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  • Bentham Science (CrossRef)  (14)
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  • 1
    Language: English
    In: Current Neuropharmacology, 2011, Vol.9(5), p.1-81
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Source: Bentham Science Publishers
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  • 2
    Language: English
    In: Recent Patents on Anti-Infective Drug Discovery, 2010, Vol.5(3), p.181-194
    Description: Despite the improvements in HCV-therapy achieved in the last 20 years, the occurrence of high frequency of non-responders and of therapy-related side effects has lead to an ongoing interest in optimizing duration and dosage of current antiviral regimens as well as to the research and development of new antiviral treatment. Recently, the discovery of a system for in vitro HCV replication provided a useful tool for a better understanding of the viral life cycle followed by the discovery of new compounds that unlike classical drugs specifically target fundamental steps of this process. The aim of this review is to provide an update on the preclinical and clinical development of novel anti-HCV treatments targeting the first steps of the viral life cycle. The recent patents in this review article discuss the new perspectives in HCV therapy.
    Keywords: Hcv ; Entry Inhibitors ; Preclinical Development ; Clinical Development ; Hcv-Therapy ; Antiviral Treatment ; Replication ; Anti-Hcv Treatments ; Flavivirus ; Chronic ; Acute ; Cirrhosis ; Hepatocellular ; Glomerulonephritis ; Cryoglobulinemia ; Porphyria Cutanea Tarda ; Lymphoproliferative ; Liver Transplantation ; Hcc ; Prognosis ; Fibrosis ; Ifn-Alpha ; Ribavirin ; Peginterferon ; Peg-Ifn ; Viral Rna ; Anaemia ; Thrombocytopenia ; Hepacivirus ; Flaviviridae ; Heterodimer ; Glycosaminoglycans ; Glycoprotein ; Drug Design ; Albumin ; Boceprevir ; Telaprevir ; Albinterferon Alpha-2b ; Luciferase Assay ; Liver-Upa-Scid ; Viral Envelope ; Epitopes ; Monoclonal Antibodies ; Plasma Donor Antibodies ; Polyclonal Antibodies ; Hcv-Genotypes ; Glycosylation ; Glycans ; Cyanovirin-N ; High-Mannose Oligosaccharides ; Iminosugars ; Bvdv ; Adenovirus ; Vaccinia Virus ; Canary Pox Virus ; Alphavirus ; Cd81 ; Tetraspanin ; Endocytosis ; Claudin-1 ; Occludin ; Cldn1 ; Chlorpromazine ; Chloroquine ; Concanamycin A ; Bafilomycin ; Heparin ; Heparinase ; Lamiridosins ; Phosphorothioate ; Oligonucleotides (Ps-Ons) ; Arbidol ; C5a ; Amphipathic-Helical Peptide ; Paramyxoviruses ; Sp-30 ; Pro 206 ; Civacir ; Itx5061 ; Rep 9ac ; Jtk-652 ; Immune Serum Globulin ; Placebo ; Monotherapy ; Clinical Trials ; Lamiaceae
    ISSN: 1574-891X
    E-ISSN: 2212-4071
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  • 3
    Language: English
    In: Current Neuropharmacology, 2019, Vol.17(9), p.861-873
    Description: 〈p〉Three inhibitors of type-B monoamine oxidase (MAOB), selegiline, rasagiline, and safinamide, are used for the treatment of Parkinson’s disease (PD). All three drugs improve motor signs of PD, and are effective in reducing motor fluctuations in patients undergoing long-term L-DOPA treatment. The effect of MAOB inhibitors on non-motor symptoms is not uniform and may not be class-related. Selegiline and rasagiline are irreversible inhibitors forming a covalent bond within the active site of MAOB. In contrast, safinamide is a reversible MAOB inhibitor, and also inhibits voltage- sensitive sodium channels and glutamate release. Safinamide is the prototype of a new generation of multi-active MAOB inhibitors, which includes the antiepileptic drug, zonisamide. Inhibition of MAOB-mediated dopamine metabolism largely accounts for the antiparkinsonian effect of the three drugs. Dopamine metabolism by MAOB generates reactive oxygen species, which contribute to nigro-striatal degeneration. Among all antiparkinsonian agents, MAOB inhibitors are those with the greatest neuroprotective potential because of inhibition of dopamine metabolism, induction of neurotrophic factors, and, in the case of safinamide, inhibition of glutamate release. The recent development of new experimental animal models that more closely mimic the progressive neurodegeneration associated with PD will allow to test the hypothesis that MAOB inhibitors may slow the progression of PD.〈/p〉
    Keywords: Selegiline Rasagiline Safinamide Maob Basal Ganglia Parkinson&Amp;#39;S Disease Glutamate Release.
