Pub Date : 2019-07-20DOI: 10.1007/s11481-019-09864-z
K. Liao, F. Niu, R. Dagur, Meng He, C. Tian, Guoku Hu
{"title":"Intranasal Delivery of lincRNA-Cox2 siRNA Loaded Extracellular Vesicles Decreases Lipopolysaccharide-Induced Microglial Proliferation in Mice","authors":"K. Liao, F. Niu, R. Dagur, Meng He, C. Tian, Guoku Hu","doi":"10.1007/s11481-019-09864-z","DOIUrl":"https://doi.org/10.1007/s11481-019-09864-z","url":null,"abstract":"","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2019-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11481-019-09864-z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43947392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-07-18DOI: 10.1007/s11481-019-09866-x
Zichun Zhao, Jin-Sheng Fu, Shiping Li, Zhenzhong Li
{"title":"Neuroprotective Effects of Genistein in a SOD1-G93A Transgenic Mouse Model of Amyotrophic Lateral Sclerosis","authors":"Zichun Zhao, Jin-Sheng Fu, Shiping Li, Zhenzhong Li","doi":"10.1007/s11481-019-09866-x","DOIUrl":"https://doi.org/10.1007/s11481-019-09866-x","url":null,"abstract":"","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2019-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11481-019-09866-x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48188247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-06-01Epub Date: 2016-09-17DOI: 10.1007/s11481-016-9709-2
S Alex Marshall, Kyle H McKnight, Allyson K Blose, Donald T Lysle, Todd E Thiele
Excessive ethanol consumption alters the neuroimmune system and particularly impacts the cytokine milieu of the CNS. Cytokine dysregulation has been shown to underlie addictive-like behaviors including alcohol abuse; however, many studies focus primarily on the proinflammatory cytokine profile during alcohol dependence. The current study furthers this research by determining the impact of excessive ethanol consumption on interleukin-10 (IL-10) and interleukin-4 (IL-4) activity in a model of non-dependent binge consumption called the "drinking in the dark" (DID) paradigm. Furthermore, the ability of IL-10 to modulate ethanol consumption was tested using site-directed pharmacology. Immunohistochemistry analyses determined that ethanol decreased IL-10 by 50 % in the basolateral amygdala (BLA) but had no effect on IL-4. Neither IL-10 nor IL-4, however, were altered in the central amygdala (CEA). Enzyme linked immunosorbent assays confirmed that IL-10 was decreased in the amygdala but not in the serum, suggesting changes of this cytokine with the DID paradigm are restricted to the central nervous system. Finally, bilateral infusions of IL-10 into the BLA, but not CeA, reduced binge-like drinking and corresponding blood ethanol concentrations without impacting either locomotor activity or anxiety-like behavioral correlates. Together, these data support the idea that alcohol abuse dysregulates specific anti-inflammatory cytokines; however, ameliorating alcohol-induced effects on cytokines, like IL-10, may prove to be an effective therapy in curbing excessive consumption.
