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  • 1
    Language: English
    In: Expert Review of Neurotherapeutics, 01 September 2012, Vol.12(9), pp.1057-1059
    Description: Evaluation of: de Tommaso M, Ceci E, Pica C et al. Serum levels of N-acetyl-aspartate in migraine and tension-type headache. J. Headache Pain 13(5), 389-394 (2012). Migraine is a common neurological disorder producing significant personal and societal burden. In the evaluated study, serum concentrations of N-acetyl aspartate (NAA), a biomarker of neuronal integrity, was found to be decreased in patients suffering from migraine with aura. These interesting results suggest a dual clinical readout. Since migraine-with-aura patients show an increased risk for stroke; the evaluation of serum levels of NAA is crucial in the control of the conventional risk factors. In addition, the therapeutic metabolite monitoring of NAA may be helpful in the assessment of the chronicization process.
    Keywords: Cardiocerebral Comorbidity ; Chronicization Process ; CNS Neuronal Dysfunction ; Migraine With Aura ; Serum N-Acetyl Aspartate ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 1473-7175
    E-ISSN: 1744-8360
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  • 2
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States, March 19, 2013, Vol.110(12), p.4804(6)
    Description: Epigenetic mechanisms are involved in the pathophysiology of depressive disorders and are unique potential targets for therapeutic intervention. The acetylating agent L-acetylcarnitine (LAC), a well-tolerated drug, behaves as an antidepressant by the epigenetic regulation of type 2 metabotropic glutamate (mGlu2) receptors. It caused a rapid and long-lasting antidepressant effect in Flinders Sensitive Line rats and in mice exposed to chronic unpredictable stress, which, respectively, model genetic and environmentally induced depression. In both models, LAC increased levels of acetylated H3K27 bound to the Grm2 promoter and also increased acetylation of NF-KB-p65 subunit, thereby enhancing the transcription of Grm2 gene encoding for the mGlu2 receptor in hippocampus and prefrontal cortex. Importantly, LAC reduced the immobility time in the forced swim test and increased sucrose preference as early as 3 d of treatment, whereas 14 d of treatment were needed for the antidepressant effect of chlorimipramine. Moreover, there was no tolerance to the action of LAC, and the antidepressant effect was still seen 2 wk after drug withdrawal. Conversely, NF-kB inhibition prevented the increase in mGlu2 expression induced by LAC, whereas the use of a histone deacetylase inhibitor supported the epigenetic control of mGlu2 expression. Finally, LAC had no effect on mGlu2 knockout mice exposed to chronic unpredictable stress, and a single injection of the mGlu2/3 receptor antagonist LY341495 partially blocked LAC action. The rapid and long-lasting antidepressant action of LAC strongly suggests a unique approach to examine the epigenetic hypothesis of depressive disorders in humans, paving the way for more efficient antidepressants with faster onset of action. doi/10.1073/pnas.1216100110
    Keywords: Antidepressants -- Research ; Antidepressants -- Analysis ; Depression (Mood disorder) -- Research ; Depression (Mood disorder) -- Analysis
    ISSN: 0027-8424
    Source: Cengage Learning, Inc.
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  • 3
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 19 March 2013, Vol.110(12), pp.4804-4809
    Description: Epigenetic mechanisms are involved in the pathophysiology of depressive disorders and are unique potential targets for therapeutic intervention. The acetylating agent L-acetylcarnitine (LAC), a welltolerated drug, behaves as an antidepressant by the epigenetic regulation of type 2 metabotropic glutamate (mGlu2) receptors. It caused a rapid and long-lasting antidepressant effect in Flinders Sensitive Line rats and in mice exposed to chronic unpredictable stress, which, respectively, model genetic and environmentally induced depression. In both models, LAC increased levels of acetylated H3K27 bound to the Grm2 promoter and also increased acetylation of NF-KB-p65 subunit, thereby enhancing the transcription of Grm2 gene encoding for the mGlu2 receptor in hippocampus and prefrontal cortex. Importantly, LAC reduced the immobility time in the forced swim test and increased sucrose preference as early as 3 d of treatment, whereas 14 d of treatment were needed for the antidepressant effect of chlorimipramine. Moreover, there was no tolerance to the action of LAC, and the antidepressant effect was still seen 2 wk after drug withdrawal. Conversely, NF-κB inhibition prevented the increase in mGlu2 expression induced by LAC, whereas the use of a histone deacetylase inhibitor supported the epigenetic control of mGlu2 expression. Finally, LAC had no effect on mGlu2 knockout mice exposed to chronic unpredictable stress, and a single injection of the mGlu2/3 receptor antagonist LY341495 partially blocked LAC action. The rapid and long-lasting antidepressant action of LAC strongly suggests a unique approach to examine the epigenetic hypothesis of depressive disorders in humans, paving the way for more efficient antidepressants with faster onset of action.
