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Current hypotheses regarding the pathophysiology of anxiety disorders emphasize an imbalance between neuronal excitation and inhibition, characterized by reduced Gamma-aminobutyric acid (GABA) inhibition and excessive glutamatergic activity, which contributes to neuronal hyperexcitability and the manifestation of anxious behaviors (111)

As genome-wide technologies expand, so will our ability to decode folate-related risk

Regen Med 2006;1(4):563574

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The impact of oxidative stress of environmental origin on the onset of placental diseases

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