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  • 1
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 23 December 2014, Vol.111(51), pp.18333-8
    Description: Previous studies have provided extensive evidence that administration of cannabinoid drugs after training modulates the consolidation of memory for an aversive experience. The present experiments investigated whether the memory consolidation is regulated by endogenously released cannabinoids. The experiments first examined whether the endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) are released by aversive training. Inhibitory avoidance training with higher footshock intensity produced increased levels of AEA in the amygdala, hippocampus, and medial prefrontal cortex (mPFC) shortly after training in comparison with levels assessed in rats trained with lower footshock intensity or unshocked controls exposed only to the training apparatus. In contrast, 2-AG levels were not significantly elevated. The additional finding that posttraining infusions of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which selectively increases AEA levels at active synapses, administered into the basolateral complex of the amygdala (BLA), hippocampus, or mPFC enhanced memory strongly suggests that the endogenously released AEA modulates memory consolidation. Moreover, in support of the view that this emotional training-associated increase in endocannabinoid neurotransmission, and its effects on memory enhancement, depends on the integrity of functional interactions between these different brain regions, we found that disruption of BLA activity blocked the training-induced increases in AEA levels as well as the memory enhancement produced by URB597 administered into the hippocampus or mPFC. Thus, the findings provide evidence that emotionally arousing training increases AEA levels within prefrontal-limbic circuits and strongly suggest that this cannabinoid activation regulates emotional arousal effects on memory consolidation.
    Keywords: Anandamide ; Cannabinoid Receptors ; Emotional Arousal ; Endocannabinoids ; Inhibitory Avoidance ; Emotions ; Memory ; Arachidonic Acids -- Metabolism ; Endocannabinoids -- Metabolism ; Limbic System -- Physiology ; Polyunsaturated Alkamides -- Metabolism ; Prefrontal Cortex -- Physiology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 2
    In: Medicine & Science in Sports & Exercise, 2013, Vol.45(1), pp.29-35
    Description: PURPOSE: Anabolic androgenic steroids (AAS) are synthetic androgen-like compounds that are abused in sport communities despite their adverse effects. Nerve growth factor (NGF) influences neuronal differentiation and survival, and it also mediates higher brain functions such as learning and memory. Changes in NGF expression have been implicated in neurodegenerative disorders, including Alzheimer disease. Hence, we decided to study the effect of chronic AAS exposure on brain NGF profile, NGF-dependent cholinergic function, and related behavioral performance. METHODS: Male Wistar rats were injected for 4 wk with either nandrolone or stanozolol at daily doses (5.0 mg·kg, s.c.) that are considered equivalent to those abused by humans. NGF levels and NGF receptor (TrkA and p75NTR) expression were measured in the hippocampus and in the basal forebrain. Choline acetyltransferase expression was evaluated in basal forebrain. Spatial learning and memory were assessed using the Morris water maze. RESULTS: AAS treatment caused region-specific changes in the expression of NGF and its receptors. Both nandrolone and stanozolol increased NGF levels in the hippocampus and reduced NGF levels in the basal forebrain, reduced p75NTR expression in the hippocampus, and failed to affect TrkA expression in the basal forebrain. Finally, AAS treatment reduced the expression of choline acetyltransferase in the basal forebrain and impaired the behavioral performance in the Morris water maze. CONCLUSION: The evidence that supraphysiological doses of AAS cause neurotrophic unbalance and related behavioral disturbances raises the concern that AAS abuse in humans may affect mechanisms that lie at the core of neuronal plasticity.
