Review of the choice and use of antidepressant drugs

Bleakley, Stephen

doi:10.1002/pnp.311

Cited by 25 publications

(8 citation statements)

References 15 publications

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“…The prevalence of antidepressant use has gradually increased around the world, especially the adverse of selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) as first-line treatment options in depression [ 13 ]. Antidepressants elevate the transmission of one or more of the monoamines: serotonin, nor-adrenaline, or dopamine [ 14 ]. They are classified according to their mechanism of action: tricyclic and tetracyclic antidepressants (TCAs and TeCAs), SSRIs, serotonin antagonist and reuptake inhibitors (SARIs), monoamine oxidase inhibitors (MAOIs), and SNRIs.…”

Section: Introductionmentioning

confidence: 99%

Antidepressants, sertraline and paroxetine, increase calcium influx and induce mitochondrial damage-mediated apoptosis of astrocytes

et al. 2017

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The impacts of antidepressants on the pathogenesis of dementia remain unclear despite depression and dementia are closely related. Antidepressants have been reported may impair serotonin-regulated adaptive processes, increase neurological side-effects and cytotoxicity. An ‘astroglio-centric’ perspective of neurodegenerative diseases proposes astrocyte dysfunction is involved in the impairment of proper central nervous system functioning. Thus, defining whether antidepressants are harmful to astrocytes is an intriguing issue. We used an astrocyte cell line, primary cultured astrocytes and neuron cells, to identify the effects of 11 antidepressants which included selective serotonin reuptake inhibitors, a serotonin-norepinephrine reuptake inhibitor, tricyclic antidepressants, a tetracyclic antidepressant, a monoamine oxide inhibitor, and a serotonin antagonist and reuptake inhibitor. We found that treatment with 10 μM sertraline and 20 μM paroxetine significantly reduced cell viability. We further explored the underlying mechanisms and found induction of the [Ca2+]i level in astrocytes. We also revealed that sertraline and paroxetine induced mitochondrial damage, ROS generation, and astrocyte apoptosis with elevation of cleaved-caspase 3 and cleaved-PARP levels. Ultimately, we validated these mechanisms in primary cultured astrocytes and neuron cells and obtained consistent results. These results suggest that sertraline and paroxetine cause astrocyte dysfunction, and this impairment may be involved in the pathogenesis of neurodegenerative diseases.

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Section: Introductionmentioning

confidence: 99%

Antidepressants, sertraline and paroxetine, increase calcium influx and induce mitochondrial damage-mediated apoptosis of astrocytes

et al. 2017

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“…Presently, the selective serotonin reuptake inhibitors (SSRIs) represent the most widely used class of antidepressant medications and these agents have largely replaced tricyclic antidepressant (TCA) drugs because of their proven efficacy and favorable side effect profile (Anderson and Edwards 2001). SSRIs are currently recommended as the first-line treatment for depression (Bleakley 2009). The neurotransmitter serotonin (5-HT) has recently been linked to AD pathology in part because serotonergic receptors densely populate the hippocampus (Schiapparelli et al 2005), the brain region crucial for short-and long-term episodic memory, which is principally affected in this disease (Bird and Burgess 2008).…”

Section: Introductionmentioning

confidence: 99%

Study of the effect of antidepressant drugs and donepezil on aluminum-induced memory impairment and biochemical alterations in rats

et al. 2014

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Alzheimer's disease is the leading cause of dementia in the elderly. Depression is a common psychiatric disorder affecting individuals across life span and often arises in the context of pre-dementia, dementia, and Alzheimer's disease. The present study aimed to investigate the effects of the antidepressant drugs clomipramine (14.2 and 56.9 μmol/kg), fluoxetine (14.5 and 57.8 μmol/kg), and sertraline (14.6 and 58.4 μmol/kg) compared with acetylcholinesterase inhibitor donepezil (12 μmol/kg) on oxidative stress, memory impairment, and depressant-like behavior in a model of Alzheimer's disease induced by prolonged intraperitoneal administration of aluminum chloride (AlCl 3 ) (10 mg/kg/day for 60 days) in rats. Results indicated that the latency to find the hidden platform in Morris water maze (MWM) test increased by 100 %, while the immobility duration in forced swimming test (FST) increased by 51 % in AlCl 3 -treated rats. The administration of AlCl 3 resulted in increased brain malondialdehyde (MDA) by 58.6 % and nitric oxide (nitrite) concentrations by 71.7 %, while reduced glutathione (GSH) decreased by 35.6 % compared with the vehicle-treated group. Catalase and paraoxonase 1 (PON1) activities in the brain decreased by 41.8 and 18.3 %, respectively. Serum acetylcholinesterase (AChE) increased by 47.8 % and brain butyrylcholinesterase (BuChE) decreased by 23.1 % after AlCl 3 treatment. In AlCl 3 -treated rats, memory performance in the MWM test improved following donepezil and the highest dose of clomipramine, fluoxetine, and sertraline. The immobility duration in the FST was decreased by sertraline. Significant decrease in brain MDA occurred after treatment with clomipramine, fluoxetine, and a lower dose of sertraline. Reduced glutathione level increased by donepezil, clomipramine, and 57.8 μmol/kg fluoxetine. The level of nitric oxide decreased by donepezil (42.6 %), clomipramine (45.0 and 62.9 %), fluoxetine (21.9 and 40.9 %), and 14.6 μmol/kg sertraline (28.7 %). Catalase activity was restored by donepezil, fluoxetine, and sertraline and markedly increased by 56.9 μmol/kg clomipramine. Paraoxonase 1 activity was increased by 14.2 μmol/kg clomipramine. BuChE activity was unaltered, but AChE activity was decreased by donepezil, clomipramine, and fluoxetine compared with the AlCl 3 control group. AlCl 3 resulted in neurodegeneration (gliosis), extensive dark neurons with corkscrew dendrites, and degeneration of some Purkinje cell. Following donepezil treatment, no dark neurons were observed, while increased granular cell layer was observed after the administration of a high dose of clomipramine, fluoxetine, or sertraline. The results suggested that in rats treated with AlCl 3 , (i) donepezil, sertraline, clomipramine, and fluoxetine improve memory performance; (ii) sertraline was particularly effective in improving depressive-like behavior in this model and might be of value in the treatment of depressive symptoms associated with Alzheimer's disease; (iii) donepezil, clomipramine, and fluoxetine alleviated oxi...

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“…Although the pathophysiology of MDD has not been fully understood, it involves several mechanisms, including serotonergic, noradrenergic, dopaminergic, and glutamatergic alterations, increased central and peripheral inflammation, hypothalamic-pituitary-adrenal (HPA) axis abnormalities, vascular changes, and decreased neurogenesis and neuroplasticity [ 2 ]. Current treatment focuses on antidepressants that inhibit monoamine neurotransmitter reuptake, elevate synaptic monoamine concentrations [ 3 ], and combine these with psychotherapy. However, less than 50% of patients respond to first-line antidepressant treatment or psychotherapy thus, in patients with treatment-resistant major depression (TRD), defined as an insufficient response to at least two antidepressant treatments [ 4 ], the use of electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation (rTMS), and vagus nerve stimulation (VNS) has also been employed with moderate efficacy.…”

Section: Introductionmentioning

confidence: 99%