A. Novelli, M. Fernández-Sánchez, A. Pérez-Gómez, D. Cabrera-Garcia, J. Salas-Puig, Robert Lipsky, A. Marini
{"title":"Marine Toxins, Neurodegeneration and Neuroprotection","authors":"A. Novelli, M. Fernández-Sánchez, A. Pérez-Gómez, D. Cabrera-Garcia, J. Salas-Puig, Robert Lipsky, A. Marini","doi":"10.1166/AJNN.2011.1030","DOIUrl":"https://doi.org/10.1166/AJNN.2011.1030","url":null,"abstract":"","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2011-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75501543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T. Summavielle, L. Cunha, D. Damiani, J. Bravo, Z. Binienda, A. Koverech, A. Virmani
Acetyl-L-carnitine (ALC) has been shown to be neuroprotective, in a dose and time dependent manner, through a variety of processes, including: membrane stabilization, ionic homeostasis, increased expression of key proteins, decreased expression of iNOS and increased resistance to neurotoxic events. Recently, we successfully demonstrated that pre-treatment with ALC confers effective neuroprotection against MDMA-induced neurotoxicity, preventing mitochondrial oxidative damage and, most importantly, preventing the typical MDMA-induced serotonin loss. However, the mechanisms underlying these actions are still unclear. In the present work, we have exposed PC12 cells to 1 M and 100 M methamphetamine (METH) to evaluate the action of ALC (0.01, 0.05, 0.1, 0.5 and 1 mM) on dopamine (DA) function. Intra and extracellular levels of DA were measured by HPLC-EC, both after a 24 or 72 h incubation period. We show that ALC by itself increases intracellular levels of DA, which may be a direct consequence of the ALC role on tyrosine biosynthesis. We also report that ALC is capable of increasing intracellular DA levels even in the presence of high METH doses and that ALC seems to prevent METH-induced DA release, which may be regulated through ALC direct action on important membrane components.
{"title":"Neuroprotective Action of Acetyl-L-Carnitine on Methamphetamine-Induced Dopamine Release","authors":"T. Summavielle, L. Cunha, D. Damiani, J. Bravo, Z. Binienda, A. Koverech, A. Virmani","doi":"10.1166/AJNN.2011.1022","DOIUrl":"https://doi.org/10.1166/AJNN.2011.1022","url":null,"abstract":"Acetyl-L-carnitine (ALC) has been shown to be neuroprotective, in a dose and time dependent manner, through a variety of processes, including: membrane stabilization, ionic homeostasis, increased expression of key proteins, decreased expression of iNOS and increased resistance to neurotoxic events. Recently, we successfully demonstrated that pre-treatment with ALC confers effective neuroprotection against MDMA-induced neurotoxicity, preventing mitochondrial oxidative damage and, most importantly, preventing the typical MDMA-induced serotonin loss. However, the mechanisms underlying these actions are still unclear. In the present work, we have exposed PC12 cells to 1 M and 100 M methamphetamine (METH) to evaluate the action of ALC (0.01, 0.05, 0.1, 0.5 and 1 mM) on dopamine (DA) function. Intra and extracellular levels of DA were measured by HPLC-EC, both after a 24 or 72 h incubation period. We show that ALC by itself increases intracellular levels of DA, which may be a direct consequence of the ALC role on tyrosine biosynthesis. We also report that ALC is capable of increasing intracellular DA levels even in the presence of high METH doses and that ALC seems to prevent METH-induced DA release, which may be regulated through ALC direct action on important membrane components.","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2011-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89610499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G Oxenkrug, K L Tucker, P Requintina, P Summergrad
