أمراض الجهاز العصبي المركزي (Arabic Wikipedia)

Analysis of information sources in references of the Wikipedia article "أمراض الجهاز العصبي المركزي" in Arabic language version.

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ajnr.org

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archive.org

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doi.org

  • Cacabelos R، Torrellas C، Fernández-Novoa L، López-Muñoz F (2016). "Histamine and Immune Biomarkers in CNS Disorders". Mediators Inflamm. ج. 2016: 1924603. DOI:10.1155/2016/1924603. PMC:4846752. PMID:27190492. Neuroimmune dysregulation is a common phenomenon in different forms of central nervous system (CNS) disorders. Cross-links between central and peripheral immune mechanisms appear to be disrupted as reflected by a series of immune markers (CD3, CD4, CD7, HLA-DR, CD25, CD28, and CD56) which show variability in brain disorders such as anxiety, depression, psychosis, stroke, Alzheimer's disease, Parkinson's disease, attention-deficit hyperactivity disorder, migraine, epilepsy, vascular dementia, mental retardation, cerebrovascular encephalopathy, multiple sclerosis, brain tumors, cranial nerve neuropathies, mental retardation, and posttraumatic brain injury.{{استشهاد بدورية محكمة}}: صيانة الاستشهاد: دوي مجاني غير معلم (link)
  • Ruffle JK (نوفمبر 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". Am J Drug Alcohol Abuse. ج. 40 ع. 6: 428–437. 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: 1109–1122. 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"
  • 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.
  • "MNT - ADHD Is A Genetic Neurodevelopmental Disorder, Scientists Reveal". Medicalnewstoday.com. DOI:10.1016/S0140-6736. مؤرشف من الأصل في 2019-05-19. اطلع عليه بتاريخ 2013-10-30.
  • "Adult ADHD significantly increases risk of common form of dementia, study finds". Sciencedaily.com. 6 فبراير 2011. DOI:10.1111/j.1468-1331.2010.03064.x. مؤرشف من الأصل في 2019-04-27. اطلع عليه بتاريخ 2013-10-30.
  • Puschmann A، Bhidayasiri R، Weiner WJ. "Synucleinopathies from bench to bedside". Parkinsonism Relat Disord. 18 Suppl 1: S24-7. DOI:10.1016/S1353-8020(11)70010-4. PMID:22166445.
  • Lipton JO، Sahin M (أكتوبر 2014). "The neurology of mTOR". Neuron. ج. 84 ع. 2: 275–291. DOI:10.1016/j.neuron.2014.09.034. PMC:4223653. PMID:25374355.
    Neurological Disorders Associated with Dysfunctional mTOR Pathway Signaling
  • Sáez-Llorens X، McCracken GH (يونيو 2003). "Bacterial meningitis in children". Lancet. ج. 361 ع. 9375: 2139–48. DOI:10.1016/S0140-6736(03)13693-8. PMID:12826449.
  • Wu، Jau-Ching؛ Ko، Chin-Chu؛ Yen، Yu-Shu؛ Huang، Wen-Cheng؛ Chen، Yu-Chun؛ Liu، Laura؛ Tu، Tsung-Hsi؛ Lo، Su-Shun؛ Cheng، Henrich (1 يوليو 2013). "Epidemiology of cervical spondylotic myelopathy and its risk of causing spinal cord injury: a national cohort study". Neurosurgical Focus. ج. 35 ع. 1: E10. DOI:10.3171/2013.4.FOCUS13122. PMID:23815246. مؤرشف من الأصل في 2020-04-14.
  • Shedid، Daniel؛ Benzel، Edward C. (2007). "CERVICAL SPONDYLOSIS ANATOMY". Neurosurgery. ج. 60 ع. SUPPLEMENT: S1–7–S1–13. DOI:10.1227/01.neu.0000215430.86569.c4. مؤرشف من الأصل في 2020-02-25.
  • Burns A، Iliffe S (5 فبراير 2009). "Alzheimer's disease". المجلة الطبية البريطانية. ج. 338: b158. DOI:10.1136/bmj.b158. PMID:19196745. {{استشهاد بدورية محكمة}}: الوسيط |doi-access=subscription غير صالح (مساعدة)

empr.com

epilepsy.com

genome.gov

go.com

abcnews.go.com

hdsa.org

  • "Huntington's Disease". Hdsa.org. مؤرشف من الأصل في 2016-09-12. اطلع عليه بتاريخ 2013-10-30.

healthdirect.gov.au

healthfully.com

hearthealthywomen.org

  • "Stroke". Hearthealthywomen.org. مؤرشف من الأصل في 2013-06-24. اطلع عليه بتاريخ 2013-10-30.

hindawi.com

jci.org

kidshealth.org

mayoclinic.org

medicalnewstoday.com

medicinenet.com

myelopathy.org

  • "The Science of CSM". Myelopathy.org: an online resource for cervical spondylotic myelopathy. مؤرشف من الأصل في 2015-11-18. اطلع عليه بتاريخ 2015-11-05.

