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Fluoxetine and vortioxetine reverse depressive-like phenotype and memory deficits induced by amyloid-β (1-42) oligomers in mice: implication of transforming growth factor-β1 and oxidative stress
A long-term treatment with antidepressants reduces the risk to develop AD and different second-generation antidepressants such as selective serotonin reuptake inhibitors (SSRIs) are currently studied for their neuroprotective properties in AD. An impairment of neurotrophic factors signaling seems to be a common pathophysiological event in depression and AD. In particular a deficit of transforming growth factor-β1 (TGF-β1) and increased oxidative stress have been found both in depression and AD. In the present work the SSRI fluoxetine and the new multimodal antidepressant vortioxetine were tested for their ability to prevent memory deficits and depressive-like phenotype in a non-transgenic mouse model of AD (i.c.v. Aβ1-42 injection) by rescue of TGF-β1 signaling. The same drugs were also tested for their ability to modulate the expression of pro-oxidant genes as well as of genes related to the antioxidant machinery.
New augmentation strategy in depression: Galanin (1-15) enhances the behavioral effects of Fluoxetine in the olfactory bulbectomy rat
Comparing the antidepressant-like efficacy of ketamine, cannabidiol and fluoxetine in male and female adolescent rats
Early-life exposure to fluoxetine induces specific prefrontal cortical circuit alterations in adult mice
The effect of fluoxetine on behaviour and BDNF epigenetic regulation depends on the individual experience of the environment
Fluoxetine enhances perceptual learning and luminance perception during adulthood
Opposing effects of Postnatal and Juvenile Fluoxetine treatment on Emotional Behaviour, Protein translation, and Bioenergetics
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