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Relevant bibliographies by topics / Phenelzine

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Academic literature on the topic 'Phenelzine'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Journal articles on the topic "Phenelzine"

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&NA;. "Phenelzine see Amitriptyline/phenelzine." Reactions Weekly &NA;, no. 375 (1991): 11. http://dx.doi.org/10.2165/00128415-199103750-00067.

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Gold, Douglas G., and S. Hossein Fatemi. "Phenelzine–Opiate–Induced Delirium Complicated by Phenelzine Withdrawal." Journal of Pharmacy Technology 19, no. 1 (2003): 19–22. http://dx.doi.org/10.1177/875512250301900106.

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Objective: To report a case of delirium involving a drug interaction of the antidepressant phenelzine in combination with an opiate and to discuss the exacerbation of delirium secondary to a withdrawal syndrome caused by the abrupt discontinuation of phenelzine. Case Summary: A 67-year-old white woman with a history of major depression and chronic anxiety developed delirium shortly after the postsurgical administration of opioid analgesics. In addition, she was taking the antidepressant phenelzine and had been maintained on this medication for approximately 20 years. Her presenting symptoms included combativeness, auditory and visual hallucinations, and persecutory delusions. After development of the delirium, the patient's phenelzine medication was abruptly discontinued, introducing a withdrawal syndrome that further aggravated her condition. Discussion: This case emphasizes the importance of the potentially fatal drug interaction involving phenelzine and opiates and addresses the adverse consequences of abruptly discontinuing phenelzine during phenelzine–opiate–induced delirium. Phenelzine–opiate interactions and phenelzine withdrawal should be considered as possible etiologies of delirium in patients with a history of phenelzine use. Conclusions: Less widely prescribed antidepressants such as phenelzine may be unfamiliar to contemporary clinicians, resulting in adverse consequences for patients, such as phenelzine–opiate drug interactions and phenelzine withdrawal.

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&NA;. "Phenelzine." Reactions Weekly &NA;, no. 304 (1990): 10. http://dx.doi.org/10.2165/00128415-199003040-00039.

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&NA;. "Phenelzine." Reactions Weekly &NA;, no. 1096 (2006): 19–20. http://dx.doi.org/10.2165/00128415-200610960-00057.

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&NA;. "Phenelzine." Reactions Weekly &NA;, no. 362 (1991): 10–11. http://dx.doi.org/10.2165/00128415-199103620-00044.

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&NA;. "Phenelzine." Reactions Weekly &NA;, no. 597 (1996): 10. http://dx.doi.org/10.2165/00128415-199605970-00032.

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&NA;. "Phenelzine." Reactions Weekly &NA;, no. 498 (1994): 10. http://dx.doi.org/10.2165/00128415-199404980-00049.

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&NA;. "Phenelzine." Reactions Weekly &NA;, no. 508 (1994): 12. http://dx.doi.org/10.2165/00128415-199405080-00061.

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&NA;. "Phenelzine." Reactions Weekly &NA;, no. 744 (1999): 10. http://dx.doi.org/10.2165/00128415-199907440-00031.

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&NA;. "Phenelzine." Reactions Weekly &NA;, no. 652 (1997): 11. http://dx.doi.org/10.2165/00128415-199706520-00030.

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Dissertations / Theses on the topic "Phenelzine"

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Paslawski, Teresa M. "The antipanic drug phenelzine and its effects on GABA and related amino acids." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0004/NQ29091.pdf.

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Salsali, Mahnaz. "Effects of the monoamine oxidase inhibitors, tranylcypromine and phenelzine, on selected cytochrome P450 enzymes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ60342.pdf.

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Cebak, John. "MITOCHONDRIAL AND NEUROPROTECTIVE EFFECTS OF PHENELZINE RELATED TO SCAVENGING OF NEUROTOXIC LIPID PEROXIDATION PRODUCTS." UKnowledge, 2015. http://uknowledge.uky.edu/neurobio_etds/12.