nih.gov

pubmed.ncbi.nlm.nih.gov

  • Cacabelos R، Torrellas C، Fernández-Novoa L، López-Muñoz F (2016). "Histamine and Immune Biomarkers in CNS Disorders". Mediators Inflamm. ج. 2016: 1924603. DOI:10.1155/2016/1924603. PMC:4846752. PMID:27190492. Neuroimmune dysregulation is a common phenomenon in different forms of central nervous system (CNS) disorders. Cross-links between central and peripheral immune mechanisms appear to be disrupted as reflected by a series of immune markers (CD3, CD4, CD7, HLA-DR, CD25, CD28, and CD56) which show variability in brain disorders such as anxiety, depression, psychosis, stroke, Alzheimer's disease, Parkinson's disease, attention-deficit hyperactivity disorder, migraine, epilepsy, vascular dementia, mental retardation, cerebrovascular encephalopathy, multiple sclerosis, brain tumors, cranial nerve neuropathies, mental retardation, and posttraumatic brain injury.{{استشهاد بدورية محكمة}}: صيانة الاستشهاد: دوي مجاني غير معلم (link)
  • Nestler EJ (ديسمبر 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. ج. 15 ع. 4: 431–443. PMC:3898681. PMID:24459410.
  • Ruffle JK (نوفمبر 2014). "Molecular neurobiology of addiction: what's all the (Δ)FosB about?". Am J Drug Alcohol Abuse. ج. 40 ع. 6: 428–437. 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: 1109–1122. 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"
  • 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.
  • Puschmann A، Bhidayasiri R، Weiner WJ. "Synucleinopathies from bench to bedside". Parkinsonism Relat Disord. 18 Suppl 1: S24-7. DOI:10.1016/S1353-8020(11)70010-4. PMID:22166445.
  • Lipton JO، Sahin M (أكتوبر 2014). "The neurology of mTOR". Neuron. ج. 84 ع. 2: 275–291. DOI:10.1016/j.neuron.2014.09.034. PMC:4223653. PMID:25374355.
    Neurological Disorders Associated with Dysfunctional mTOR Pathway Signaling
  • Sáez-Llorens X، McCracken GH (يونيو 2003). "Bacterial meningitis in children". Lancet. ج. 361 ع. 9375: 2139–48. DOI:10.1016/S0140-6736(03)13693-8. PMID:12826449.
  • Wu، Jau-Ching؛ Ko، Chin-Chu؛ Yen، Yu-Shu؛ Huang، Wen-Cheng؛ Chen، Yu-Chun؛ Liu، Laura؛ Tu، Tsung-Hsi؛ Lo، Su-Shun؛ Cheng، Henrich (1 يوليو 2013). "Epidemiology of cervical spondylotic myelopathy and its risk of causing spinal cord injury: a national cohort study". Neurosurgical Focus. ج. 35 ع. 1: E10. DOI:10.3171/2013.4.FOCUS13122. PMID:23815246. مؤرشف من الأصل في 2020-04-14.
  • Burns A، Iliffe S (5 فبراير 2009). "Alzheimer's disease". المجلة الطبية البريطانية. ج. 338: b158. DOI:10.1136/bmj.b158. PMID:19196745. {{استشهاد بدورية محكمة}}: الوسيط |doi-access=subscription غير صالح (مساعدة)
  • Walitza S، Melfsen S، Herhaus G، Scheuerpflug P، Warnke A، Müller T، Lange KW، Gerlach M. "Association of Parkinson's disease with symptoms of attention deficit hyperactivity disorder in childhood". J Neural Transm Suppl ع. 72: 311–5. PMID:17982908.

ncbi.nlm.nih.gov

  • Cacabelos R، Torrellas C، Fernández-Novoa L، López-Muñoz F (2016). "Histamine and Immune Biomarkers in CNS Disorders". Mediators Inflamm. ج. 2016: 1924603. DOI:10.1155/2016/1924603. PMC:4846752. PMID:27190492. Neuroimmune dysregulation is a common phenomenon in different forms of central nervous system (CNS) disorders. Cross-links between central and peripheral immune mechanisms appear to be disrupted as reflected by a series of immune markers (CD3, CD4, CD7, HLA-DR, CD25, CD28, and CD56) which show variability in brain disorders such as anxiety, depression, psychosis, stroke, Alzheimer's disease, Parkinson's disease, attention-deficit hyperactivity disorder, migraine, epilepsy, vascular dementia, mental retardation, cerebrovascular encephalopathy, multiple sclerosis, brain tumors, cranial nerve neuropathies, mental retardation, and posttraumatic brain injury.{{استشهاد بدورية محكمة}}: صيانة الاستشهاد: دوي مجاني غير معلم (link)
  • Nestler EJ (ديسمبر 2013). "Cellular basis of memory for addiction". Dialogues Clin. Neurosci. ج. 15 ع. 4: 431–443. PMC:3898681. PMID:24459410.
  • Olsen CM (ديسمبر 2011). "Natural rewards, neuroplasticity, and non-drug addictions". Neuropharmacology. ج. 61 ع. 7: 1109–1122. 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"
  • Lipton JO، Sahin M (أكتوبر 2014). "The neurology of mTOR". Neuron. ج. 84 ع. 2: 275–291. DOI:10.1016/j.neuron.2014.09.034. PMC:4223653. PMID:25374355.
    Neurological Disorders Associated with Dysfunctional mTOR Pathway Signaling

ninds.nih.gov

nimh.nih.gov

meshb.nlm.nih.gov

rcn.com

users.rcn.com

sciencedaily.com

ssa.gov

ssdrc.com

thejns.org

web.archive.org

webmd.com

who.int

wisegeek.com

wkhealth.com

content.wkhealth.com