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Academic literature on the topic 'Antidepressants Mechanisms of action'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Antidepressants Mechanisms of action"

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Kozlovskii, V. L., M. Yu Popov, D. N. Kosterin, and O. V. Lepik. "Heterogeneity of the mechanisms of action of antidepressants." V.M. BEKHTEREV REVIEW OF PSYCHIATRY AND MEDICAL PSYCHOLOGY, no. 1 (April 12, 2021): 11–17. http://dx.doi.org/10.31363/2313-7053-2021-1-11-17.

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The article discusses the heterogeneous mechanisms of the pharmacodynamics of antidepressants that underlie the therapeutic response. Sharing the similar clinical activity, antidepressants determine the development of drug-induced homeostasis by means of different molecular mechanisms (selective or nonselective blockade of monoamine reuptake, inhibition of monoamine oxidase, blockade of certain monoamine receptors). However, an increase of serotonin and other monoamines concentrations in the synapses of the central nervous system is only the initiating factor in the development of specific clinical effects. The latter are probably determined by other neurochemical effects, including changes in the density of postsynaptic receptors and an increase in the synthesis of neurotrophic factors. However, the primary mechanisms that increase monoamine concentrations in the synapses might not always “work properly”, leading to the lack of efficacy of the initial antidepressant, while the probability of the therapeutic response to the subsequent antidepressant remains rather high. Thus, the efficacy of an antidepressant may depend on the baseline differences in the neurochemical state contributing to the pathological “depressive” homeostasis. The heterogeneous neurochemical effects of antidepressants can determine the dissociation of existing neuronal interactions, leading to the development of the new — druginduced — homeostasis. At the same time, it is possible that stimulation of general neurotrophic processes by antidepressants may contribute to the progression and chronicity of pathology due to the ambiguous influence on certain stages of the pathological process. This determines the significance of neurophysiological studies of central disturbances in depression and search of fundamentally new neurochemical targets for the treatment of depressive states associated with various mental disorders.
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Amidfar, Meysam, and Yong-Ku Kim. "Recent Developments on Future Antidepressant-related Serotonin Receptors." Current Pharmaceutical Design 24, no. 22 (October 19, 2018): 2541–48. http://dx.doi.org/10.2174/1381612824666180803111240.

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Conventional serotonin-enhancing antidepressants including selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs) have shown effectiveness in the treatment of major depression, but their significant limitations such as slowness of action have led to intensive research efforts to develop new antidepressants. Increased synaptic neurotransmission of serotonin (5-hdroxytryptamine; 5-HT) through orchestration of stimulation and blockade of various subtypes of 5-HT receptors is involved in the mechanisms of action of SSRIs. Agonists at the 5-HT1A, 5-HT1B, 5-HT2C, 5-HT4, and 5-HT6 receptors and antagonists at the 5-HT1A, 5-HT2A, 5-HT2C, 5-HT3, 5- HT6, and 5-HT7 receptors have shown antidepressant properties in clinical and preclinical studies. However, paradoxical antidepressant-like effects of both agonists and antagonists at particular 5-HT receptors suggest the need to consider the neurochemical mechanisms of each 5-HT receptor subtype. Therefore, better knowledge of the involvement of individual 5-HT receptors in the mechanisms of action of currently used antidepressants as well as antidepressant effects of selective ligands of 5- HT receptor subtypes will provide opportunities for the development of future antidepressants with more rapid onset of action, fewer side effects, and better efficacy than SSRIs.
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Leonard, B. E. "Mechanisms of Action of Antidepressants." CNS Drugs 4, Supplement 1 (1995): 1–12. http://dx.doi.org/10.2165/00023210-199500041-00003.

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GARATTINI, S., C. BARBUI, and B. SARACENO. "Antidepressant agents: from tricyclics to serotonin uptake inhibitors." Psychological Medicine 28, no. 5 (September 1998): 1169–78. http://dx.doi.org/10.1017/s0033291798007090.

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Background. The number of antidepressant drugs available in the market has grown rapidly in the last few years. The present paper underlines some of the pre-clinical and clinical problems that call close attention from the regulatory authorities when approving new drugs.Methods. We present here a review of the literature.Results. A wide heterogeneity in the action of the various antidepressants precludes any single theory about the pathogenesis and therapy of depression. Antidepressant activity, in fact, may be achieved by acting on a number of different monoaminergic mechanisms. The variety in the neurochemical effects of antidepressants is not reflected in clinical trials, which tend to stereotypy. In many cases clinical trials aim at demonstrating equivalence rather than differences in efficacy. Regulatory authorities should, therefore, pay attention in accepting the equivalence of effects of a new drug in relation to a reference one: most clinical trials of new antidepressant drugs do not have the power to detect clinically relevant differences.Conclusions. Unconventional new pre-clinical tests are needed to generate antidepressants with a different mechanism of action. Clinical studies are needed to promote objective comparative evaluation of the cost, benefits and toxic effects of new antidepressants.
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Murawiec, Sławomir, and Marek Krzystanek. "Symptom Cluster-Matching Antidepressant Treatment: A Case Series Pilot Study." Pharmaceuticals 14, no. 6 (May 31, 2021): 526. http://dx.doi.org/10.3390/ph14060526.