    Keywords: Anabolic Agents -- Adverse Effects ; Androgens -- Adverse Effects ; Hippocampus -- Drug Effects ; Nandrolone -- Adverse Effects ; Nerve Growth Factor -- Metabolism ; Performance-Enhancing Substances -- Adverse Effects ; Stanozolol -- Adverse Effects;
    ISSN: 0195-9131
    E-ISSN: 15300315
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  • 3
    Language: English
    In: Current pharmaceutical design, 2014, Vol.20(15), pp.2457
    Keywords: Alzheimer Disease -- Etiology ; Amyloid Beta-Peptides -- Physiology
    ISSN: 13816128
    E-ISSN: 1873-4286
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 4
    Language: English
    In: Current Pharmaceutical Design, 2015, Vol.21(11), p.1357-1357
    Keywords: Pharmacy, Therapeutics, & Pharmacology;
    ISSN: 1381-6128
    E-ISSN: 1873-4286
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  • 5
    Language: English
    In: Current Pharmaceutical Design, 2014, Vol.20(15), p.2457-2457
    Keywords: Pharmacy, Therapeutics, & Pharmacology;
    ISSN: 1381-6128
    E-ISSN: 1873-4286
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  • 6
    Language: English
    In: Current pharmaceutical design, 2015, Vol.21(11), pp.1357
    Keywords: Mental Disorders -- Etiology ; Stress, Psychological -- Complications
    ISSN: 13816128
    E-ISSN: 1873-4286
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 7
    Language: English
    In: European Journal of Pharmacology, 15 December 2017, Vol.817, pp.22-29
    Description: Chronic stress is considered a widely accepted risk factor for the development of neuropsychiatric and neurological disorders. Indeed, high cortisol levels, and, thus, hypothalamic pituitary adrenal (HPA)-axis dysregulation, have been indicated as the most frequent alteration in patients affected by depression, as well as by Alzheimer's disease (AD). Furthermore, depressive state has been pointed as an early manifestation of AD, advocating an overlap between these neuropathological events. We have previously demonstrated that central soluble beta amyloid 1-42 (Aβ) administration peptide induces a depressive like-behavior in rats, with altered HPA axis activation, reduced cortical serotonin and neurotrophin levels. The crucial role of Aβ in stress response is becoming more and more evident, indeed many reports indicate that its release is increased in stressful conditions and stress-based paradigm. Furthermore, it has been reported that stress controls Aβ production and/or clearance. Chronic stress is responsible of inducing neuroinflammation processes and reduced serotoninergic tone, both pathophysiological mechanisms proposed in the association of depression with another chronic disease, such as diabetes. Likewise, AD has also been indicated as type 3 diabetes, considering the large body of literature that suggests common biological bases. Thus, the main aim of the present review is to evaluate the most recent literature findings in humans and animal models in regard to the role of Aβ in stress response and in relation to the biological substrates and pathological pathways common to AD and comorbid diseases, such as depression and diabetes.
    Keywords: Amyloid Beta ; Stress ; Hpa Axis ; Depression ; Diabetes ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0014-2999
    E-ISSN: 1879-0712
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  • 8
    Language: English
    In: Molecules, 01 February 2018, Vol.23(2), p.411
    Description: In recent years, an increasing number of studies have been published, focusing on the potential therapeutic use of small catalytic agents with strong biological properties. So far, most of these works have only regarded specific clinical fields, such as oncology, infectivology and general pathology, in particular with respect to the treatment of significant inflammatory processes. However, interesting data on possible therapeutic applications of small molecules for the treatment of neuropsychiatric and neurodegenerative illnesses are emerging, especially with respect to the possibility to modulate the cellular redox state. Indeed, a crucial role of redox dysregulation in the pathogenesis of these disorders has been widely demonstrated by both pre-clinical and clinical studies, being the reduction of the total amount of free radicals a promising novel therapeutic approach for these diseases. In this review, we focused our interest on studies published during the last ten years reporting therapeutic potential of small molecules for the treatment of neuropsychiatric and neurodegenerative disorders, also based on the biological efficiency of these compounds in detecting intracellular disturbances induced by increased production of reactive oxygen species.
    Keywords: Small Molecules ; Neuropsychiatric Disorders ; Neurodegenerative Disorders ; Redox Modulation ; Oxidative Stress ; Chemistry
    E-ISSN: 1420-3049
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  • 9
    Language: English
    In: Frontiers in Psychiatry, Oct 25, 2017
    Description: In recent years, several studies claiming the finding of a specific biomarker for the identification of the “high-risk state” to develop psychosis, first psychotic episode, as well as the prediction of the individual response to antipsychotics have been published. Together with genetic reports, numerous publications in this field have been focused on inflammation and stress response blood biomarkers, as well as on indicators of redox dysregulation. In this review, we focus on human studies found in PubMed from January 1 st 2010 to January 31 st 2017, describing the clinical use of these biomarkers to detect the “premorbid” psychotic state and early phases of the disease. Their pharmacological implications in predicting and monitoring the individual response to antipsychotic medication is also discussed.
    Keywords: Inflammation – Patient Outcomes ; Biological Markers – Research ; Antipsychotic Agents – Dosage and Administration
    ISSN: 1664-0640
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  • 10
    Language: English
    In: Pharmacological Research, May 2016, Vol.107, pp.195-204
    Description: Redox dysregulation occurs following a disequilibrium between reactive oxygen species (ROS) producing and degrading systems, i.e. mitochondria, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases and nitric oxide synthase (NOS) on one hand and the principal antioxidant system, the glutathione, on the other hand. Increasing recent evidence points towards a pathogenetic role of an altered redox state in the development of several mental disorders, such as anxiety, bipolar disorders, depression, psychosis, autism and post-traumaticstress disorders (PTSD). In this regard, pharmacological targeting of the redox state regulating systems in the brain has been proposed as an innovative and promising therapeutic approach for the treatment of these mental diseases. This review will summarize current knowledge obtained from both pre-clinical and clinical studies in order to descant ⿿lights and shadows⿿ of targeting pharmacologically both the producing and degrading reactive oxygen species (ROS) systems in psychiatric disorders.
    Keywords: Redox Regulation Systems ; Psychiatric Disorders ; Nadph Oxidase ; Nitric Oxide ; Reactive Oxygen Species ; Glutathione ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 1043-6618
    E-ISSN: 1096-1186
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