إدمان (Arabic Wikipedia)

Analysis of information sources in references of the Wikipedia article "إدمان" in Arabic language version.

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asam.org

doi.org

  • Angres DH، Bettinardi-Angres K (أكتوبر 2008). "The disease of addiction: origins, treatment, and recovery". Disease-a-Month. ج. 54 ع. 10: 696–721. DOI:10.1016/j.disamonth.2008.07.002. PMID:18790142.
  • Ruffle JK (نوفمبر 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". Am. J. Drug Alcohol Abuse. ج. 40 ع. 6: 428–37. DOI:10.3109/00952990.2014.933840. PMID:25083822.
    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.
  • Olsen CM (ديسمبر 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. ج. 61 ع. 7: 1109–22. DOI:10.1016/j.neuropharm.2011.03.010. PMC:3139704. PMID:21459101. Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (Komisaruk et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009). ... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al, 2006; Aiken, 2007; Lader, 2008)."Table 1: Summary of plasticity observed following exposure to drug or natural reinforcers"
  • Volkow ND، Koob GF، McLellan AT (يناير 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. ج. 374 ع. 4: 363–371. DOI:10.1056/NEJMra1511480. PMID:26816013. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
    Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
  • Nestler EJ (أكتوبر 2008). "Review. Transcriptional mechanisms of addiction: role of DeltaFosB". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. ج. 363 ع. 1507: 3245–55. DOI:10.1098/rstb.2008.0067. PMC:2607320. PMID:18640924. Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch – from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure – cited earlier (Renthal et al. in press). The mechanism responsible for ΔFosB repression of c-fos expression is complex and is covered below. ...
    Examples of validated targets for ΔFosB in nucleus accumbens ... GluR2 ... dynorphin ... Cdk5 ... NFκB ... c-Fos

    Table 3
  • Berridge KC (أبريل 2012). "From prediction error to incentive salience: mesolimbic computation of reward motivation". Eur. J. Neurosci. ج. 35 ع. 7: 1124–43. DOI:10.1111/j.1460-9568.2012.07990.x. PMC:3325516. PMID:22487042.
  • Edwards S (2016). "Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder". Neuroscience for Addiction Medicine: From Prevention to Rehabilitation - Constructs and Drugs. Progress in Brain Research. ج. 223. ص. 63–76. DOI:10.1016/bs.pbr.2015.07.005. ISBN:978-0-444-63545-7. PMID:26806771.
  • Berridge KC، Kringelbach ML (مايو 2015). "Pleasure systems in the brain". Neuron. ج. 86 ع. 3: 646–664. DOI:10.1016/j.neuron.2015.02.018. PMC:4425246. PMID:25950633.

drugpolicy.org

mssm.edu

neuroscience.mssm.edu

  • "Glossary of Terms". Mount Sinai School of Medicine. Department of Neuroscience. اطلع عليه بتاريخ 2015-02-09.

nih.gov

pubmed.ncbi.nlm.nih.gov

  • Angres DH، Bettinardi-Angres K (أكتوبر 2008). "The disease of addiction: origins, treatment, and recovery". Disease-a-Month. ج. 54 ع. 10: 696–721. DOI:10.1016/j.disamonth.2008.07.002. PMID:18790142.
  • Ruffle JK (نوفمبر 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". Am. J. Drug Alcohol Abuse. ج. 40 ع. 6: 428–37. DOI:10.3109/00952990.2014.933840. PMID:25083822.
    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.
  • Olsen CM (ديسمبر 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. ج. 61 ع. 7: 1109–22. DOI:10.1016/j.neuropharm.2011.03.010. PMC:3139704. PMID:21459101. Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (Komisaruk et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009). ... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al, 2006; Aiken, 2007; Lader, 2008)."Table 1: Summary of plasticity observed following exposure to drug or natural reinforcers"
  • Nestler EJ (ديسمبر 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. ج. 15 ع. 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.
  • Volkow ND، Koob GF، McLellan AT (يناير 2016). "Neurobiologic Advances from the Brain Disease Model of Addiction". N. Engl. J. Med. ج. 374 ع. 4: 363–371. DOI:10.1056/NEJMra1511480. PMID:26816013. Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe.
    Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder.
  • Nestler EJ (أكتوبر 2008). "Review. Transcriptional mechanisms of addiction: role of DeltaFosB". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. ج. 363 ع. 1507: 3245–55. DOI:10.1098/rstb.2008.0067. PMC:2607320. PMID:18640924. Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch – from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure – cited earlier (Renthal et al. in press). The mechanism responsible for ΔFosB repression of c-fos expression is complex and is covered below. ...
    Examples of validated targets for ΔFosB in nucleus accumbens ... GluR2 ... dynorphin ... Cdk5 ... NFκB ... c-Fos

    Table 3
  • Berridge KC (أبريل 2012). "From prediction error to incentive salience: mesolimbic computation of reward motivation". Eur. J. Neurosci. ج. 35 ع. 7: 1124–43. DOI:10.1111/j.1460-9568.2012.07990.x. PMC:3325516. PMID:22487042.
  • Edwards S (2016). "Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder". Neuroscience for Addiction Medicine: From Prevention to Rehabilitation - Constructs and Drugs. Progress in Brain Research. ج. 223. ص. 63–76. DOI:10.1016/bs.pbr.2015.07.005. ISBN:978-0-444-63545-7. PMID:26806771.
  • Berridge KC، Kringelbach ML (مايو 2015). "Pleasure systems in the brain". Neuron. ج. 86 ع. 3: 646–664. DOI:10.1016/j.neuron.2015.02.018. PMC:4425246. PMID:25950633.