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Despite treating depression with antidepressants, their effectiveness is often insufficient. Comparative effectiveness studies and meta-analyses show the effectiveness of antidepressants; however, they do not provide clear indications as to the choice of a specific antidepressant. The rational choice of antidepressants may be based on matching their mechanisms of action to the symptomatic profiles of depression, reflecting the heterogeneity of symptoms in different patients. The authors presented a series of cases of patients diagnosed with depression in whom at least one previous antidepressant treatment was shown to be ineffective before drug targeted symptom cluster-matching treatment (SCMT). The presented pilot study shows for the first time the effectiveness of SCMT in the different clusters of depressive symptoms. All the described patients obtained recovery from depressive symptoms after introducing drug-targeted SCMT. Once validated in clinical trials, SCMT might become an effective and rational method of selecting an antidepressant according to the individual profile of depressive symptoms, the mechanism of their formation, and the mechanism of drug action. Although the study results are preliminary, SCMT can be a way to personalize treatment, increasing the likelihood of improvement even in patients who meet criteria for treatment-resistant depression.
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Thase, Michael E. "New medications for treatment-resistant depression: a brief review of recent developments." CNS Spectrums 22, S1 (December 2017): 39–48. http://dx.doi.org/10.1017/s1092852917000876.

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There is a great unmet need for new medications with novel mechanisms of action that can effectively treat patients who do not benefit from standard antidepressant therapies. After a period in which it seemed as if the pharmaceutical pipeline for new antidepressants was going dry, the past decade has witnessed renewed interest, beginning with discovery of the antidepressant effects of ketamine. This article briefly highlights more recent research on ketamine and other investigational antidepressants.
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Borowicz-Reutt, Kinga K. "How Antidepressant Drugs Affect the Antielectroshock Action of Antiseizure Drugs in Mice: A Critical Review." International Journal of Molecular Sciences 22, no. 5 (March 3, 2021): 2521. http://dx.doi.org/10.3390/ijms22052521.

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Depression coexists with epilepsy, worsening its course. Treatment of the two diseases enables the possibility of interactions between antidepressant and antiepileptic drugs. The aim of this review was to analyze such interactions in one animal seizure model—the maximal electroshock (MES) in mice. Although numerous antidepressants showed an anticonvulsant action, mianserin exhibited a proconvulsant effect against electroconvulsions. In most cases, antidepressants potentiated or remained ineffective in relation to the antielectroshock action of classical antiepileptic drugs. However, mianserin and trazodone reduced the action of valproate, phenytoin, and carbamazepine against the MES test. Antiseizure drug effects were potentiated by all groups of antidepressants independently of their mechanisms of action. Therefore, other factors, including brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factor (GDNF) modulation, should be considered as the background for the effect of drug combinations.
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Ochi, Taichi, Natalya M. Vyalova, Innokentiy S. Losenkov, Diana Z. Paderina, Ivan V. Pozhidaev, Anton J. M. Loonen, German G. Simutkin, Nikolay A. Bokhan, Bob Wilffert, and Svetlana A. Ivanova. "Preliminary Pharmacogenetic Study to Explore Putative Dopaminergic Mechanisms of Antidepressant Action." Journal of Personalized Medicine 11, no. 8 (July 27, 2021): 731. http://dx.doi.org/10.3390/jpm11080731.

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Background: There is sufficient evidence that interference of dopaminergic neurotransmission contributes to the therapeutic effects of antidepressants in unipolar and bipolar depression. Methods: Hamilton depression rating scale (HAMD 17) scores of 163 at least moderately ill patients with major depressive disorders were used to establish treatment response. HAMD 17 score status was measured before initiation, after two weeks, and after four weeks of treatment with various antidepressants. The possible association between response and genotype in a total of 14 variants of dopamine neurotransmission-related proteins was investigated. Results: DRD4 rs11246226 CA heterozygous patients were found with a greater improvement of HAMD 17 score when compared to homozygous C patients during 0–2 weeks and 0–4 weeks. Patients with MAOB rs1799836 heterozygous GA and homozygous A also demonstrated improved scores during 2–4 weeks and 0–4 weeks. Conclusions: The results are preliminary due to the limited population size and the small number of variants. Further research into the involvement of habenular dopamine D4 receptors in the antidepressant response is desirable.
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Dabetić, Marija, Milica Nešić, Uroš Dabetić, and Milan Latas. "Antidepressants and COVID-19: A case report and review of the literature." Engrami 44, no. 1 (2022): 89–99. http://dx.doi.org/10.5937/engrami43-39941.

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Introduction. Anti-inflammatory potential of antidepressants was observed before the COVID-19 pandemic. However, it recently regained spotlight when studies with large number of patients showed that antidepressants reduced the risk of intubation and death in COVID-19 symptomatic infection. Also, the response to antidepressants seems to be more rapid in post-COVID depression that in non-COVID19 related depression. The aim of this paper to review the literature regarding the effects and mechanisms of action of antidepressants in COVID-19 infection and post-COVID sequalae, and to present a case repot of a typical outpatient with post-COVID depression. Conclusion. Post-COVID depression is a common sequela of COVID-19 infection. Selective serotonin reuptake inhibitors elicit a rapid and efficient response in patients with post-COVID depression, which may be explained by their anti-inflammatory properties. Timely screening and treatment of post-COVID psychiatric disorders can significantly decrease the burden of COVID-19 pandemic both at the individual and societal level. Also, it is discussed how the pandemic studies of antidepressant mechanisms of actions provided new insights on the aetiology of depression.
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Frazer, A. "P.1.045 Mechanisms of action of antidepressants." European Neuropsychopharmacology 7 (September 1997): S149. http://dx.doi.org/10.1016/s0924-977x(97)88494-5.

