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Although previous studies have largely assigned depressive symptoms to the three monoamine neurotransmitters (dopamine, norepinephrine, or serotonin), we describe a specific peripheral glutamatergic dysfunction (decreased GDH activity in K2 relatively control) that accompanies distinct clinical DE phenotypes with a predominance of parkinsonian neurological symptoms

For optimal assimilation, the time and conditions of intake therefore play a key role

This piece is part of a series that dives deeper into this years iteration of our flagship research piece, Charting Disruption

Structural insights into the mechanism of the sodium/iodide symporter