volunteers appear to be very poor [107]. Some other attribute to consider is the interindividual variability of volunteers, because information technology could be an important reason that masks the cerebral effect of these drugs.

There are also several ethical considerations about the use of psychostimulants in good for you people. Currently, caffeine is the stimulant well-nigh commonly used to get alertness. However, the misuse of MPH and modafinil is growing among students, since these drugs are cheap and easy to obtain illegally.

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6. Perspectives

Drug abuse and addiction to legal and illegal substances take become a major challenge in western adult and developing societies. Growing prove has shown that the onset age of drug consumption is effectually 15 years. At this age, the central nervous arrangement is still under maturation. Childhood and adolescence are critical stages for neural and social development. Therefore, worldwide increasing prevalence of drug abuse amongst teenagers will certainly have an outcome on scholar performance. All the prove described in the present review suggests that teenagers that swallow drugs risk deleterious consequences in their academic growth, since the neural mechanisms targeted past these drugs may have long-term impacts on cognitive functions. Therefore, prevention initiatives and public wellness programs must be implemented in schools to protect children and teenagers from escalating drug utilise.

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seven. Conclusion

In summary, the show regarding the possible long-term detrimental effects of teenage drug consumption on learning and memory adds to the increased risk of developing mental disorders, and therefore it should be included in public wellness information campaigns that seek to encourage delaying and/or reducing drug consumption at this stage of life. The scientific information obtained from studies such equally those described above will exist of little use without adequate public policies aimed at alleviating this serious problem.

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Written By

Claudia Juárez-Portilla, Tania Molina-Jiménez, Jean-Pascal Morin, Gabriel Roldán-Roldán and Rossana Citlali Zepeda

Submitted: August 3rd, 2017 Reviewed: October 21st, 2017 Published: Dec 20th, 2017

© 2017 The Writer(southward). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in whatsoever medium, provided the original work is properly cited.

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Source: https://www.intechopen.com/chapters/58183

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