{"title":"Modulation of Binge-like Ethanol Consumption by IL-10 Signaling in the Basolateral Amygdala.","authors":"S Alex Marshall, Kyle H McKnight, Allyson K Blose, Donald T Lysle, Todd E Thiele","doi":"10.1007/s11481-016-9709-2","DOIUrl":"10.1007/s11481-016-9709-2","url":null,"abstract":"<p><p>Excessive ethanol consumption alters the neuroimmune system and particularly impacts the cytokine milieu of the CNS. Cytokine dysregulation has been shown to underlie addictive-like behaviors including alcohol abuse; however, many studies focus primarily on the proinflammatory cytokine profile during alcohol dependence. The current study furthers this research by determining the impact of excessive ethanol consumption on interleukin-10 (IL-10) and interleukin-4 (IL-4) activity in a model of non-dependent binge consumption called the \"drinking in the dark\" (DID) paradigm. Furthermore, the ability of IL-10 to modulate ethanol consumption was tested using site-directed pharmacology. Immunohistochemistry analyses determined that ethanol decreased IL-10 by 50 % in the basolateral amygdala (BLA) but had no effect on IL-4. Neither IL-10 nor IL-4, however, were altered in the central amygdala (CEA). Enzyme linked immunosorbent assays confirmed that IL-10 was decreased in the amygdala but not in the serum, suggesting changes of this cytokine with the DID paradigm are restricted to the central nervous system. Finally, bilateral infusions of IL-10 into the BLA, but not CeA, reduced binge-like drinking and corresponding blood ethanol concentrations without impacting either locomotor activity or anxiety-like behavioral correlates. Together, these data support the idea that alcohol abuse dysregulates specific anti-inflammatory cytokines; however, ameliorating alcohol-induced effects on cytokines, like IL-10, may prove to be an effective therapy in curbing excessive consumption.</p>","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2017-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5357210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47414902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-05-04DOI: 10.1080/10428194.2016.1233544
Qingsheng Li, Woong-Ki Kim
We thank Sahu et al. for their comments on our paper ‘Pregnancy: part of life in chronic myelogenous leukemia.’[1] The issues highlighted in their submission are highly relevant and important to a setting where resources are constrained and optimal standards of care may be difficult to achieve. This situation is commonly encountered in developing countries where access to drugs and the ability to closely monitor disease by advanced molecular diagnostics is limited. Management of chronic myelogenous leukemia (CML) in unusual clinical situations such as pregnancy requires an individualized approach directed toward optimizing care to ensure favorable outcomes for both the parent and the fetus wherever possible. As shown in our paper, close monitoring of disease status by quantitative polymerase chain reaction (PCR)based testing and judicious use of available therapies can be used effectively to manage such patients. Although both the hydroxyurea and leukocyte apheresis are useful adjuncts to therapy in some conditions, there is little evidence to recommend these as the mainstay of management in all cases. Despite emerging data describing favorable outcomes in the fetuses of patients exposed to Imatinib and some other tyrosine kinase inhibitors (TKIs) in the early stages of pregnancy, it is important to consider that these agents were immediately withdrawn at the time pregnancy was detected thereby minimizing exposure where possible.[2–4] Adverse fetal outcomes were documented in cases where Imatinib was not discontinued early.[5] In this respect, interferon-based therapy appears to be the least likely to result in adverse maternal or fetal outcomes and can also provide some measure of disease control beyond cytoreduction alone. We recognize that there are likely to be differences in practice in resource-constrained settings and appreciate the difficulties that may be associated in managing complex issues such as pregnancy in CML, particularly in a younger patient population. This scenario effectively demonstrates the premise of our article that with the life expectancy of CML patients now being nearly the same as that of normal individuals. Efforts are necessary to ensure that pregnancy and childbirth can also be an achievable milestone without compromising disease control.