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Dissertations / Theses on the topic "Antidepressants Mechanisms of action"

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Mann, Catherine. "Mechanisms of action of antidepressant drugs: Presynaptic and postreceptor mechanisms." Thesis, University of Ottawa (Canada), 1992. http://hdl.handle.net/10393/10600.

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The etiology of clinical depression is unknown, but thought to be related to an impairment in brain transmission of monoamines. Depression is treated with antidepressant drugs which, regardless of classification, ultimately result in increased efficacy of aminergic transmission. Tricyclic antidepressants are known to inhibit the presynaptic uptake of amines. [3H]Imipramine, the prototype tricyclic antidepressant and a potential biological marker in depression, binds to both high- and a low-affinity sites in the brain. The high-affinity binding of [3H]imipramine to its binding site on the serotonin (5-HT) neuronal transporter has been shown to be a sodium-dependent process. However, that of [3H]paroxetine, a novel and selective 5-HT uptake inhibitor, has not yet been investigated. Because of a discrepancy between the onset of uptake-blocking effect and alleviation of depressive symptoms, the blockage of uptake is probably not the only pharmacological action of antidepressants underlying their clinical effect. Recent studies have reported decreases in beta-adrenoceptor and 5-HT2 receptor numbers following long-term treatment with antidepressants, and suggested that an adaptive change in amine receptors may be more relevent for the clinical effect. However, not all 5-HT uptake inhibitors elicit this downregulation. Recent research has thus centred on elucidating changes in the signal transduction apparatus of aminergic neurons. The 5-HT2 receptor in the brain is coupled to the phosphoinositide turnover cascade and protein kinase C (PKC) activity. The subcellular distribution of PKC following chronic antidepressant treatment has not yet been investigated. This study was undertaken (1) To compare the sodium dependence of [3H]paroxetine binding and [3H]5-HT uptake in rat diencephalon in order to confirm whether paroxetine binds to the 5-HT recognition site on the transporter, and (2) to investigate the effects of both acute and chronic antidepressant treatment on PKC location and activity (both basal and 5-HT2 receptor agonist (DOI)-challenged) in rat cortex and hippocampus. Results indicate that, antidepressant drugs induce differing but significant effects on PKC activity in the subcellular fractions of neurons both after acute and chronic treatment. These changes in PKC activity may alter transduction of cellular signals evoked by the binding of 5-HT to receptors. (Abstract shortened by UMI.)
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Tabaka, John. "Mechanisms of action of antidepressants and their combination for major depressive disorder treatment: a theoretical and clinical approach." Thesis, McGill University, 2014. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=121186.