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Lipid peroxidation is a key contributor to the pathophysiology of traumatic brain injury (TBI). Traditional antioxidant therapies are intended to scavenge the free radicals responsible for either the initiation or propagation of lipid peroxidation (LP). However, targeting free radicals after TBI is difficult as they rapidly react with other cellular macromolecules, and thus has a limited post-injury time window in which they may be intercepted by a radical scavenging agent. In contrast, our laboratory has begun testing an antioxidant approach that scavenges the final stages of LP i.e. formation of carbonyl-containing breakdown products. By scavenging breakdown products such as the highly reactive and neurotoxic aldehydes (often referred to as “carbonyls”) 4-hydroxynonenal (4-HNE) and acrolein (ACR), we are able to prevent the covalent modification of cellular proteins that are largely responsible for posttraumatic neurodegeneration. Without intervention, carbonyl additions render cellular proteins non-functional which initiates the loss of ionic homeostasis, mitochondrial failure, and subsequent neuronal death. Phenelzine (PZ) is an FDA-approved monoamine oxidase (MAO) inhibitor traditionally used for the treatment of depression. Phenelzine also possesses a hydrazine functional group capable of covalently binding neurotoxic carbonyls. The hypothesis of this dissertation is that carbonyl scavenging with PZ will exert an antioxidant neuroprotective effect in the traumatically injured rat brain mechanistically related to PZ’s hydrazine moiety reacting with the lipid peroxidation (LP)-derived reactive aldehydes 4-hydroxynonenal (4-HNE) and acrolein (ACR). Data from our ex vivo experiments demonstrate that the exogenous application of 4-HNE or ACR significantly reduced respiratory function and increased markers of oxidative damage in isolated non-injured rat cortical mitochondria, whereas PZ pre-treatment significantly prevented mitochondrial dysfunction and oxidative modification of mitochondrial proteins in a concentration-related manner. Additionally, PZ’s neuroprotective scavenging mechanism was confirmed to require the presence of a hydrazine moiety based on experiments with a structurally similar MAO inhibitor, pargyline, which lacks the hydrazine group and did not protect the isolated mitochondria from 4-HNE and ACR. Our in vivo work demonstrates that subcutaneous injections of PZ following TBI in the rat are able to significantly protect brain mitochondrial respiratory function, decrease markers of oxidative damage, protect mitochondrial calcium buffering capacity, and increase cortical tissue sparing without decreasing neuronal cytoskeletal spectrin degradation. These results confirm that PZ is capable of protecting mitochondrial function and providing neuroprotection after experimental TBI related to scavenging of neurotoxic LP degradation products.

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Kulbe, Jacqueline Renee. "NEUROPROTECTIVE STRATEGIES FOLLOWING EXPERIMENTAL TRAUMATIC BRAIN INJURY: LIPID PEROXIDATION-DERIVED ALDEHYDE SCAVENGING AND INHIBITION OF MITOCHONDRIAL PERMEABILITY TRANSITION." UKnowledge, 2019. https://uknowledge.uky.edu/neurobio_etds/22.

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Traumatic brain injury (TBI) represents a significant health crisis. To date there are no FDA-approved pharmacotherapies available to prevent the neurologic deficits caused by TBI. Following TBI, dysfunctional mitochondria generate reactive oxygen and nitrogen species, initiating lipid peroxidation (LP) and the formation of LP-derived neurotoxic aldehydes, which bind mitochondrial proteins, exacerbating dysfunction and opening of the mitochondrial permeability pore (mPTP), resulting in extrusion of mitochondrial sequestered calcium into the cytosol, and initiating a downstream cascade of calpain activation, spectrin degradation, neurodegeneration and neurologic impairment. As central mediators of the TBI secondary injury cascade, mitochondria and LP-derived neurotoxic aldehydes make promising therapeutic targets. In fact, Cyclosporine A (CsA), an FDA-approved immunosuppressant capable of inhibiting mPTP has been shown to be neuroprotective in experimental TBI. Additionally, phenelzine (PZ), an FDA-approved non-selective irreversible monoamine oxidase inhibitor (MAOI) class antidepressant has also been shown to be neuroprotective in experimental TBI due to the presence of a hydrazine (-NH-NH2) moiety allowing for the scavenging of LP-derived neurotoxic aldehydes. The overall goal of this dissertation is to further examine the neuroprotective effects of the mPTP inhibitor, CsA, and the LP-derived neurotoxic aldehyde scavenger, PZ, using a severe controlled cortical impact injury (CCI) model in 3-month old male Sprague-Dawley rats. First, the effects of CsA on cortical synaptic and non-synaptic mitochondria, two heterogeneous populations, are examined. Our results indicate that compared to non-synaptic mitochondria, synaptic mitochondria sustain greater damage 24h following CCI and are protected to a greater degree by CsA. Second, the neuroprotective effects of a novel 72h continuous subcutaneous infusion of CsA combined with PZ are compared to monotherapy. Following CCI, our results indicate that individually both CsA and PZ attenuate modification of mitochondrial proteins by LP-derived neurotoxic aldehydes, PZ is able to maintain mitochondrial respiratory control ratio and cytoskeletal integrity, but together, PZ and CsA, are unable to improve and in some cases negate monotherapy neuroprotective effects. Finally, the effects of PZ (MAOI, aldehyde scavenger), pargyline (PG, MAOI, non-aldehyde scavenger) and hydralazine (HZ, non-MAOI, aldehyde scavenger) are compared. Our results indicate that PZ, PG, and HZ are unable to improve CCI-induced deficits to learning and memory as measured by Morris water maze (post-CCI D3-7). Of concern, PZ animals lost a significant amount of weight compared to all other group, possibly due to MAOI effects. In fact, in uninjured cortical tissue, PZ administration leads to a significant increase in norepinephrine and serotonin. Additionally, although PZ, PG, and HZ did not lead to a statistically significant improvement in cortical tissue sparing 8 days following CCI, the HZ group saw a 10% improvement over vehicle. Overall, these results indicate that pharmacotherapies which improve mitochondrial function and decrease lipid peroxidation should continue to be pursued as neuroprotective approaches to TBI. However, further pursuit of LP-derived aldehyde scavengers for clinical use in TBI may require the development of hydrazine (-NH-NH2)-compounds which lack additional confounding mechanisms of action.