    ISSN: 1570-159X
    E-ISSN: 1875-6190
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  • 4
    Language: English
    In: Current Neuropharmacology, 2016, Vol.14(1), p.41-47
    Description: Schizophrenia and Bipolar Disorder are chronic psychiatric disorders, both considered as “major psychosis” they are thought to share some pathogenetic factors involving a dysfunctional 〈i〉gene x environment〈/i〉 interaction. Alterations in the glutamatergic transmission have been suggested to be involved in the pathogenesis of psychosis. Our group developed an epigenetic model of schizophrenia originated by Prenatal Restraint Stress (PRS) paradigm in mice. PRS mice developed some behavioral alterations observed in schizophrenic patients and classic animal models of schizophrenia, i.e. deficits in social interaction, locomotor activity and prepulse inhibition. They also showed specific changes in promoter DNA methylation activity of genes related to schizophrenia such as reelin, BDNF and GAD67, and altered expression and function of mGlu2/3 receptors in the frontal cortex. Interestingly, behavioral and molecular alterations were reversed by treatment with mGlu2/3 agonists. Based on these findings, we speculate that pharmacological modulation of these receptors could have a great impact on early phase treatment of psychosis together with the possibility to modulate specific epigenetic key protein involved in the development of psychosis. 〈/p〉 〈p〉 In this review, we will discuss in more details the specific features of the PRS mice as a suitable epigenetic model for major psychosis. We will then focus on key proteins of chromatin remodeling machinery as potential target for new pharmacological treatment through the activation of metabotropic glutamate receptors. 〈/p〉
    Keywords: Dna Methylation Epigenetics Mglu Receptors Prenatal Stress Psychosis.
    ISSN: 1570-159X
    E-ISSN: 1875-6190
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  • 5
    Language: English
    In: Current drug targets, 2018, Vol.19(6), pp.636-650
    Description: It is known that an increased oxidative stress is present in a wide range of diseases and, given the vulnerability of the central nervous system, its involvement has been in particular investigated in neurological and psychiatric diseases, including anxiety disorders. In this review, we analyse the studies that have been conducted on the effects of oxidative stress modulators in anxiety, focusing on their possible clinical use. While preclinical studies have shown a clear anxiolytic-like effect of different oxidative stress modulators, less significant results have been obtained from clinical studies. After having reviewed the possible reasons for the discrepancy between preclinical and clinical data, we encourage further studies aimed at better investigating the utility of the modulation of oxidative stress in humans, as an adjunctive therapy of the traditional integrated psychotherapeutic and pharmacological approach.
