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Migraine: diagnosis and treatment
Published in Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby, Headache in Clinical Practice, 2018
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby
The currently available antidepressants consist of a number of different classes of drugs with different mechanisms of action: MAOIs: (a) selective and reversible; (b) nonselective and irreversible;monoamine reuptake inhibitors: (a) nonselective TCAs; (b) selective serotonin reuptake inhibitors (SSRIs); (c) selective serotonin and norepinephrine reuptake inhibitors (SNRIs);monoamine receptor targeted drugs: (a) serotonin (trazadone, trazodone); (b) norepinephrine β2 NE antagonist (mirtazepine, mirtazapine); (c) dopamine (bupropion).
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Published in Calver Pang, Ibraz Hussain, John Mayberry, Pre-Clinical Medicine, 2017
Calver Pang, Ibraz Hussain, John Mayberry
This question focuses on psychopharmacology. Central nervous system drugs can act as simulators (agonists) or blockers (antagonists) of neurotransmitter receptors. Antidepressants include selective serotonin reuptake inhibitors (first-line treatment for moderate to severe depression), tricyclics (block reuptake of serotonin and noradrenaline), and non-selective monoamine reuptake inhibitors. Drugs used to treat schizophrenia include typical and atypical antipsychotics and clozapine. Advantages of atypical antipsychotics are fewer side effects, different available preparations and differing side-effect profiles that can be matched to patient characteristics. This group of drugs is now used as first-line treatment in schizophrenia. Typical antipsychotics are well known for their side effects and toxicity, for example, extrapyramidal side effects (parkinsonism, acute dystonia, akathasia, tardive dyskinesia) and neuroleptic malignant syndrome (severe rigidity, hyperthermia, autonomic lability and increased creatine phosphokinase). Benzodiazepines can be used to treat anxiety and work by acting as full agonists at GABA-benzodiazepine receptors leading to enhancement of GABA.
Amelioration of modified chronic unpredictable stress using Celastrus paniculatus seed oil alone and in combination with fluoxetine
Published in Drug and Chemical Toxicology, 2023
Sanjana Chahuan, Sania Grover, Shamsher Singh
Besides oxidative stress and neuroinflammation, monoamine theory is of major concern in depression. It has been seen that the breakdown of monoamines (dopamine, serotonin, and norepinephrine) by enzymes like MAO and reuptake of these monoamines are blameworthy to cause depression. Therefore, to upregulate these monoamines two pharmacotherapeutic approaches are in trend, i.e., either the use of MAO inhibitors like tranylcypromine, phenelzine, or monoamine reuptake inhibitors like fluoxetine (FLU) (selective serotonin reuptake inhibitor (SSRI)), venlafaxine (selective norepinephrine reuptake inhibitor), and nefazodone (serotonin-norepinephrine reuptake inhibitor) (Fajemiroye et al. 2016). Moreover, elevated corticosterone levels are also liable for the development of depression. Hypothalamic-pituitary-adrenal (HPA) axis is supposed to play a vital role in regulating the levels of glucocorticoids through a negative feedback mechanism. But under the influence of stress, the dysregulation of this HPA axis and failure of the negative feedback mechanism takes place, resulting in high glucocorticoid (corticosterone) levels in the blood which may further leads to the genesis of depression (Ali et al. 2015).
Machine learning, pharmacogenomics, and clinical psychiatry: predicting antidepressant response in patients with major depressive disorder
Published in Expert Review of Clinical Pharmacology, 2022
William V. Bobo, Bailey Van Ommeren, Arjun P. Athreya
Kautzky and colleagues similarly leveraged clustering and RFs to predict response after 4 weeks of treatment with antidepressants or electroconvulsive therapy (ECT) using 12 SNPs in or near HTR2A (rs643627, rs6313), COMT (rs4680), ST8SIA2 (rs8035760, rs3784723), PPP3CC (rs7430, rs10108011), and BDNF (rs6265, rs11030101, rs11030104, and rs12273363) in 225 depressed participants in the Group for the Study of Resistant Depression (GSRD) cohort [59,60]. MDD diagnoses were confirmed using a modified version of the Mini-International Neuropsychiatric Interview (MINI), version 5.0.0 [61]. SNPs were selected based on literature review. Study drugs included selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), noradrenaline reuptake inhibitors (NARIs), tricyclic and tetracyclic antidepressants, and monoamine reuptake inhibitors (MAOIs). There was no stratification based on antidepressants or intervention types. Response to treatment was defined as achieving a HAMD score ≤17 after one or two adequate trials of antidepressants. The RF model was trained using 10-fold cross-validation, and the trained models were not validated in an external dataset. A four-factor RF model incorporating three SNPs (rs6265, rs6313, and rs7430) and melancholic depressive subtype was associated with a 4-fold higher chance of positive treatment response compared with other patients (OR 4.22, 95% CI 1.43–12.49).
Use of non-cancer drugs and survival among patients with pancreatic adenocarcinoma: a nationwide registry-based study in Norway
Published in Acta Oncologica, 2021
Nathalie C. Støer, Gauthier Bouche, Pan Pantziarka, Erica K. Sloan, Bettina K. Andreassen, Edoardo Botteri
The use of beta-blockers was not associated with pancreatic cancer mortality. The HR for patients using non-selective beta-blockers compared to non-users was 0.85, 95% CI 0.69–1.05 (Table 2) and for high dose non-selective beta-blocker users it was 0.74, 95% CI 0.54–1.01 (Table 3). When compared to patients using diuretics and/or calcium channel blockers and/or ACE inhibitors, non-selective beta-blocker users had a significantly lower mortality (HR: 0.67, 95% CI 0.47–0.96, Table 4). Metastatic patients using angiotensin receptor blockers had lower pancreatic cancer mortality (HR: 0.84, 95% CI 0.72–0.99) compared to non-users (Table 2). No other drugs were associated with pancreatic cancer mortality. Results were similar in non-metastatic and metastatic pancreatic cancer patients, in patients resected and not resected for their primary tumour (data not shown), and no interactions with sex were observed. In an exploratory analysis, no significant heterogeneity between non-selective monoamine reuptake inhibitors and selective serotonin reuptake inhibitors was observed (p = 0.220).