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MacKenzie, Erin Margaret. "Neurochemical and neuroprotective aspects of phenelzine and its active metabolite B-phenylethylidenehydrazine." Phd thesis, 2009. http://hdl.handle.net/10048/721.

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Phenelzine (PLZ) is a monoamine oxidase (MAO) inhibitor that also inhibits the activity of GABA-transaminase (GABA-T), causing significant and long-lasting increases in brain GABA levels. Inhibition of MAO prior to PLZ administration has been shown to prevent the GABAergic effects of the drug, strongly suggesting that a metabolite of PLZ formed by the action of MAO is responsible for the GABAergic effects. While PLZ has been used clinically for decades for its antidepressant and antipanic effects, it has more recently been shown to be neuroprotective in an animal model of ischemia. The aim of the experiments described in this thesis was to identify the active metabolite of PLZ, and to determine the neurochemical mechanisms by which PLZ and this metabolite exert their neuroprotective effects (with a particular focus on degenerative mechanisms observed in cerebral ischemia and Alzheimers disease (AD)). The development of an analytical assay for -phenylethylidenehydrazine (PEH) was a major breakthrough in this project and permitted the positive identification of this compound as the active metabolite of PLZ. Further experiments demonstrated that PLZ and PEH could be neuroprotective in cerebral ischemia and AD not only by reducing excitotoxicity via increased GABAergic transmission, but also by (a) increasing brain ornithine, which could potentially lead to a decrease in glutamate synthesis and/or a decrease in polyamines (whose metabolism produces toxic aldehydes); (b) inhibiting the activity of human semicarbazide-sensitive amine oxidase (SSAO), an enzyme whose activity is increased in AD producing excessive amounts of the toxic aldehyde formaldehyde (FA); (c) by sequestering FA in vitro, forming a non-reactive hydrazone product. Since PEH appears to mediate or share the neurochemical effects of PLZ, two propargylated analogs of PEH were synthesized and tested for their potential as PEH prodrugs. Surprisingly these analogs were not particularly effective prodrugs in vivo, but they possessed an interesting neurochemical properties on their own (the ability to elevate brain levels of glycine), and warrant further investigation as potential antipsychotic agents. Together, these results suggest that PLZ and its active metabolite, PEH, should be further investigated for their neuroprotective potential in cerebral ischemia and in AD.<br>Neurochemistry

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MacKenzie, Erin Margaret. "Neurochemical and neuroprotective aspects of phenelzine and its active metabolite [Beta]-phenylethylidenehydrazine." 2009. http://hdl.handle.net/10048/721.

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Thesis (Ph.D.)--University of Alberta, 2009.<br>A thesis submitted to the Faculty of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Neurochemistry, Department of Psychiatry. Title from pdf file main screen (viewed on October 23, 2009). Includes bibliographical references.

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Musgrave, Travis. "Amino acid and biogenic amine concentrations during experimental autoimmune encephalomyelitis and the disease-modifying effects of phenelzine treatment." Master's thesis, 2011. http://hdl.handle.net/10048/1950.

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The project described in this thesis began with a broad analysis of the changes to amino acid and biogenic amine concentrations in the central nervous system (CNS) during experimental autoimmune encephalomyelitis (EAE) in mice, an animal model of Multiple Sclerosis (MS). That study identified deficits in specific neurotransmitters during EAE that I targeted pharmacologically using the antidepressant drug phenelzine. Phenelzine administration substantially influenced the concentrations of amino acids and biogenic amines in EAE mice in a manner likely to be therapeutic. In the final experiment, I treated EAE mice chronically with phenelzine; This treatment was associated with significant improvements in motor abilities compared to vehicle treated animals. In an open field, improvements were also observed in behavioural indices of depression, physical sickness and anxiety. The results of this thesis may offer new insights into the pathogenesis of EAE and MS and indicate the disease-modifying potential of phenelzine treatment in MS.