Interferon-gamma (IFNG), a pro-inflammatory cytokine, increases concentrations of neopterin, a stable pteridine derivative, due to IFNG-induced transcriptional activation of the rate-limiting enzyme of pteridines biosynthesis. Neopterin concentrations were reported to correlate with metabolic syndrome (MetS), the cause of increased mortality risk, in subjects of European ancestry. We were interested to assessed neopterin correlations with clinical markers of MetS and mortality risk in population with a different genetic background, i.e., Puerto Ricans residents of Boston. Since inflammation is associated with pyridoxal-5'-phosphate (PLP) deficiency, we assessed correlations of neopterin with PLP. Plasma neopterin concentrations were evaluated in 592 adult (45-75 years of age) participants of Boston Puerto Rican Health Study. Neopterin concentrations correlated with abdominal obesity (waist circumference, r = 0.085, p < 0.038), HDL cholesterol (r = -0.15, p < 0.0001), insulin resistance (HOMA-IR, r = 0.08, P < 0.03), and plasma pyridoxal-5'-phosphate (PLP (r = -0.13, P = 0.002). Neopterin concentrations of >16 nmol/L at baseline were associated with the increased risk of mortality in 113 subjects followed for 6 years. The present results together with previously reported data in European subjects suggest a similar pattern of neopterin correlations with MetS and mortality risk in population with different genetic backgrounds. PLP is a cofactor of IFNG-induced key enzymes of tryptophan-kynurenine metabolism. Since PLP deficiency is associated with the increased production of diabetogenic kynurenine derivative, xanthurenic acid, our results suggest that up-regulated IFNG production might contribute to the development of insulin resistance. Assessment of neopterin concentrations might help to monitor the activity of IFNG-inducible inflammation associated with aging-associated medical and psychiatric disorders.
干扰素- γ (IFNG)是一种促炎细胞因子，由于IFNG诱导了蝶啶生物合成限速酶的转录激活，从而增加了新蝶呤(一种稳定的蝶啶衍生物)的浓度。据报道，在欧洲血统的受试者中，新蝶呤浓度与代谢综合征(MetS)相关，这是导致死亡风险增加的原因。我们有兴趣评估新蝶呤与具有不同遗传背景的人群(即波士顿的波多黎各居民)中met临床标志物和死亡风险的相关性。由于炎症与吡哆醛-5'-磷酸(PLP)缺乏有关，我们评估了新蝶呤与PLP的相关性。对592名波士顿波多黎各健康研究参与者(45-75岁)的血浆新蝶呤浓度进行了评估。新蝶呤浓度与腹部肥胖(腰围，r = 0.085, p < 0.038)、高密度脂蛋白胆固醇(r = -0.15, p < 0.0001)、胰岛素抵抗(HOMA-IR, r = 0.08, p < 0.03)、血浆吡多醛-5′-磷酸(PLP) (r = -0.13, p = 0.002)相关。113名受试者随访6年，基线时新蝶呤浓度>16 nmol/L与死亡风险增加相关。目前的结果与先前报道的欧洲受试者数据表明，在不同遗传背景的人群中，新蝶呤与MetS和死亡风险的相关性模式相似。PLP是ifng诱导的色氨酸-犬尿氨酸代谢关键酶的辅助因子。由于PLP缺乏与致糖尿病犬尿氨酸衍生物黄嘌呤酸的产生增加有关，我们的研究结果表明，IFNG产生的上调可能有助于胰岛素抵抗的发展。评估新蝶呤浓度可能有助于监测与衰老相关的医学和精神疾病相关的ifng诱导炎症的活性。
{"title":"Neopterin, a Marker of Interferon-Gamma-Inducible Inflammation, Correlates with Pyridoxal-5'-Phosphate, Waist Circumference, HDL-Cholesterol, Insulin Resistance and Mortality Risk in Adult Boston Community Dwellers of Puerto Rican Origin.","authors":"G Oxenkrug, K L Tucker, P Requintina, P Summergrad","doi":"10.1166/ajnn.2011.1024","DOIUrl":"https://doi.org/10.1166/ajnn.2011.1024","url":null,"abstract":"<p><p>Interferon-gamma (IFNG), a pro-inflammatory cytokine, increases concentrations of neopterin, a stable pteridine derivative, due to IFNG-induced transcriptional activation of the rate-limiting enzyme of pteridines biosynthesis. Neopterin concentrations were reported to correlate with metabolic syndrome (MetS), the cause of increased mortality risk, in subjects of European ancestry. We were interested to assessed neopterin correlations with clinical markers of MetS and mortality risk in population with a different genetic background, i.e., Puerto