    ISSN: 00278424
    Source: Archival Journals (JSTOR)
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  • 4
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 19 March 2013, Vol.110(12), pp.4804-9
    Description: Epigenetic mechanisms are involved in the pathophysiology of depressive disorders and are unique potential targets for therapeutic intervention. The acetylating agent L-acetylcarnitine (LAC), a well-tolerated drug, behaves as an antidepressant by the epigenetic regulation of type 2 metabotropic glutamate (mGlu2) receptors. It caused a rapid and long-lasting antidepressant effect in Flinders Sensitive Line rats and in mice exposed to chronic unpredictable stress, which, respectively, model genetic and environmentally induced depression. In both models, LAC increased levels of acetylated H3K27 bound to the Grm2 promoter and also increased acetylation of NF-ĸB-p65 subunit, thereby enhancing the transcription of Grm2 gene encoding for the mGlu2 receptor in hippocampus and prefrontal cortex. Importantly, LAC reduced the immobility time in the forced swim test and increased sucrose preference as early as 3 d of treatment, whereas 14 d of treatment were needed for the antidepressant effect of chlorimipramine. Moreover, there was no tolerance to the action of LAC, and the antidepressant effect was still seen 2 wk after drug withdrawal. Conversely, NF-ĸB inhibition prevented the increase in mGlu2 expression induced by LAC, whereas the use of a histone deacetylase inhibitor supported the epigenetic control of mGlu2 expression. Finally, LAC had no effect on mGlu2 knockout mice exposed to chronic unpredictable stress, and a single injection of the mGlu2/3 receptor antagonist LY341495 partially blocked LAC action. The rapid and long-lasting antidepressant action of LAC strongly suggests a unique approach to examine the epigenetic hypothesis of depressive disorders in humans, paving the way for more efficient antidepressants with faster onset of action.
    Keywords: Acetylcarnitine -- Pharmacology ; Antidepressive Agents -- Pharmacology ; Epigenesis, Genetic -- Drug Effects ; Hippocampus -- Metabolism ; Nerve Tissue Proteins -- Biosynthesis ; Prefrontal Cortex -- Metabolism ; Receptors, Metabotropic Glutamate -- Biosynthesis
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 5
    In: Journal of Paediatrics and Child Health, December 2015, Vol.51(12), pp.1214-1220
    Description: To purchase or authenticate to the full-text of this article, please visit this link: http://onlinelibrary.wiley.com/doi/10.1111/jpc.12927/abstract Byline: Mario Barreto, Melania Evangelisti, Luigi Principessa, Maurizio Simmaco, Valentina Negro, Luana Lionetto, Martina Campisano, Maria Pia Villa Keywords: asthma; child; functional gastrointestinal disorder; inflammation; intestinal permeability; recurrent respiratory symptom Aim Increased intestinal permeability has been reported in asthmatic subjects as well as in patients with gastrointestinal disease, thus suggesting the involvement of all the mucosal immune system. We aimed to assess intestinal permeability according to recurrent respiratory and gastrointestinal symptoms in children with asthma and children with functional gastrointestinal disorders (FGIDs). Methods In 108 outpatients aged 3-14 years (45 asthmatic, 63 with FGIDs), we measured the urinary lactulose/mannitol (L/M) ratio, performed allergy skin prick tests and administered questionnaires for recurrent respiratory and gastrointestinal symptoms starting from at least 2 months which persisted over the previous 4 weeks. L/M ratios were compared with previously reported normal values yielded by our chromatographic method (liquid chromatography-mass spectrometry). Results High L/M ratios (〉0.030) were less frequent in asthmatic children than in children with FGIDs (9/45: 20% vs. 41/63: 65%, P 〈 0.001). High L/M ratios were associated with gastrointestinal symptoms in 8/9 asthmatic (P 〈 0.05) and 39/41 subjects with FGIDs (P 〈 0.005). L/M ratios were not associated with respiratory symptoms or atopy. In a regression model, a high L/M was predicted by low height, absence of asthma and presence of gastrointestinal symptoms (r = 0.72, P 〈 0.001). Conclusions Increased intestinal permeability is associated with recurrent gastrointestinal symptoms rather than with recurrent respiratory symptoms in both asthmatic children and those with FGIDs. Our findings do not support the hypothesis of mucosal intestinal damage following an inflammatory stimulus in the respiratory mucosa. Article Note: Conflict of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