{"title":"Reply to Letter to the Editor","authors":"Qingsheng Li, Woong-Ki Kim","doi":"10.1080/10428194.2016.1233544","DOIUrl":"https://doi.org/10.1080/10428194.2016.1233544","url":null,"abstract":"We thank Sahu et al. for their comments on our paper ‘Pregnancy: part of life in chronic myelogenous leukemia.’[1] The issues highlighted in their submission are highly relevant and important to a setting where resources are constrained and optimal standards of care may be difficult to achieve. This situation is commonly encountered in developing countries where access to drugs and the ability to closely monitor disease by advanced molecular diagnostics is limited. Management of chronic myelogenous leukemia (CML) in unusual clinical situations such as pregnancy requires an individualized approach directed toward optimizing care to ensure favorable outcomes for both the parent and the fetus wherever possible. As shown in our paper, close monitoring of disease status by quantitative polymerase chain reaction (PCR)based testing and judicious use of available therapies can be used effectively to manage such patients. Although both the hydroxyurea and leukocyte apheresis are useful adjuncts to therapy in some conditions, there is little evidence to recommend these as the mainstay of management in all cases. Despite emerging data describing favorable outcomes in the fetuses of patients exposed to Imatinib and some other tyrosine kinase inhibitors (TKIs) in the early stages of pregnancy, it is important to consider that these agents were immediately withdrawn at the time pregnancy was detected thereby minimizing exposure where possible.[2–4] Adverse fetal outcomes were documented in cases where Imatinib was not discontinued early.[5] In this respect, interferon-based therapy appears to be the least likely to result in adverse maternal or fetal outcomes and can also provide some measure of disease control beyond cytoreduction alone. We recognize that there are likely to be differences in practice in resource-constrained settings and appreciate the difficulties that may be associated in managing complex issues such as pregnancy in CML, particularly in a younger patient population. This scenario effectively demonstrates the premise of our article that with the life expectancy of CML patients now being nearly the same as that of normal individuals. Efforts are necessary to ensure that pregnancy and childbirth can also be an achievable milestone without compromising disease control.","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2017-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10428194.2016.1233544","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44886815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-03-01Epub Date: 2016-10-03DOI: 10.1007/s11481-016-9711-8
Kristen A McLaurin, Landhing M Moran, Hailong Li, Rosemarie M Booze, Charles F Mactutus
Approximately 50 % of HIV-1 seropositive individuals develop HIV-1 associated neurocognitive disorders (HAND), which commonly include alterations in executive functions, such as inhibition, set shifting, and complex problem solving. Executive function deficits in HIV-1 are fairly well characterized, however, relatively few studies have explored the elemental dimensions of neurocognitive impairment in HIV-1. Deficits in temporal processing, caused by HIV-1, may underlie the symptoms of impairment in higher level cognitive processes. Translational measures of temporal processing, including cross-modal prepulse inhibition (PPI), gap-prepulse inhibition (gap-PPI), and gap threshold detection, were studied in mature (ovariectomized) female HIV-1 transgenic (Tg) rats, which express 7 of the 9 HIV-1 genes constitutively throughout development. Cross-modal PPI revealed a relative insensitivity to the manipulation of interstimulus interval (ISI) in HIV-1 Tg animals in comparison to control animals, extending previously reported temporal processing deficits in HIV-1 Tg rats to a more advanced age, suggesting the permanence of temporal processing deficits. In gap-PPI, HIV-1 Tg animals exhibited a relative insensitivity to the manipulation of ISI in comparison to control animals. In gap-threshold detection, HIV-1 Tg animals displayed a profound differential sensitivity to the manipulation of gap duration. Presence of the HIV-1 transgene was diagnosed with 91.1 % accuracy using gap threshold detection measures. Understanding the generality and permanence of temporal processing deficits in the HIV-1 Tg rat is vital to modeling neurocognitive deficits observed in HAND and provides a key target for the development of a diagnostic screening tool.