    Keywords: Oxidative Stress Modulators ; Anxiety Disorders ; Anxiety Models ; Lipid Peroxidation ; Reactive Nitrogen Species ; Reactive Oxygen Species. ; Anti-Anxiety Agents -- Pharmacology ; Anxiety Disorders -- Drug Therapy ; Oxidative Stress -- Drug Effects
    ISSN: 13894501
    E-ISSN: 1873-5592
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  • 6
    Language: English
    In: Current Pharmaceutical Design, 2013, Vol.19(36), p.6480-6490
    Description: The term "Autism Spectrum" is often used to describe disorders that are currently classified as Pervasive Developmental Disorders. These disorders are typically characterized by social deficits, communication difficulties, stereotyped or repetitive behaviors and/or cognitive delays or mental retardation; sometimes they present high comorbidity rates with epilepsy. Although these diagnoses share some common features, individuals with these disorders are thought to be "on the spectrum" because of differences in severity across these domains. Recent advances in the genetics of autism spectrum disorders (ASDs) are offering new valuable insights into molecular and cellular mechanisms of pathology. Of particular interest are transgenic technologies that allowed the engineering of several mouse models mimicking different kinds of monogenic heritable forms of ASDs. These transgenic models provide excellent opportunities to explore in detail cellular and molecular mechanisms underlying disease pathology and to identify novel targets for therapeutic intervention. Increasing evidence suggests that the pathophysiological core of the murine model is primarily due to changes in normal synaptic transmission and plasticity. Here, we will extensively review the synaptic alterations across different animal models of ASDs and recapitulate the pharmacological strategies aimed at rescuing hippocampal plasticity phenotypes. We describe how pharmacological modulation of mGlu5 receptor, through the use of positive or negative allosteric modulators (depending on the specific disorder), may represent a promising therapeutic strategy for ASDs treatment.
    Keywords: Synaptic Plasticity Long-Term Potentiation Long-Term Depression Monogenic Autism Mglurs.
    ISSN: 1381-6128
    E-ISSN: 1873-4286
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  • 7
    Language: English
    In: Recent Patents on CNS Drug Discovery, 2015, Vol.10(1), p.55-64
    Description: Osteoporotic hip fracture needs a specific approach and treatment, since elderly patients are at high risk for adverse outcomes after surgery. In particular, delirium often occurs in the peri-operative period, and it is associated with death, hospital-acquired complications, persistent cognitive impairments, poor functional recovery after surgery and increased healthcare costs. 〈/p〉〈p〉 The pre-operative assessment of the risk factors for delirium improves the preventive measures. The delirium diagnostic tools should be included in the standard of orthogeriatric cure for hip fracture. Given the increasing complexity of the clinical pictures, we present a review of the available treatment options for delirium in patients with hip fracture. The metabolic pre-operative disorders and the management of co-morbid diseases are specific targets of treatment in order to optimize the outcomes after surgery. In particular, elderly patients with Alzheimer's disease are highly vulnerable to hip fracture and delirium, and they are severely frail with reduced physiologic reserves. 〈/p〉〈p〉 An integrated approach combining environmental and pharmacological strategies is useful in the delirium treatment, with a close collaboration between the orthopedic and geriatric team.
    Keywords: Alzheimer'S Disease Bdnf Cortisol Hip Fracture Metabolism Neurotransmission.
    ISSN: 1574-8898
    E-ISSN: 2212-3954
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  • 8
    Language: English
    In: Current Genomics, 2013, Vol.14(2), p.147-156
    Description: Late-onset Alzheimer's disease (LOAD) is the most common form of dementia in the elderly. LOAD has a complex and largely unknown etiology with strong genetic determinants. Genetics of LOAD is known to involve several genetic risk factors among which the Apolipoprotein E (APOE) gene seems to be the major recognized genetic determinant. Recent efforts have been made to identify other genetic factors involved in the pathophysiology of LOAD such as genes associated with a deficit of neurotrophic factors in the AD brain. Genetic variations of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), and transforming-growth-factor-β1 (TGF-β1) are known to increase the risk to develop LOAD and have also been related to depression susceptibility in LOAD. Transforming-Growth-Factor-β1 (TGF- β1) is a neurotrophic factor that exerts neuroprotective effects against β-amyloid-induced neurodegeneration. Recent evidence suggests that a specific impairment in the signaling of TGF-β is an early event in the pathogenesis of AD. TGF-β1 protein levels are predominantly under genetic control, and the TGF-β1 gene, located on chromosome 19q13.1–3, contains several single nucleotide polymorphisms (SNPs) upstream and in the transcript region, such as the SNP at codon +10 (T/C) and +25 (G/C), which is known to influence the level of expression of TGF-β1. In the present review, we summarize the current literature on genetic risk factors for LOAD, focusing on the role of the TGF-β1 gene, finally discussing the possible implications of these genetic studies for the selection of patients eligible for neuroprotective strategies in AD.
