Comparing the effect of fluoxetine, escitalopram, and sertraline, on the level of BDNF and depression in preclinical and clinical studies: a systematic review

Talaee, Nastaran; Azadvar, Shataw; Khodadadi, Sanaz; Abbasi, Nahal; Asli-Pashaki, Zahra Najafi; Mirabzadeh, Yasaman; Kholghi, Gita; Akhondzadeh, Shahin; Vaseghi, Salar

doi:10.1007/s00228-024-03680-y

Cited by 4 publications

(1 citation statement)

References 217 publications

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“…In one recent review, the levels of BDNF in preclinical and clinical studies are analyzed side-by-side. Interestingly, conflicting results were found in animal studies while in humans, the anti-depressant effect of drugs (including fluoxetine) seems not to depend on BDNF ( Talaee et al, 2024 ). We now summarize the available literature in the field focusing first on animal models and second, on studies with patients, and separating detrimental effects ( Table 1 ) from positive effects ( Table 2 ).…”

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confidence: 99%

The multifaceted effects of fluoxetine treatment on cognitive functions

Ampuero,

Luarte,

Flores

et al. 2024

Front. Pharmacol.

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Fluoxetine, the prototypical selective serotonin reuptake inhibitor (SSRI), is widely used to treat major depressive disorder (MDD) and a variety of other central nervous system conditions, primarily due to its established clinical safety profile. Although its efficacy in treating depression is well-recognized, the impact of fluoxetine on cognitive functions remains inconsistent and elusive. In this review, we first examine the well-substantiated biological mechanisms underlying fluoxetine’s antidepressant effects, which include serotonin reuptake inhibition and activation of TrkB receptors—key to brain-derived neurotrophic factor (BDNF) signaling. Subsequently, we delve into the cognitive side effects observed in both preclinical and clinical studies, affecting domains such as memory, attention, and executive functions. While certain studies indicate cognitive improvements in patients with underlying disorders, there is also evidence of negative effects, influenced by variables like gender, duration of treatment, age, disease pathology, and the specifics of cognitive testing. Significantly, the negative cognitive outcomes reported in preclinical research often involve healthy, non-diseased animals. This review underscores the necessity for heightened caution in fluoxetine prescription and further investigation into its potentially detrimental cognitive effects, even when used prophylactically.

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Section: Introductionmentioning

confidence: 99%

The multifaceted effects of fluoxetine treatment on cognitive functions

Ampuero,

Luarte,

Flores

et al. 2024

Front. Pharmacol.

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New Insights into Contradictory Changes in Brain-Derived Neurotrophic Factor (BDNF) in Rodent Models of Posttraumatic Stress Disorder (PTSD)

Ghaffarzadegan,

Akhondzadeh,

Nikasa

et al. 2024

Neurochem Res

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Hesperidin produces antidepressant effects by activating AMPA receptor: enhancing synaptic proteins to promote hippocampal neuronal activities

Pang,

Cao

2024

Behavioural Pharmacology

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Hesperidin treatments reduce depressive symptoms in mouse models of depression, but the mechanism that mediates its antidepressant effects is unclear. This study shows that hesperidin exerts its antidepressant effects by activating α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor to promote synaptic and neuronal function in the hippocampus. The optimal dose of hesperidin (10 mg/kg) for the antidepressant potential was determined after 7 consecutive days of treatments, demonstrating decreased latency to eat and increased food consumption in novelty suppressed feeding, and decreased immobility time in tail suspension test (TST). Moreover, the optimal dose also reversed the depressive phenotypes of Institute of Cancer Research mice exposed to chronic unpredictable mild stress (CUMS), including reduced immobility time in the TST and increased sucrose preference in the sucrose preference test. In addition, hesperidin increased the expression of AMPA receptor protein (Glur1) and synaptic proteins (BDNF, PSD95, synapsin1) in the hippocampus of CUMS-exposed mice. Furthermore, inhibition of AMPA receptor activity by NBQX blocked the effect of hesperidin in reversing the depressive phenotypes, upregulated the expression of synaptic proteins (BDNF, PSD95, synapsin1) and cFOS-positive cells in the hippocampus, and increased the number of Ki67-positive cells in the dentate gyrus of the hippocampus of CUMS-exposed mice. These results help to further understand the antidepressant mechanism of hesperidin and provide new ideas for the future development of antidepressant drugs.

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Comparing the effect of fluoxetine, escitalopram, and sertraline, on the level of BDNF and depression in preclinical and clinical studies: a systematic review

Cited by 4 publications

References 217 publications

The multifaceted effects of fluoxetine treatment on cognitive functions

The multifaceted effects of fluoxetine treatment on cognitive functions

New Insights into Contradictory Changes in Brain-Derived Neurotrophic Factor (BDNF) in Rodent Models of Posttraumatic Stress Disorder (PTSD)

Hesperidin produces antidepressant effects by activating AMPA receptor: enhancing synaptic proteins to promote hippocampal neuronal activities

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