    Keywords: Asthma ; Child ; Functional Gastrointestinal Disorder ; Inflammation ; Intestinal Permeability ; Recurrent Respiratory Symptom
    ISSN: 1034-4810
    E-ISSN: 1440-1754
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  • 6
    In: Psychiatry and Clinical Neurosciences, December 2018, Vol.72(12), pp.864-875
    Description: Byline: Ilaria Cuomo, Daria Piacentino,Georgios D. Kotzalidis, Luana Lionetto, Sergio De Filippis Keywords: bipolar disorder; depression; global functioning; lacosamide; mania Aim Bipolar disorder (BD) is often treated with anticonvulsants. Lacosamide has not been tested in BD. We assessed its effects in a hospital setting in patients with BD without epilepsy. Methods We treated 102 consecutive hospitalized patients with acute BD with lacosamide 50-300 mg/day. We compared this sample with a retrospective sample treated with other antiepileptics (OAE). We rated patients after 3, 7, 15, and 30 days of treatment with the Brief Psychiatric Rating Scale, Young Mania Rating Scale, Hamilton Depression Rating Scale, Hamilton Anxiety Rating Scale, Clinical Global Impressions - Severity, and Global Assessment of Functioning. Results Patients receiving lacosamide were significantly younger and had fewer mixed episodes at intake, and less substance use disorder comorbidity than those receiving OAE. Both groups showed positive effects on all measures. The two groups did not differ on any clinical measure at baseline, but from the 3rd day on, lacosamide patients fared better than OAE patients on the Young Mania Rating Scale and Clinical Global Impressions - Severity and worse on the Hamilton Anxiety Rating Scale. From the 15th day, OAE patients scored better on the Brief Psychiatric Rating Scale. Global Assessment of Functioning scores were significantly more improved in the lacosamide patients. Age, substance use disorder comorbidity, episode type, and educational level significantly affected results. No interactions were found amongst these parameters. Conclusion Lacosamide was effective in reducing psychopathology, mania, depression, and anxiety and in improving global functioning in patients with BD-I/II disorder in the short term, with few side-effects. Lacosamide improved mania, clinical severity, and global functioning better than OAE at doses lower than those used in epilepsy. CAPTION(S): Table S1. Intragroup comparisons of effects of treatments vs baseline at the different time-points considered (cut-off P 〈 0.007). Table S2. Effect sizes of treatments on all considered measures for all groups. Table S3. Intragroup comparisons for substance use disorders (SUD) comorbid vs SUD non-comorbid subsamples (cut-off P 〈 0.007, save for age, P 〈 0.05).
    Keywords: Bipolar Disorder ; Depression ; Global Functioning ; Lacosamide ; Mania
    ISSN: 1323-1316
    E-ISSN: 1440-1819
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  • 7
    Language: English
    In: The Journal of Headache and Pain, 2015, Vol.16(Supplement 1), pp.1-1
    Description: Drugs used in the treatment of migraine have been recently reported to be highly associated with the occurrence of clinically significant drug-drug interactions (DDIs). The multiple drug therapy regimen is widely used for migraine treatment, particularly for chronic migraine. In fact, additional pharmacological agents are usually administered during an acute migraine attack in patient chronically treated with prophylactic therapy. The wide variety of drugs available for migraine prophylactic and acute treatment, and consequently their pharmacological interactions, might complicate the choice of a safe combination therapy. The most frequently used drugs for the prophylactic therapy of migraine belong to the antiepileptic, β-blockers, tricyclic, SSRIs and SNRIs antidepressants and antihistamine medications while acute migraine attacks are treated with triptans, NSAIDs and ergot derivatives. Moreover, in the last few years several of the latter drugs have been combined in new formulations for clinical use in order to improve treatment efficacy and, consequently, the compliance of the patient. Drug-drug interactions might occur at receptors level, both in the Central Nervous System (CNS) and in the periphery, at the major metabolic pathways levels (i.e., CYP450 enzymes) and at the protein binding level. One of the most widely known examples of the severity of such interactions is represented by the serotoninergic syndrome induced by the co-administration of serotoninergic antidepressants and triptans.