    Keywords: Alzheimer’s Disease ; Depression ; Drugs ; Genetic Polymorphism ; Risk Factor ; Transforming-Growth-Factor-Β1
    ISSN: 1389-2029
    E-ISSN: 1875-5488
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  • 9
    Language: English
    In: Current Neuropharmacology, 2006, Vol.4(3), p.173-173
    Description: Although morphine is still the gold-standard for the treatment of pathological pain, the increasing knowledge of the mechanisms that regulate pain threshold breaks the ground for the development of new potent and safe analgesic drugs. Hopefully, these drugs will relieve some forms of pain that are partially resistant to opiates, such as neuropathic pain. This issue of Current Neuropharmacology includes a series of excellent reviews that summarize the current knowledge and the most exciting perspectives on the neurobiology of pain. The opening review by Dr. Marchettini and collaborators is a nice clinical classification of peripheral neuropathies, which are a major source of neuropathic pain. If present, pain associated with peripheral neuropathies is extremely disabling, and its treatment is one of the major challenges in neuroscience. The two following reviews by Dr. Story and Dr. Mc Naughton's group focus on the role of Trp channels in heat sensation and inflammatory pain. One of these channels, named TrpV1, is expressed by neurons of dorsal root ganglia, and responds to heat, protons, inflammatory mediators, and capsaicin. An increased sensitivity of the TrpV1 channel is central to the pathophysiology of heat hyperalgesia in inflammatory pain. The review by the group of Dr. Negri and Dr. Melchiorri describes the role of prokineticins and their receptors in the modulation of pain. Prokineticins are the mammalian homologs of Bv8, a small protein extracted from the frog skin that behaves as a potent hyperalgesic agent. The regulation of pain moves from the periphery to the CNS in the review by Dr. Tao and Dr. Johns, which describes the role of PDZ-domain-containing proteins associated with NMDA receptors in persistent pain. The review by the group of Dr. Maione and Dr. Rossi explores the complex interaction between metabotropic glutamate receptors and cannabinoid receptors in the periaqueductal grey, a region of the brainstem that is critical for the regulation of pain threshold. These two classes of receptors are considered as potential targets for novel analgesic drugs. Along this line, the review by Dr. Chiechio and collaborators describes the mechanism of action of Lacetylcarnitine, a drug that is currently used for the treatment of neuropathic pain. L-Acetylcarnitine up-regulates the expression of a particular metabotropic glutamate receptor subtype, the mGlu2 receptor, which inhibits neurotransmission at the synapse between primary afferent pathways and neurons in the dorsal horns of the spinal cord. Finally, the elegant review by Dr. Manzanares, Dr. Julian, and Dr. Carrascosa describes the multifaceted role of the cannabinoid system in pain transmission, and the potential therapeutic implications for the management of acute and chronic pain. Taken together, the articles included in the issue offer an original view of the molecular and transsynaptic mechanisms underlying inflammatory and neuropathic pain, and are particularly helpful for basic scientists and clinicians interested in the neuropharmacology of pain.
    Keywords: Psychosis;
    ISSN: 1570-159X
    E-ISSN: 1875-6190
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  • 10
    Language: English
    In: Current Pharmaceutical Biotechnology, 2016, Vol.17(10), p.926-929
    Description: Many unsolved practical issues, from technical and scientific to ethical, legal and economic topics, are slowing down the translation of Personalized Medicine principles into medical practice. The Italian Society of Personalized Medicine exposes here its point of view, based on the real-world practice of precision medicine carried-out in Italian healthcare structures.
    Keywords: H2020 Personalized Medicine Precision Medicine.
    ISSN: 1389-2010
    E-ISSN: 1873-4316
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