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Background: Annually, an estimated 8.2% of Canadians aged 18 or older are affected by major depressive disorder (MDD). Nearly half of those suffering from MDD will fail to achieve remission while also having an inadequate response to an initial and continuous 6-week single antidepressant treatment. This failure to remit or respond to monotherapy, referred to as treatment-resistant depression (TRD), affects more than 30% of those suffering from MDD. The addition of a second antidepressant to improve upon the effects or alleviate the side-effects of the initial antidepressant has repeatedly shown encouraging therapeutic benefits. Unfortunately, the use of combination therapy in clinical settings has remained relatively low. Objective: With knowledge and understanding of the mechanisms of action of each of the seven different classes of antidepressants attained from preclinical studies (in vitro and in vivo electrophysiology) conducted at the Neurobiological Psychiatry Unit (NPU) at McGill University, the therapeutic efficacy of combination therapy can be maximized and adverse interactions and events minimized. The main goal of this thesis was to review the extensive literature concerning antidepressant studies conducted at the NPU as well as the clinical literature from PubMed and OvidSP in order to discern the most efficacious antidepressants and antidepressant combination treatments. The data collected from the literature was critically compared with the clinical database of the Mood Disorders Clinic (MDC) at the McGill University Health Centre (MUHC), in order to establish the clinical pertinence of using antidepressant combinations. Methods: A literature review was conducted to discern the most frequently prescribed antidepressants and efficacious antidepressant combination treatments. Subsequently, we analyzed the database of the MUHC; 133 outpatients with a current DSM-IV diagnosis of MDD aged 18 years or older were included in this study. Sociodemographic and clinical information of each patient was obtained during his or her initial diagnostic evaluation by a multidisciplinary team and chart review. Patients were also asked to complete a self-reported BDI-II questionnaire in order to assess the severity of depressive symptoms. Statistical analyses between prescribed antidepressant combinations and symptom severity were performed to determine effectiveness. A critical comparison of the findings from the literature with the clinical information obtained from patients referred to the MDC was conducted. Results: Significantly more women than men were diagnosed with MDD. Within the six months of their initial diagnostic evaluation, 87.2% of the patients had been prescribed an antidepressant. The most frequently prescribed antidepressant was a selective serotonin reuptake inhibitor (SSRI), followed by a serotonin-norepinephrine reuptake inhibitor (SNRI) and bupropion. Consistent with the literature, the most frequent antidepressant combination treatments were i) SSRI + bupropion, ii) SNRI + bupropion, and iii) SNRI + mirtazapine. No significant difference was found between antidepressant combination treatments and mean total BDI-II scores. Conclusions: Clinical findings were generally consistent with the literature. The literature supported the use of antidepressant combinations for effective and time-efficient treatment of MDD, particularly at the beginning of treatment, yet psychiatrists still appeared hesitant on using this approach. The combinations of bupropion with an SSRI or SNRI were found to be the most efficacious combinations, receiving frequent support in the literature and in this study. Limitations: Low completion rate of the BDI-II resulted in the powers of performed tests to be lower than the desired powers, thus reducing the likelihood of detecting a difference when one may have actually existed. A larger cohort of patients could allow for clinically meaningful differences to be observed.
Contexte: Chaque année, on estime que 8.2% des Canadiens âgés de 18 ans ou plus sont touchés par un trouble dépressif majeur (TDM). Près de la moitié des personnes souffrant de TDM ne parviendra pas à atteindre la rémission tout en ayant une réponse inadéquate au premier traitement antidépresseur pris seul durant 6 semaines continues. Ce défaut de rémission ou de répondre à la monothérapie, appelée dépression résistante au traitement (DRT), affecte plus de 30% des personnes souffrant de TDM. L'ajout d'un second antidépresseur pour améliorer les effets du médicament ou atténuer les effets secondaires de l'antidépresseur a montré à maintes reprises d'encourageants avantages thérapeutiques. Malheureusement, l'utilisation de la thérapie de combinaison dans les milieux cliniques reste relativement faible. Objectif: L'objectif principal de ce travail de recherche était de revisiter la littérature scientifique, à partir des études précliniques menées sur les antidépresseurs chez l'unité de Psychiatrie Neurobiologique à l'université McGill et des études cliniques à partir de PubMed/OvidSP, afin de comprendre le mécanisme d'action des antidépresseurs et les combinaisons possibles les plus efficaces. Ces données de la littérature ont été ensuite comparées avec une banque de données cliniques du programme de troubles de l'humeur du centre universitaire de santé McGill (CUSM), qui est un centre de soins tertiaires psychiatriques, avec le but d'établir la pertinence clinique de l'utilisation des combinaisons d'antidépresseurs. Méthodes: Une revue des études publiés dans la littérature a été effectuée pour discerner les antidépresseurs les plus prescrits et les combinaisons d'antidépresseurs les plus efficaces. Par la suite, nous avons analysé la banque de données du CUSM; 133 patients en consultation externe ayant un diagnostic du DSM-IV de TDM âgés de 18 ans ou plus ont été inclus dans cette étude. Les renseignements sociodémographiques et cliniques de chaque patient ont été obtenus au cours de sa première évaluation diagnostique par une équipe pluridisciplinaire et examen des dossiers. Les patients ont également été invités à remplir un questionnaire d'auto-évaluation de BDI-II afin d'évaluer la sévérité des symptômes dépressifs. Des analyses statistiques entre les combinaisons d'antidépresseurs prescrits et la sévérité des symptômes ont été effectuées. Une comparaison critique de ces résultats de la littérature avec les données cliniques de la banque du CUSM a été réalisée. Résultats: Beaucoup plus de femmes que d'hommes ont été diagnostiqués avec TDM. Dans les six mois suivant leur diagnostic initial, 87.2% des patients avaient été prescrit un antidépresseur. L'antidépresseur le plus prescrit est un ISRS, suivi par un IRSNa et le bupropion. Conformément à la documentation, les traitements combinés d'antidépresseurs les plus fréquents étaient i) ISRS + bupropion, ii) IRSNa + bupropion, et iii) IRSNa + mirtazapine. Aucune différence significative n'a été observée entre les traitements de combinaisons d'antidépresseurs et la moyenne totale des résultats du BDI-II. Conclusions: Les résultats cliniques étaient généralement conformes aux études passées. Les études sont favorables à l'utilisation de combinaisons d'antidépresseurs pour le traitement efficace et plus rapide de TDM, en particulier au début du traitement, mais les psychiatres semblaient encore hésitants sur l'utilisation de cette approche. Les combinaisons de bupropion avec un ISRS ou IRSNa se sont révélées être les combinaisons les plus efficaces, bénéficiant d'un soutien fréquent dans les études passées et dans cette étude. Limitations:Le faible taux d'achèvement du questionnaire BDI-II ont abouti à des pouvoirs de tests effectués à être plus faible que les pouvoirs voulus, réduisant ainsi la probabilité de détecter une différence qui peut avoir réellement existé. Une cohorte plus importante de patients pourrait permettre d'observer des différences cliniquement significatives.
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Mustafa, M. R. "Involvement of noradrenergic mechanisms in the antidepressant action of rolipram." Thesis, Cardiff University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378451.

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Coull, Moyra Ann. "Signal transduction mechanisms in affective disorders and antidepressant drug action." Thesis, St George's, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393163.

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Petermann, Markus. "Identifying the mechanisms of antidepressant drug action in mice lacking brain serotonin." Doctoral thesis, Humboldt-Universität zu Berlin, 2021. http://dx.doi.org/10.18452/23035.