    Keywords: Medicine;
    ISSN: 1129-2369
    E-ISSN: 1129-2377
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  • 8
    Language: English
    In: Pharmacogenomics, August 2014, Vol.15(11), pp.1539-50
    Description: Pediatric migraine is a disabling condition that can affect the everyday activities and emotional states of children. Due to the multifactorial character of the pathology and the variety of the disease's phenotypes, establishment of an effective treatment is often challenging. Pharmacological treatment is often administered off-label and includes very different drugs, from analgesics to antidepressants. Since interindividual variability in therapy response commonly causes inefficacy and an exacerbation of symptoms, pharmacogenetics may help to decrease the prescription rate of useless or unsafe drugs. If there are many drugs used in migraine, then there are even more candidate or established pharmacogenetic markers that are implicated in clinical profiles. This article presents the current situation regarding the pharmacogenetics of drugs used in pediatric migraine.
    Keywords: Cyp450 ; Ugt ; Childhood ; Migraine ; Pharmacogenetics ; Analgesics -- Therapeutic Use ; Migraine Disorders -- Drug Therapy
    ISSN: 14622416
    E-ISSN: 1744-8042
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  • 9
    Language: English
    In: PLoS ONE, 01 January 2016, Vol.11(9), p.e0163105
    Description: BACKGROUND:5-FU based chemotherapy is the most common first line regimen used for metastatic colorectal cancer (mCRC). Identification of predictive markers of response to chemotherapy is a challenging approach for drug selection. The present study analyzes the predictive role of 5-FU degradation rate (5-FUDR) and genetic polymorphisms (MTHFR, TSER, DPYD) on survival. MATERIALS AND METHODS:Genetic polymorphisms of MTHFR, TSER and DPYD, and the 5-FUDR of homogenous patients with mCRC were retrospectively studied. Genetic markers and the 5-FUDR were correlated with clinical outcome. RESULTS:133 patients affected by mCRC, treated with fluoropyrimidine-based chemotherapy from 2009 to 2014, were evaluated. Patients were classified into three metabolic classes, according to normal distribution of 5-FUDR in more than 1000 patients, as previously published: poor-metabolizer (PM) with 5-FU-DR ≤ 0,85 ng/ml/106 cells/min (8 pts); normal metabolizer with 0,85 〈 5-FU-DR 〈 2,2 ng/ml/106 cells/min (119 pts); ultra-rapid metabolizer (UM) with 5-FU-DR ≥ 2,2 ng/ml/106 cells/min (6 pts). PM and UM groups showed a longer PFS respect to normal metabolizer group (14.5 and 11 months respectively vs 8 months; p = 0.029). A higher G3-4 toxicity rate was observed in PM and UM, respect to normal metabolizer (50% in both PM and UM vs 18%; p = 0.019). No significant associations between genes polymorphisms and outcomes or toxicities were observed. CONCLUSION:5-FUDR seems to be significantly involved in predicting survival of patients who underwent 5-FU based CHT for mCRC. Although our findings require confirmation in large prospective studies, they reinforce the concept that individual genetic variation may allow personalized selection of chemotherapy to optimize clinical outcomes.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 10
    Language: English
    In: European Child & Adolescent Psychiatry, 2017, Vol.26(12), pp.1433-1441
    Description: This study aims at determining serum levels of tryptophan and other metabolites of the kynurenine pathway in children with attention deficit hyperactivity disorder (ADHD) compared to healthy controls. Such metabolites interact with glutamate receptors in the central nervous system, potentially modulating mechanisms that are pivotal in ADHD and thus potentially representing peripheral biomarkers of the disorder. We measured serum levels of tryptophan and some metabolites of the kynurenine pathway in 102 children with ADHD and 62 healthy controls by liquid chromatography–tandem mass spectrometry (LC–MS/MS). As compared to healthy controls, children with ADHD showed a reduction in serum levels of anthranilic acid (−60%), kynurenic acid (−11.2%), and xanthurenic acid (−12.5%). In contrast, serum levels of tryptophan (+11.0%) and kynurenine (+48.6%) were significantly enhanced, and levels of quinolinic acid were unchanged in children with ADHD. In a logistic regression model, the presence of ADHD was predicted by low anthranilic acid and high tryptophan levels. These findings support the involvement of the kynurenine pathway in the pathophysiology of ADHD and suggest that anthranilic acid and tryptophan levels should be investigated as potential peripheral biomarker for ADHD.
    Keywords: ADHD ; Biomarker ; Kynurenines ; Children ; Neurobiology
    ISSN: 1018-8827
    E-ISSN: 1435-165X
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