Ricans residents of Boston. Since inflammation is associated with pyridoxal-5'-phosphate (PLP) deficiency, we assessed correlations of neopterin with PLP. Plasma neopterin concentrations were evaluated in 592 adult (45-75 years of age) participants of Boston Puerto Rican Health Study. Neopterin concentrations correlated with abdominal obesity (waist circumference, r = 0.085, p < 0.038), HDL cholesterol (r = -0.15, p < 0.0001), insulin resistance (HOMA-IR, r = 0.08, P < 0.03), and plasma pyridoxal-5'-phosphate (PLP (r = -0.13, P = 0.002). Neopterin concentrations of >16 nmol/L at baseline were associated with the increased risk of mortality in 113 subjects followed for 6 years. The present results together with previously reported data in European subjects suggest a similar pattern of neopterin correlations with MetS and mortality risk in population with different genetic backgrounds. PLP is a cofactor of IFNG-induced key enzymes of tryptophan-kynurenine metabolism. Since PLP deficiency is associated with the increased production of diabetogenic kynurenine derivative, xanthurenic acid, our results suggest that up-regulated IFNG production might contribute to the development of insulin resistance. Assessment of neopterin concentrations might help to monitor the activity of IFNG-inducible inflammation associated with aging-associated medical and psychiatric disorders.</p>","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2011-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3269817/pdf/nihms336786.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30438849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Selected Peer-Reviewed Articles from the 10th International Conference on Neuroprotective Agents (ICNA 2010)","authors":"R. Andrews, T. Patterson, W. Slikker","doi":"10.1166/AJNN.2011.1033","DOIUrl":"https://doi.org/10.1166/AJNN.2011.1033","url":null,"abstract":"","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2011-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80659920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"AJNN is Established as a Lead Neuroscience Journal","authors":"H. Sharma","doi":"10.1166/AJNN.2010.1011","DOIUrl":"https://doi.org/10.1166/AJNN.2010.1011","url":null,"abstract":"","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2010-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81880086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The etiology, pathogenesis, clinical findings and actual therapeutic questions in the patients under the age of 45 with ischemic attacks of cerebral blood circulation form a varied and complex nature of syndrome of early cerebrovascular disease. The epidemiologic peculiarties of the affected contingent and the scale social aspects of the disease are at the root of large amount of multifactor examinations and tracing of the described problem. A case is presented of a 39-year old female patient with early cerebrovascular disease on the ground of isolated stenoses of both medial cerebral arteries-high-grade stenosis (70%) for the left arteria cerebri media (MCA) and low-grade stenosis (40%) for the right MCA. In the process of the wide differential diagnostic plan, no risk and etiological factors have been specified, excepting described intracranial stenoses for the first appearance of cerebral infarctions in the young age. A short analysis has been accomplished of conventional and specific etiological factors for ischemic anomalies of cerebral blood circulation in the age group under 45 as well as a review of the therapeutic possibilities in the medical algorithm of the cerebrovascular disease.
