Antidepressants have a delayed onset of action due to neuroplastic adaptation processes
Multiple studies and reviews support the concept that conventional antidepressants have a delayed therapeutic onset because they rely on gradual neuroplastic adaptations, such as altered BDNF signaling and synaptic rewiring.
The retrieved papers consistently support the neuroplasticity hypothesis of antidepressant action, explicitly connecting the delayed onset of traditional monoaminergic antidepressants to slow neuroplastic adaptations such as BDNF synthesis, TrkB activation, and synaptic rewiring.
E. Castrén, L. Monteggia. Brain-Derived Neurotrophic Factor Signaling in Depression and Antidepressant Action.. 2021. https://doi.org/10.1016/j.biopsych.2021.05.008
Paper 0 links antidepressant action and mood disorders to neurotrophic factors and neuronal plasticity mechanisms like BDNF signaling.
See more details
Marion J F Levy, Fabien Boulle, Harry W Steinbusch, Daniël L A van den Hove, Gunter Kenis, Laurence Lanfumey. Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression.. 2018. https://doi.org/10.1007/s00213-018-4950-4
Paper 6 notes that while traditional antidepressants still exhibit a delayed onset of action, they exert beneficial therapeutic effects by enhancing neurotrophic signaling and synaptic plasticity.
Tomi Rantamäki, Ipek Yalcin. Antidepressant drug action--From rapid changes on network function to network rewiring.. 2016. https://doi.org/10.1016/j.pnpbp.2015.06.001
Paper 8 associates the delayed onset of monoamine-based antidepressants with their slow ability to increase synaptic plasticity and neuronal excitability via altered neurotrophic signaling.
The paper trail · every fact has a biography
Challenge the receipt
Citation formatting by citeproc-js (Frank Bennett) and the Citation Style Language project. Source and licenses.
Terms · Privacy · How verdicts work · Dispute this receipt