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Serotonin gilt als Hauptangriffsstelle gängiger Antidepressiva bei schweren Depressionen, wie bspw. selektive Serotonin-Wiederaufnahmehemmer (SSRI), und -Enhancer (SSRE). Es bleibt offen, ob SSRI / E ausschließlich über die Manipulation des Serotoninspiegels wirken, oder ob alternative Signalwege daran beteiligt sind. Ansatzpunkte hierfür sind beispielsweise die neurotrophen Signalwege (spez. Brain derived neurotophic factor, BDNF) oder die Hypothalamus-Hypophysen-Nebennieren- (HPA) – Signalwege des Stressachsensystems. Ebenfalls wurde in Nagetiermodellen beobachtet, dass mit der Dysregulation des zentralen Serotoninsystems bei schweren Depressionen, ein Rückgang der Neurogenese im Gyrus dentatus des Hippocampus einhergeht. Ziel dieser Arbeit war, das Zusammenspiel von Serotonin, BDNF, adulter Neurogenese und der Stressachse zu untersuchen. Zentrum der Studien ist ein Mausmodell, mit einer genetischen Depletion des zentralen Serotonin-synthetisierenden Enzyms Tryptophanhydroxylase 2 (sog. Tph2-/- Mäuse). Es wurden die physiologische Reaktionen auf die Behandlung mit gängigen Antidepressiva abhängig von der Abwesenheit von Serotonin untersucht, um mögliche alternative Signalwege aufzeigen zu können. Die bekannte Zunahme der Neurogenese nach SSRI/SSRE-Behandlung wurde in Wildtyptieren beobachtet, während die Therapie in Tph2-/- Mäusen keine direkte kausale Wirkung zeigte. Im Gegensatz dazu waren die BDNF-Spiegel in depressionsrelevanten Hirnregionen in Tph2-/- Mäusen nach SSRI, signifikant verringert. Auch zeigen die Studien eine neurobiologische Relevanz von Serotonin im ZNS, bei den antidepressiven Mechanismen einer Elektrokonvulsiven Krampftherapie. Ebenfalls deuten erhöhte Neurogeneseraten bei lebenslanger Abwesenheit von Serotonin im ZNS, Therapiemethoden-unabhängig, möglicherweise auf eine modulierte Stressreaktion hin. Untersuchungen der Parameter des HPA-Stressachsensystems, wiesen auf einen grundlegend veränderten Stresshormonspiegel in Tph2-/- Mäusen hin.
Serotonin, the "molecule of happiness" is an important target for antidepressants. The mainly prescribed drugs in major depression are selective serotonin re-uptake inhibitors (SSRI); but recently, SSR-enhancer (SSRE) have also attracted clinical attention. However, only a quarter of patients responds to treatment. It needs to be determined, whether SSRI/E act solely via manipulating serotonin levels or whether other pathways are involved, e.g. neurotrophic signaling (brain-derived neurotrophic factor, BDNF) or the hypothalamus-pituitary-adrenal (HPA)-axis. Furthermore, in major depression, dysregulation of central serotonin signaling is accompanied with a decline in hippocampal neurogenesis, as has been observed in rodent models. At the center of this thesis is a mouse model deficient in the central serotonin-synthesizing enzyme, tryptophan hydroxylase 2 (Tph2-/- mice). I have investigated physiological responses to antidepressant treatment in the absence of brain serotonin, and the possible role of alternative pathways. I observed the typical increase in neurogenesis upon SSRI treatment in WT mice, while it had no effect in Tph2-/- mice. In contrast, BDNF levels were significantly decreased in Tph2-/- mice after treatment with no effect in WT control mice. Furthermore, my results show a critical role of brain serotonin in the neurobiological effects of electroconvulsive seizure. Surprisingly, in animals lacking central serotonin, increased neurogenesis was observed independently of the treatment. The gathered data indicated an altered stress response; therefore, parameters of the HPA-axis have been studied, indicating a downregulated HPA system in Tph2-/-animals in baseline state, but showed no difference in treatment or feedback control. This thesis gives insight into the mechanisms of antidepressant action and reveals ideas for novel pathways involved in the process that could be used as targets in therapeutic approaches and further research in major depression.
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Petermann, Markus [Verfasser]. "Identifying the mechanisms of antidepressant drug action in mice lacking brain serotonin / Markus Petermann." Berlin : Humboldt-Universität zu Berlin, 2021. http://d-nb.info/1237268524/34.

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Pariante, Carmine Maria. "The in vitro effects of antidepressants on the glucocorticoid receptor and the potential relevance for the mechanism of action of this class of drugs." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406497.

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Abdel-Razaq, Wesam. "Molecular mechanisms of monoamine neurotransmitter modulatory antidepressant actions." Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435767.

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Neves, António Luís Alexandre. "Tratamento farmacológico da depressão." Master's thesis, [s.n.], 2015. http://hdl.handle.net/10284/5309.

