What is the primary mechanism of action (MOA) of SAMe in treating depression?

The primary mechanism of action of SAMe (S-adenosylmethionine) in treating depression is its ability to increase monoamines in the brain. SAMe is a naturally occurring compound involved in methylation processes, which are crucial for the synthesis and maintenance of neurotransmitters such as serotonin, norepinephrine, and dopamine. These neurotransmitters are critical for regulating mood, and increases in their levels are often associated with improvements in depressive symptoms.

The action of SAMe on monoamines suggests that it can help elevate mood by promoting the production of these important neurotransmitters. Research indicates that SAMe can enhance the bioavailability of monoamines, contributing to its potential effectiveness as an antidepressant. This mechanism aligns with how many traditional antidepressants operate, although through different pathways, which highlights SAMe's relevance in the biological treatment of depression.

The other options focus on different mechanisms or outcomes that are not the primary action of SAMe. Reducing inflammation, inhibiting serotonin reuptake, and enhancing vitamin absorption do not accurately describe the primary function of SAMe in the context of its role as an antidepressant.