Dependeco (medicino): Malsamoj inter versioj
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Dependeco estas [[malsano]] kiu estas karakterizita per sindeviga engaĝiĝo en rekompensado de stimuloj, malgraŭ malbonaj sekvoj.<ref name="Nestler">Nestler EJ (Decembro 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681. PMID 24459410. "Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict."</ref><ref name="Glossary">"Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. [http://neuroscience.mssm.edu/nestler/glossary.html] Alirita la 2an de Majo 2016.</ref><ref>Angres DH, Bettinardi-Angres K (Oktobro 2008). "The disease of addiction: origins, treatment, and recovery". Dis Mon 54 (10): 696–721. doi:10.1016/j.disamonth.2008.07.002. PMID 18790142.</ref><ref>Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 364–365, 375. ISBN 9780071481274. "The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...
compulsive eating, shopping, gambling, and sex–so-called “natural addictions”– Indeed, addiction to both drugs and behavioral rewards may arise from similar dysregulation of the mesolimbic dopamine system."</ref><ref name="Taylor">Taylor SB, Lewis CR, Olive MF (Februaro 2013). "The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans". Subst. Abuse Rehabil. 4: 29–43. doi:10.2147/SAR.S39684. PMC 3931688. PMID 24648786. "Initial drug use can be attributed to the ability of the drug to act as a reward (ie, a pleasurable emotional state or positive reinforcer), which can lead to repeated drug use and dependence.8,9 A great deal of research has focused on the molecular and neuroanatomical mechanisms of the initial rewarding or reinforcing effect of drugs of abuse. ...
The tremendous need for more effective pharmacological treatments for psychostimulant addiction is a mainstay of contemporary addiction research. However, the recent downsizing of many major pharmaceutical companies away from psychiatric indications (including addiction) due to the lack of efficacy of experimental compounds in humans may require a sea change in the translational research approach.212,213 A new emphasis on larger-scale biomarker, genetic, and epigenetic research focused on the molecular targets of mental disorders has been recently advocated.212 In addition, the integration of cognitive and behavioral modification of circuit-wide neuroplasticity (ie, computer-based training to enhance executive function) may prove to be an effective adjunct-treatment approach for addiction, particularly when combined with cognitive enhancers.198,213–216 Furthermore, in order to be effective, all pharmacological or biologically based treatments for addiction need to be integrated into other established forms of addiction rehabilitation, such as cognitive behavioral therapy, individual and group psychotherapy, behavior-modification strategies, twelve-step programs, and residential treatment facilities."</ref> Ĝi povas esti konsiderita kiel malsano aŭ biologia proceso kaŭzanta tiajn kondutojn.<ref name="Nestler"/><ref name="American">American Society for Addiction Medicine (2012). "Definition of Addiction".</ref> La du trajtoj kiuj karakterizas ĉiujn kutimigajn stimulojn estas ke ili [[Plifortigo|plifortikigas]] (t.e., ili pliigas la verŝajnecon ke persono serĉos ripetan eksponiĝon al ili) kaj interne rekompensantaj (t.e., io perceptis kiel esti pozitiva aŭ dezirinda).<ref name="Nestler"/><ref>"Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. [http://neuroscience.mssm.edu/nestler/glossary.html] Alirita la 2an de Majo 2016.</ref><ref name="Taylor">Taylor SB, Lewis CR, Olive MF (February 2013). "The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans". Subst. Abuse Rehabil. 4: 29–43. doi:10.2147/SAR.S39684. PMC 3931688. PMID 24648786. "Initial drug use can be attributed to the ability of the drug to act as a reward (ie, a pleasurable emotional state or positive reinforcer), which can lead to repeated drug use and dependence.8,9 A great deal of research has focused on the molecular and neuroanatomical mechanisms of the initial rewarding or reinforcing effect of drugs of abuse. ...
The tremendous need for more effective pharmacological treatments for psychostimulant addiction is a mainstay of contemporary addiction research. However, the recent downsizing of many major pharmaceutical companies away from psychiatric indications (including addiction) due to the lack of efficacy of experimental compounds in humans may require a sea change in the translational research approach.212,213 A new emphasis on larger-scale biomarker, genetic, and epigenetic research focused on the molecular targets of mental disorders has been recently advocated.212 In addition, the integration of cognitive and behavioral modification of circuit-wide neuroplasticity (ie, computer-based training to enhance executive function) may prove to be an effective adjunct-treatment approach for addiction, particularly when combined with cognitive enhancers.198,213–216 Furthermore, in order to be effective, all pharmacological or biologically based treatments for addiction need to be integrated into other established forms of addiction rehabilitation, such as cognitive behavioral therapy, individual and group psychotherapy, behavior-modification strategies, twelve-step programs, and residential treatment facilities."</ref>
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Dependeco estas malsano de la
The strong correlation between chronic drug exposure and ΔFosB provides novel opportunities for targeted therapies in addiction (118), and suggests methods to analyze their efficacy (119). Over the past two decades, research has progressed from identifying ΔFosB induction to investigating its subsequent action (38). It is likely that ΔFosB research will now progress into a new era – the use of ΔFosB as a biomarker. ...
Conclusions
ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a ‘‘molecular switch’’ (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction."</ref> [10] δFosB, gena transkripcifaktoro, estas kritika komponento kaj ofta faktoro en la evoluo de praktike ĉiuj formoj de kondutismaj kaj drogaj dependecoj; [9] [10] [11] [12] du jardekoj da esplorado en la rolon de δFosB en dependeco montris ke dependeco ekestas, kaj la rilata sindeviga konduto intensigas aŭ malintensigas, kune kun la genetika troesprimo de δFosB en la D1-speco mezaj dornaj neŭronoj de la nukleackumbens; [1] [9] [10] [11] pro la kaŭza rilato inter δFosB esprimo kaj dependecoj, ĝi estas utiligita preclinical kiel dependecbiosigno. [1] [9] [11] δFosB esprimo en tiuj neŭronoj rekte kaj pozitive reguligas drogmem-administracion kaj kompenssentemigon tra pozitiva plifortikigo, malpliigante sentemon al malemo.
[noto 1] [1] [9] Dependeco postulas altan paspagon sur individuoj kaj socio kiel tutaĵo tra la rektaj malutiloj de medikamentoj, rilataj sankostoj, longperspektivaj komplikaĵoj (ekz., pulma kancero kun fumtabako, hepatcirozo kun trinkado de alkoholo, aŭ metamfetaminbuŝo de intravejna metamfetamino), la funkciaj sekvoj de ŝanĝita neŭrala plastikeco en la cerbo, kaj la sekvan perdon de produktiveco. [13] [14] [15] Klasikaj markostampoj de dependeco inkludas difektitan kontrolon de substancoj aŭ konduto, okupitecon kun substanco aŭ konduto, kaj daŭran uzon malgraŭ sekvoj. [16] Kutimoj kaj padronoj asociitaj kun dependeco estas tipe karakterizitaj per tuja kontentigo (mallongperspektiva kompenso), kunligita kun malfruaj malutilaj efikoj (longperspektivaj kostoj).
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