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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas
As organizações mundias de saúde consideram a depressão uma desordem de humor apresentando muitas facetas e uma variedade de possíveis etiologias que provoca forte impacto na qualidade de vida do doente e dos seus familiares. A depressão é um problema de saúde pública, tendo em vista o aumento no número de casos e as suas consequências sociais. Uma elevada percentagem dos doentes com depressão desenvolvem a tendências para o suicídio e podem evoluir para tentativa do mesmo. A doença ocorre em todas as faixas etárias, desde os jovens até aos idosos. A prevalência média da depressão na população geral é mais comum nas mulheres com idade compreendida entre os 15 e os 29 anos e menos prevalente nos indivíduos com 50 ou mais anos. A depressão é um problema médico, passível de tratamento e, nas últimas cinco décadas, a psicofarmacologia da depressão evoluiu muito e rapidamente aumentando o número de fármacos disponíveis no mercado. Assim, atualmente o mercado dispõe de diversos antidepressivos com eficácia para o tratamento da depressão. Apesar das diferenças estruturais e do mecanismo de ação, os antidepressivos apresentam, de um modo geral, a mesma eficácia entre as diferentes classes. No entanto, a farmacocinética das substâncias podem alterar a biodisponibilidade e os efeitos adversos das mesmas, tornando-se um fator preponderante para a não adesão à terapia. A escolha do antidepressivo deverá ser baseada em vários fatores tais como: o tipo de sintomatologia, a idade, o uso concomitantes com outras terapias e a história clínica do doente. Este trabalho procura fazer uma revisão bibliográfica no âmbito do tratamento farmacológico da depressão, bem como do mecanismo de ação, da farmacocinética, dos efeitos laterais e das interações farmacológicas das diferentes classes de antidepressivos.
The mundial health organizations consider depression a mood disorder presenting many facets and a variety of possible etiologies that causes strong impact on quality of life of patients and their families. Depression is a public health problem, given the increase in the number of cases and its social consequences. A high percentage of patients with depression develop tendencies towards suicide and may progress to attempt the same. The disease occurs in all age groups, from the young to the elderly. The average prevalence of depression in the general population is more common among women aged 15 to 29 years and less prevalent in individuals with 50 or more years. The depression is a medical condition, treatable and in the last five decades the psychopharmacology of depression has evolved very quickly and increasing the number of drugs available in the market. Currently, the market offers many antidepressants effectively for the treatment of depression. Despite the structural differences and their mechanism of action, the antidepressants generally have the same efficacy between different classes. However, the pharmacokinetics of substances can alter the bioavailability and adverse effects of the same, becoming an important factor for non-adherence to therapy. The choice of the antidepressant should be based on various factors such as the type of symptoms, age, concomitant use with other therapies, and patient history. This paper seeks to make a literature review about the pharmacology of antidepressants particularly the pharmacological treatment of depression and the mechanism of action, pharmacokinetics, side effects and drug interactions thereof.
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Schroeder, Frederick Albert. "A Role for Histone Modification in the Mechanism of Action of Antidepressant and Stimulant Drugs: a Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/370.

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Depression and stimulant drug addiction each result in massive losses of health, productivity and human lives every year. Despite decades of research, current treatment regimes for depression are ineffective in approximately half of all patients. Therapy available to stimulant drug addicts is largely ineffective and moreover, dedicated treatments for drug dependence (including abuse of cocaine) are non-existent. Thus, there is a pressing need to further understanding of the molecular mechanisms underlying these disorders in order to develop novel, targeted therapeutic strategies. Chromatin remodeling, including changes in histone acetylation, has been proposed to play a role in both the etiology and treatment of depression and stimulant abuse. Histone acetyltransferases (HATs) and histone deacetylases (HDACs) regulate numerous cellular processes, including transcription, cell cycle progression and differentiation. Moreover, histone acetylation has been shown to regulate hippocampal neurogenesis, a cellular response associated with the pathogenesis and treatment of depression and stimulant abuse (Hsieh et al., 2004, Yamaguchi et al., 2004, Fischer et al., 2007). Ultimately, such basic cellular processes impact higher order function, namely cognition and emotion. Indeed, recent studies suggest that HDAC activity in selected forebrain regions, including ventral striatum and hippocampus, modulate stimulant- and antidepressantinduced behavior (Kumar et al., 2005, Tsankova et al., 2006a, Fischer et al., 2007). These reports highlight an association between chromatin remodeling and diverse behavioral changes, including changes induced by the pleiotropic HDAC inhibitor, sodium butyrate (SB), (Kumar et al., 2005, Tsankova et al., 2006a, Fischer et al., 2007). However, behavioral, brain-metabolic and molecular effects of SB treatment in the context of rodent models of depression, dopaminergic sensitization and repeated cocaine administration remained unclear. The work described in this thesis illustrates the potential for chromatin modifying drugs in mechanisms underlying the experimental pharmacology of depression and stimulant addiction. Specifically, the data presented here support the view that treatment with the short chain fatty acid, sodium butyrate enhances: (1) antidepressant-like behavioral effects of the selective serotonin reuptake inhibitor (SSRI), fluoxetine (2) locomotor sensitization induced by repeated administration of the dopamine D1/D5 receptor agonist SKF82958; and(3) brain metabolic activation upon repeated cocaine administration as evidenced by fMRI in awake rats. Furthermore, this report provides evidence that these treatment paradigms will result in chromatin modification changes associated with active transcription, in addition to increased mRNA levels of plasticity-associated genes, including brain-derived neurotrophic factor (BDNF) at key brain regions implicated in the pathogenesis of depression and stimulant addiction. To date, little is known regarding the underlying mechanisms of action mediating the enhancing effects of sodium butyrate on the various antidepressant- and stimulantrelated paradigms. Our findings underscore the potential of chromatin-modifying drugs to profoundly affect the behavioral response of an animal to antidepressant and stimulant drugs and warrants consideration in the context of developing novel therapeutic strategies.
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Books on the topic "Antidepressants Mechanisms of action"

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Polgár, László. Mechanisms of protease action. Boca Raton, Fla: CRC Press, 1989.

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Saltiel, Alan R., and Jeffrey E. Pessin. Mechanisms of Insulin Action. New York, NY: Springer New York, 2007. http://dx.doi.org/10.1007/978-0-387-72204-7.

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Woodruff, G. N., ed. Mechanisms of Drug Action. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-08026-7.

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Sakamoto, Yukiya. Glucocorticoid hormone: Mechanisms of action. Tokyo: JapanScientific Societies Press, 1986.

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Molecular mechanisms of drug action. London: Taylor & Francis, 1988.

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Gehring, Ulrich, Ernst J. M. Helmreich, and Günter Schultz, eds. Molecular Mechanisms of Hormone Action. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-75022-9.

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1936-, Gehring Ulrich, Helmreich, E. J. M. 1922-, and Schultz G. 1936-, eds. Molecular mechanisms of hormone action. Berlin: Springer-Verlag, 1989.

