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10.3892/ijo.2024.5634 4 AliA

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

DSIP-CBBBP fusion peptide and DSIP treatments demonstrated even more significant increases in neuron density compared to the model group, emphasizing the potential of these treatments in counteracting neuronal loss associated with insomnia

ANZ J Surg