MAOIs (Monoamine Oxidase Inhibitors) increase levels of Brain-Derived Neurotrophic Factor (BDNF) in the brain, particularly with chronic use, which is a key mechanism for their antidepressant and neuroplastic effects, promoting neuronal survival, growth, and synaptic plasticity, helping reverse stress-induced reductions in BDNF seen in depression.
While short use of these medications might not show this benefit, long-term use boosts BDNF in the frontal cortex, treating depression and preventing neuron damage.
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Neurotrophic factors are critical regulators of the formation and plasticity of neuronal networks. Brain-derived neurotrophic factor (BDNF) is abundant in the brain and periphery, and is found in both human serum and plasma. Animal studies have demonstrated that stress reduces BDNF expression or activity in the hippocampus and that this reduction can be prevented by treatment with antidepressant drugs.
A similar change in BDNF activity occurs in the brain of patients with major depression disorder (MDD).
Recently, clinical studies have indicated that serum or plasma BDNF levels are decreased in untreated MDD patients. Antidepressant treatment for at least four weeks can restore the decreased BDNF function up to the normal value.
Therefore, depression is associated with impaired neuronal plasticity. Suicidal behavior can be a consequence of severe impaired neuronal plasticity in the brain. Antidepressant treatment promotes increased BDNF activity as well as several forms of neuronal plasticity, including neurogenesis, synaptogenesis and neuronal maturation. BDNF could also play an important role in the modulation of neuronal networks.
Such a neuronal plastic change can positively influence mood or recover depressed mood. These alterations of BDNF levels or neuronal plasticity in MDD patients before and after antidepressant treatment can be measured through the examination of serum or plasma BDNF concentrations.
BDNF levels can therefore be useful markers for clinical response or improvement of depressive symptoms, but they are not diagnostic markers of major depression.
Lee BH, Kim YK. The roles of BDNF in the pathophysiology of major depression and in antidepressant treatment. Psychiatry Investig. 2010 Dec;7(4):231-5. doi: 10.4306/pi.2010.7.4.231. Epub 2010 Nov 23. PMID: 21253405; PMCID: PMC3022308.