{"title":"Early Cerebrovascular Disease—Clinical Characteristics and Aspects Description of a Clinical Case","authors":"D. Maslarov, D. Drenska, J. Petrova","doi":"10.1166/AJNN.2010.1013","DOIUrl":"https://doi.org/10.1166/AJNN.2010.1013","url":null,"abstract":"The etiology, pathogenesis, clinical findings and actual therapeutic questions in the patients under the age of 45 with ischemic attacks of cerebral blood circulation form a varied and complex nature of syndrome of early cerebrovascular disease. The epidemiologic peculiarties of the affected contingent and the scale social aspects of the disease are at the root of large amount of multifactor examinations and tracing of the described problem. A case is presented of a 39-year old female patient with early cerebrovascular disease on the ground of isolated stenoses of both medial cerebral arteries-high-grade stenosis (70%) for the left arteria cerebri media (MCA) and low-grade stenosis (40%) for the right MCA. In the process of the wide differential diagnostic plan, no risk and etiological factors have been specified, excepting described intracranial stenoses for the first appearance of cerebral infarctions in the young age. A short analysis has been accomplished of conventional and specific etiological factors for ischemic anomalies of cerebral blood circulation in the age group under 45 as well as a review of the therapeutic possibilities in the medical algorithm of the cerebrovascular disease.","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2010-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85378036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Schizophrenia is a chronic, severe, and disabling brain disease. Today the neuroscience and clinical researches have advanced sufficiently to develop neuroprotective approach for discovery a novel generation of compounds with neuroprotective properties. However, the use of neuroprotective agents in schizophrenia is not yet well established. There are two main targets for neuroprotective therapy: (1) neurodegenerative processes in schizophrenia (e.g., apoptosis, excitotoxicity, oxidative stress, stress sensitization, neurotrophic factor expression, and alteration of neurosteroids); and (2) clinical, and behavioral presentations of illness including psychopathological symptoms, a significant decline in cognition, psychosocial functioning and in health related quality of life (HRQL) of patients. The HRQL deficit or impairment is a core feature of schizophrenia spectrum disorders. Based on the author’s and his team research contributions for last ten years, and complementary theoretical considerations, this paper presents the Distress/Protection Vulnerability Model of HRQL impairment in schizophrenia and related disorders. This model has reshaped our understanding of schizophrenia phenotype and will be essential useful for designing more effective clinical and neuroprotective trials.
{"title":"Health-Related Quality of Life Impairment in Schizophrenia and Related Disorders as a Target for Neuroprotective Therapy","authors":"M. Ritsner","doi":"10.1166/AJNN.2010.1012","DOIUrl":"https://doi.org/10.1166/AJNN.2010.1012","url":null,"abstract":"Schizophrenia is a chronic, severe, and disabling brain disease. Today the neuroscience and clinical researches have advanced sufficiently to develop neuroprotective approach for discovery a novel generation of compounds with neuroprotective properties. However, the use of neuroprotective agents in schizophrenia is not yet well established. There are two main targets for neuroprotective therapy: (1) neurodegenerative processes in schizophrenia (e.g., apoptosis, excitotoxicity, oxidative stress, stress sensitization, neurotrophic factor expression, and alteration of neurosteroids); and (2) clinical, and behavioral presentations of illness including psychopathological symptoms, a significant decline in cognition, psychosocial functioning and in health related quality of life (HRQL) of patients. The HRQL deficit or impairment is a core feature of schizophrenia spectrum disorders. Based on the author’s and his team research contributions for last ten years, and complementary theoretical considerations, this paper presents the Distress/Protection Vulnerability Model of HRQL impairment in schizophrenia and related disorders. This model has reshaped our understanding of schizophrenia phenotype and will be essential useful for designing more effective clinical and neuroprotective trials.","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2010-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83867755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Epigenetic Modulation Expressed as Methylation Changes in DNA from Primary School Children of Two Different Geographical Environments II","authors":"Silvia Ratti, N. Vizioli, E. O. Alvarez","doi":"10.1166/AJNN.2010.1014","DOIUrl":"https://doi.org/10.1166/AJNN.2010.1014","url":null,"abstract":"","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2010-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73521673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Microglia as a Target for Inflammatory Processes and Neuroprotective Strategies","authors":"S. Skaper","doi":"10.1166/AJNN.2010.1017","DOIUrl":"https://doi.org/10.1166/AJNN.2010.1017","url":null,"abstract":"","PeriodicalId":7964,"journal":{"name":"American journal of neuroprotection and neuroregeneration","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2010-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80424814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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