ncbi.nlm.nih.gov

  • Olsen CM (ديسمبر 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. ج. 61 ع. 7: 1109–22. DOI:10.1016/j.neuropharm.2011.03.010. PMC:3139704. PMID:21459101. Functional neuroimaging studies in humans have shown that gambling (Breiter et al, 2001), shopping (Knutson et al, 2007), orgasm (Komisaruk et al, 2004), playing video games (Koepp et al, 1998; Hoeft et al, 2008) and the sight of appetizing food (Wang et al, 2004a) activate many of the same brain regions (i.e., the mesocorticolimbic system and extended amygdala) as drugs of abuse (Volkow et al, 2004). ... Cross-sensitization is also bidirectional, as a history of amphetamine administration facilitates sexual behavior and enhances the associated increase in NAc DA ... As described for food reward, sexual experience can also lead to activation of plasticity-related signaling cascades. The transcription factor delta FosB is increased in the NAc, PFC, dorsal striatum, and VTA following repeated sexual behavior (Wallace et al., 2008; Pitchers et al., 2010b). This natural increase in delta FosB or viral overexpression of delta FosB within the NAc modulates sexual performance, and NAc blockade of delta FosB attenuates this behavior (Hedges et al, 2009; Pitchers et al., 2010b). Further, viral overexpression of delta FosB enhances the conditioned place preference for an environment paired with sexual experience (Hedges et al., 2009). ... In some people, there is a transition from "normal" to compulsive engagement in natural rewards (such as food or sex), a condition that some have termed behavioral or non-drug addictions (Holden, 2001; Grant et al., 2006a). ... In humans, the role of dopamine signaling in incentive-sensitization processes has recently been highlighted by the observation of a dopamine dysregulation syndrome in some patients taking dopaminergic drugs. This syndrome is characterized by a medication-induced increase in (or compulsive) engagement in non-drug rewards such as gambling, shopping, or sex (Evans et al, 2006; Aiken, 2007; Lader, 2008)."Table 1: Summary of plasticity observed following exposure to drug or natural reinforcers"
  • Nestler EJ (ديسمبر 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. ج. 15 ع. 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.
  • Nestler EJ (أكتوبر 2008). "Review. Transcriptional mechanisms of addiction: role of DeltaFosB". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. ج. 363 ع. 1507: 3245–55. DOI:10.1098/rstb.2008.0067. PMC:2607320. PMID:18640924. Recent evidence has shown that ΔFosB also represses the c-fos gene that helps create the molecular switch – from the induction of several short-lived Fos family proteins after acute drug exposure to the predominant accumulation of ΔFosB after chronic drug exposure – cited earlier (Renthal et al. in press). The mechanism responsible for ΔFosB repression of c-fos expression is complex and is covered below. ...
    Examples of validated targets for ΔFosB in nucleus accumbens ... GluR2 ... dynorphin ... Cdk5 ... NFκB ... c-Fos

    Table 3
  • Berridge KC (أبريل 2012). "From prediction error to incentive salience: mesolimbic computation of reward motivation". Eur. J. Neurosci. ج. 35 ع. 7: 1124–43. DOI:10.1111/j.1460-9568.2012.07990.x. PMC:3325516. PMID:22487042.
  • Berridge KC، Kringelbach ML (مايو 2015). "Pleasure systems in the brain". Neuron. ج. 86 ع. 3: 646–664. DOI:10.1016/j.neuron.2015.02.018. PMC:4425246. PMID:25950633.

samhsa.gov

oas.samhsa.gov

springer.com

link.springer.com

surgeongeneral.gov

addiction.surgeongeneral.gov

  • "Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health" (PDF). Office of the Surgeon General. US Department of Health and Human Services. نوفمبر 2016. ص. 35–37, 45, 63, 155, 317, 338. مؤرشف من الأصل (PDF) في 2020-02-09. اطلع عليه بتاريخ 2017-01-28.

web.archive.org

  • "Facing Addiction in America: The Surgeon General's Report on Alcohol, Drugs, and Health" (PDF). Office of the Surgeon General. US Department of Health and Human Services. نوفمبر 2016. ص. 35–37, 45, 63, 155, 317, 338. مؤرشف من الأصل (PDF) في 2020-02-09. اطلع عليه بتاريخ 2017-01-28.
  • American Society for Addiction Medicine (2012). "Definition of Addiction". مؤرشف من الأصل في 2019-12-13.
  • مكتب الدراسات التطبيقية للولايات المتحدة الأمريكية نسخة محفوظة 20 أكتوبر 2011 على موقع واي باك مشين.[وصلة مكسورة]
  • the war on drugs، . نسخة محفوظة 08 يونيو 2018 على موقع واي باك مشين.
  • Drug War Statistics، . نسخة محفوظة 05 يوليو 2017 على موقع واي باك مشين.