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Dipple, Anthony. Mechanisms of action of chemical carcinogens. Birmingham: University of Birmingham, 1987.

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Williams, Graham R. Molecular mechanisms of thyroid hormone action. Birmingham: University of Birmingham, 1993.

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White, H. Steve. Mechanisms of action of antiepileptic drugs. West Islip, NY: Professional Communications, Inc., 2010.

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Book chapters on the topic "Antidepressants Mechanisms of action"

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Leonard, B. E. "Antidepressant Drugs." In Mechanisms of Drug Action, 203–48. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-08026-7_6.

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Ackenheil, M. "The mechanism of action of antidepressants revised." In Amine Oxidases and Their Impact on Neurobiology, 29–37. Vienna: Springer Vienna, 1990. http://dx.doi.org/10.1007/978-3-7091-9113-2_3.

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Golan, Moran, Gabriel Schreiber, and Sofia Avissar. "Regulation of G Protein Receptor Coupling, Mood Disorders and Mechanism of Action of Antidepressants." In Signal Transduction: Pathways, Mechanisms and Diseases, 63–81. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-02112-1_4.

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Sharp, Trevor. "Molecular and Cellular Mechanisms of Antidepressant Action." In Behavioral Neurobiology of Depression and Its Treatment, 309–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/7854_2012_216.

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Fišar, Zdeněk. "Pathophysiology of Mood Disorders and Mechanisms of Action of Antidepressants and Mood Stabilizers." In Endocannabinoid Regulation of Monoamines in Psychiatric and Neurological Disorders, 103–34. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7940-6_6.

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Miyamoto, S., and M. Asakura. "Protein Phosphorylation System in the Mechanism of Action of Antidepressants." In Signal Transduction in Affective Disorders, 69–84. Tokyo: Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-68479-4_6.

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Leonard, B. E. "Effect of Antidepressants on Neurotransmission: a Common Mechanism of Action?" In Current Aspects of the Neurosciences, 205–37. London: Macmillan Education UK, 1992. http://dx.doi.org/10.1007/978-1-349-12275-2_6.

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Checkley, S. A., T. H. Corn, I. B. Glass, C. Thompson, C. Franey, and J. Arendt. "Neuroendocrine and Other Studies of the Mechanism of Antidepressant Action of Desipramine." In Ciba Foundation Symposium 123 - Antidepressants and Receptor Function, 126–47. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470513361.ch8.

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Wiesel, F. A., and L. Träskman-Bendz. "The Mechanisms of Action of Antipsychotics and Antidepressant Drugs." In Neuroendocrinology of Mood, 117–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-72738-2_5.

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Stenovec, Matjaž, Baoman Li, Alexei Verkhratsky, and Robert Zorec. "Ketamine Action on Astrocytes Provides New Insights into Rapid Antidepressant Mechanisms." In Advances in Neurobiology, 349–65. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-77375-5_14.

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Conference papers on the topic "Antidepressants Mechanisms of action"

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Foote, Christopher S. "Chemical mechanisms of photodynamic action." In SPIE Institutes for Advanced Optical Technologies 6, edited by Charles J. Gomer. SPIE, 1990. http://dx.doi.org/10.1117/12.2283671.

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"The Prevalence of Depressive and Anxious Symptomatology and Use of Antidepressants Among Breast Cancer Patients :A Cross-Sectional Study ." In International Conference on Public Health and Humanitarian Action. International Federation of Medical Students' Associations - Jordan, 2022. http://dx.doi.org/10.56950/xsxm3127.

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Background: breast cancer is considered as one the most common type among women worldwide and for Jordanian citizens according to Jordan Ministry of health that there was around 1292 (38.4%) new cases of breast cancer reported in 2020, and The diagnosis of breast cancer is usually associated with psychological stress such as Anxiety and depression that is resulting from the diagnosis itself, where if it's was incurable diseases, fear of death, fear of loss, at the end previous studies show that there is a higher prevalence of depressive disorder which is up to two to three times more than the general population. Objective: Our goal in this cross-section study is to find out the prevalence of psychological and depressive disorders correlates to breast cancer (BC) in outpatient and inpatient setting as it was approved that depression is comorbid to cancer that should not be neglected. We also aim to identify risk factors of depression among study participants like cancer stage ( initial or later), income and marital status, and type of intervention chemotherapy or radiation therapy plus their treatment sessions Method: This study was conducted at king Abdullah university hospital in Irbid, King Hussein cancer center (KHCC), and queen Alia Military hospital in Amman, Jordan. More than 400 formed the study sample include inpatient and outpatient setting of breast cancer using in them Depression and anxiety assessment scale. In the inpatient setting The Hospital Anxiety and Depression Scale (HADS) instrument used, which is a 14-question instrument given to patients in a secondary care setting to screen for the presence and severity of depression and anxiety. Also, the beck depression Inventory (BDI) used, which is a self-report rating inventory that measures characteristics, attitudes, and symptoms of depression. In the outpatient setting The PHQ-9 instrument which includes nine questions given to the patient in primary care settings. The anxious symptomatology defined by using the GAD-7 instrument with a total score of 15 and above indicating a case with severe anxious symptomatology. Results: Our study findings demonstrated a higher prevalence of depressive and anxious symptomatology in the inpatient setting and advanced disease stages. In addition, the underutilization of antidepressant therapy was observed. there for we need to consider mental disorder as part of the treatment protocol for breast cancer patient. Keywords: anxiety , antidepressants medications, breast cancer, depression, inpatient, Jordan, outpatient
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Xu, Peng. "Mechanisms of action of pyrethroid insecticides." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.94894.