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Books on the topic "Phenelzine"

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Elwood, William N. Fry: A study of adolescents' use of embalming fluid with marijuana and tobacco. Texas Commission on Alcohol and Drug Abuse, 1998.

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Dougherty, Darin D., Scott L. Rauch, and Michael A. Jenike. Pharmacological Treatments for Obsessive Compulsive Disorder. Edited by Gail Steketee. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195376210.013.0061.

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Progress in treating OCD has accelerated in recent years. Effective first-line treatments include behavior therapy and medications, with overwhelming evidence supporting the efficacy of serotonergic reuptake inhibitors (SRIs). Second-line medication treatments for OCD include augmentation of SRIs with neuroleptics, clonazepam, or buspirone, with limited support for other strategies at present. Alternative monotherapies (e.g., buspirone, clonazepam, phenelzine) have more limited supporting data and require further study. Behavior therapy, and perhaps cognitive therapy, is as effective as medication and may be superior in risks, costs, and enduring benefits. Future rigorous research is needed to determine which patients respond preferentially to which medications, at what dose, and after what duration. Emerging treatments include new compounds acting via serotonergic, dopaminergic, glutamatergic, and opioid systems.

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Golier, Julia A., Andreas C. Michaelides, Maya Genovesi, Emily Chapman, and Rachel Yehuda. Pharmacological Treatment of Posttraumatic Stress Disorder. Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780199342211.003.0019.

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Although psychotherapy is considered first-line treatment for posttraumatic stress disorder (PTSD), advances have been made in pharmacological treatment. Based on controlled clinical trials, antidepressants remain the first-line pharmacological treatment. Studies suggest that selective serotonin reuptake inhibitors reduce PTSD-specific symptoms and improve global outcome. Emerging evidence suggests efficacy for venlafaxine. Other individual agents found to be efficacious include imipramine and phenelzine. Prazosin is emerging as a beneficial adjunct for PTSD-related sleep disturbances and nightmares. Some evidence suggests that atypical antipsychotics may be efficacious against a broad range of symptoms, although the risk of metabolic side effects may limit widespread use. Trials are needed to assess whether anticonvulsants, cortisol-based treatments, sympatholytics, or other novel approaches are efficacious, and how pharmacotherapy can enhance psychotherapy outcomes. These studies should consider the goals of pharmacotherapy in PTSD and the subgroups of patients or clinical presentations most likely to benefit from pharmacological interventions.

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Book chapters on the topic "Phenelzine"

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McAllister-Williams, R. Hamish, Daniel Bertrand, Hans Rollema, et al. "Phenelzine." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1805.

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Courtney, John C., Cristy Akins, and Efrain Antonio Gonzalez. "Phenelzine." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1692.

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Courtney, John C., and Cristy Akins. "Phenelzine." In Encyclopedia of Clinical Neuropsychology. Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1692.

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Courtney, John C., Cristy Akins, and Efrain Antonio Gonzalez. "Phenelzine." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1692-2.

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Liebowitz, M. R., F. M. Quitkin, J. W. Stewart, et al. "Treatment of Atypical Depression: Phenelzine, Imipramine, and Placebo." In New Results in Depression Research. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70702-5_13.

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McKenna, K. F., G. B. Baker, R. T. Coutts, G. Rauw, A. Mozayani, and T. J. Danielson. "Recent studies on the MAO inhibitor phenelzine and its possible metabolites." In Amine Oxidases and Their Impact on Neurobiology. Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9113-2_15.

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Peter, Helga. "Phenelzin." In Springer Reference Medizin. Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-642-54672-3_747-1.

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Faraj, B. A., R. Sarper, M. Camp, E. Malveaux, and Y. Tarcan. "Tyramine-Induced Brain Injury in Phenelzine-Treated Dogs: An Animal Model for Cerebral Edema." In Trace Amines. Humana Press, 1988. http://dx.doi.org/10.1007/978-1-4612-4602-2_41.

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McKenna, K. F., D. J. McManus, G. B. Baker, and R. T. Coutts. "Chronic administration of the antidepressant phenelzine and its N-acetyl analogue: effects on GABAergic function." In Amine Oxidases: Function and Dysfunction. Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9324-2_15.

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"Phenelzine." In Meyler's Side Effects of Drugs. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.01254-3.

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