{"title":"A Gap in Time: Extending our Knowledge of Temporal Processing Deficits in the HIV-1 Transgenic Rat.","authors":"Kristen A McLaurin, Landhing M Moran, Hailong Li, Rosemarie M Booze, Charles F Mactutus","doi":"10.1007/s11481-016-9711-8","DOIUrl":"10.1007/s11481-016-9711-8","url":null,"abstract":"<p><p>Approximately 50 % of HIV-1 seropositive individuals develop HIV-1 associated neurocognitive disorders (HAND), which commonly include alterations in executive functions, such as inhibition, set shifting, and complex problem solving. Executive function deficits in HIV-1 are fairly well characterized, however, relatively few studies have explored the elemental dimensions of neurocognitive impairment in HIV-1. Deficits in temporal processing, caused by HIV-1, may underlie the symptoms of impairment in higher level cognitive processes. Translational measures of temporal processing, including cross-modal prepulse inhibition (PPI), gap-prepulse inhibition (gap-PPI), and gap threshold detection, were studied in mature (ovariectomized) female HIV-1 transgenic (Tg) rats, which express 7 of the 9 HIV-1 genes constitutively throughout development. Cross-modal PPI revealed a relative insensitivity to the manipulation of interstimulus interval (ISI) in HIV-1 Tg animals in comparison to control animals, extending previously reported temporal processing deficits in HIV-1 Tg rats to a more advanced age, suggesting the permanence of temporal processing deficits. In gap-PPI, HIV-1 Tg animals exhibited a relative insensitivity to the manipulation of ISI in comparison to control animals. In gap-threshold detection, HIV-1 Tg animals displayed a profound differential sensitivity to the manipulation of gap duration. Presence of the HIV-1 transgene was diagnosed with 91.1 % accuracy using gap threshold detection measures. Understanding the generality and permanence of temporal processing deficits in the HIV-1 Tg rat is vital to modeling neurocognitive deficits observed in HAND and provides a key target for the development of a diagnostic screening tool.</p>","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11481-016-9711-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45389290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-03DOI: 10.1007/s11481-016-9724-3
Chaitanya Joshi, V. Labhasetwar, A. Ghorpade
{"title":"Destination Brain: the Past, Present, and Future of Therapeutic Gene Delivery","authors":"Chaitanya Joshi, V. Labhasetwar, A. Ghorpade","doi":"10.1007/s11481-016-9724-3","DOIUrl":"https://doi.org/10.1007/s11481-016-9724-3","url":null,"abstract":"","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2017-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11481-016-9724-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44624009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-12-27DOI: 10.1007/s11481-016-9723-4
R. Aalinkeel, Courtney S. Mangum, E. Abou-Jaoude, J. Reynolds, Maixian Liu, K. Sundquist, Neil U. Parikh, L. Chaves, M. Mammen, S. Schwartz, S. Mahajan
{"title":"Galectin-1 Reduces Neuroinflammation via Modulation of Nitric Oxide-Arginase Signaling in HIV-1 Transfected Microglia: a Gold Nanoparticle-Galectin-1 “Nanoplex” a Possible Neurotherapeutic?","authors":"R. Aalinkeel, Courtney S. Mangum, E. Abou-Jaoude, J. Reynolds, Maixian Liu, K. Sundquist, Neil U. Parikh, L. Chaves, M. Mammen, S. Schwartz, S. Mahajan","doi":"10.1007/s11481-016-9723-4","DOIUrl":"https://doi.org/10.1007/s11481-016-9723-4","url":null,"abstract":"","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2016-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11481-016-9723-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44342409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-12-26DOI: 10.1007/s11481-016-9722-5
Ross Penninkilampi, Holly M. Brothers, G. Eslick
{"title":"Safety and Efficacy of Anti-Amyloid-β Immunotherapy in Alzheimer’s Disease: A Systematic Review and Meta-Analysis","authors":"Ross Penninkilampi, Holly M. Brothers, G. Eslick","doi":"10.1007/s11481-016-9722-5","DOIUrl":"https://doi.org/10.1007/s11481-016-9722-5","url":null,"abstract":"","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2016-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11481-016-9722-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45264944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-12-16DOI: 10.1007/s11481-016-9720-7
R. Calvello, A. Cianciulli, G. Nicolardi, F. De Nuccio, L. Giannotti, Rosaria Salvatore, C. Porro, T. Trotta, M. Panaro, D. Lofrumento
{"title":"Vitamin D Treatment Attenuates Neuroinflammation and Dopaminergic Neurodegeneration in an Animal Model of Parkinson’s Disease, Shifting M1 to M2 Microglia Responses","authors":"R. Calvello, A. Cianciulli, G. Nicolardi, F. De Nuccio, L. Giannotti, Rosaria Salvatore, C. Porro, T. Trotta, M. Panaro, D. Lofrumento","doi":"10.1007/s11481-016-9720-7","DOIUrl":"https://doi.org/10.1007/s11481-016-9720-7","url":null,"abstract":"","PeriodicalId":16500,"journal":{"name":"Journal of Neuroimmune Pharmacology","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2016-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11481-016-9720-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48283975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}