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Hartman, Jorine E., Karin Klooster, Sonja Augustijn, Wouter H. Van Geffen, Justin Garner, Pallav L. Shah, Nick H. T. Ten Hacken, and Dirk-Jan Slebos. "Mechanisms of action of endobronchial coil treatment." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa3154.

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RAMPIL, I. J. "MECHANISMS AND SITES OF ACTION OF GENERAL ANAESTHETICS." In Proceedings of the Fourth International Symposium. PUBLISHED BY IMPERIAL COLLEGE PRESS AND DISTRIBUTED BY WORLD SCIENTIFIC PUBLISHING CO., 2000. http://dx.doi.org/10.1142/9781848160231_0019.

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Thomas, Oliver, Miri Zilka, Adrian Weller, and Novi Quadrianto. "An Algorithmic Framework for Positive Action." In EAAMO '21: Equity and Access in Algorithms, Mechanisms, and Optimization. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3465416.3483303.

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Dan, Sen, and Shu Gao. "Semantics-enhanced algorithm for skeleton-based action recognition." In International Conference on Mechanisms and Robotics (ICMAR 2022), edited by Zeguang Pei. SPIE, 2022. http://dx.doi.org/10.1117/12.2652191.

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Bowen, Landen A., Clayton L. Grames, Spencer P. Magleby, Robert J. Lang, and Larry L. Howell. "An Approach for Understanding Action Origami as Kinematic Mechanisms." In ASME 2013 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/detc2013-13407.

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Action origami is a field of origami dealing with models that are folded so that in their final, deployed state they exhibit motion. Hundreds of action origami models exist, many of which use complicated kinematics to achieve motion in their deployed state. Understanding the kinematics of action origami could result in a new source of concepts for deployable, movable engineering solutions. This paper presents an approach for evaluating and classifying the mechanisms that enable action origami motion. Approximately 300 action origami models are studied. Although disguised with artistic elements, it is found that most action origami models are based on a few fundamental mechanisms. A classification scheme is proposed, and a previously unused class of action origami is identified as an area for future origami art.
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Poroshina, Marina Y., L. V. Zhorina, T. A. Ogloblina, Elena B. Chernyaeva, A. V. Agronskaya, and T. I. Rokitskaya. "Accumulation and photodynamic action mechanisms of tetrasulfonated aluminum phthalocyanine." In Radiofrequency and Optical Methods of Biomedical Diagnostics and Therapy, edited by Valery V. Tuchin. SPIE, 1993. http://dx.doi.org/10.1117/12.146469.

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RESENDE ROSADO, BÁRBARA, and Ricardo Gudwin. "Analysis and Simulation of Computacional Mechanisms for Action Selection." In XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil: Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-50866.

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Reports on the topic "Antidepressants Mechanisms of action"

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Cumberledge, Susan. Biochemistry and Molecular Mechanisms of Wingless Action. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada305797.

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Frey, Scott H. Cortical Mechanisms of Multi-step Action Planning. Fort Belvoir, VA: Defense Technical Information Center, December 2010. http://dx.doi.org/10.21236/ada545175.

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Keefer, Philip, Mauricio Espinoza, Álvaro Espinoza, and Ricardo Fort. Rule Enforcement, Collective Action, and Growth: Micro Evidence and Mechanisms from Peru. Inter-American Development Bank, August 2019. http://dx.doi.org/10.18235/0001275.

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Woods, W. T., and Jr. Mechanisms of Action of Low Molecular Weight Toxins in the Cardiovascular System. Fort Belvoir, VA: Defense Technical Information Center, October 1987. http://dx.doi.org/10.21236/ada225113.

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Vernooij, D. M., R. J. A. Oostewechel, J. A. Verschoor, H. B. Axmann, F. I. D. G. Pereira da Silva, and R. B. Castelein. Understanding the mechanisms to strengthen food systems through value chain-driven action. Wageningen: Wageningen Food & Biobased Research, 2022. http://dx.doi.org/10.18174/577463.

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Piwnica-Worms, David, and Ken Blumer. Elucidating Mechanisms of Farnesyltransferase Inhibitor Action and Resistance in Breast Cancer by Bioluminescence Imaging. Fort Belvoir, VA: Defense Technical Information Center, June 2008. http://dx.doi.org/10.21236/ada491469.

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Piwnica-Worms, David. Elucidating Mechanisms of Farnesyltransferase Inhibitor Action and Resistance in Breast Cancer by Bioluminescence Imaging. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada540951.

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Piwnica-Worms, David, and Ken Blumer. Elucidating Mechanisms of Farnesyltransferase Inhibitor Action and Resistance in Breast Cancer by Bioluminescence Imaging. Fort Belvoir, VA: Defense Technical Information Center, June 2009. http://dx.doi.org/10.21236/ada510012.

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Bergey, Gregory K. Mechanisms of Action of Clostridial Neurotoxins on Dissociated Mouse Spinal Cord Neurons in Cell Culture. Fort Belvoir, VA: Defense Technical Information Center, September 1991. http://dx.doi.org/10.21236/ada244092.

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Berry, J., H. Ingolfsson, A. Javaherian, and S. Finkbeiner. Update May 2021 - Physics-based Modeling to Understand TDP-43 Mechanisms of Action in ALS. Office of Scientific and Technical Information (OSTI), May 2021. http://dx.doi.org/10.2172/1837817.

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