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Several pathogenic variants of OGT have been reported in XLID patients [39, 40], all leading to delayed development, brain abnormalities, and reduced intellectual capacity, further strengthening the connection between the O-GlcNAc system and neurodevelopment

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Diminished BDNF concentrations within the realms of the hippocampus and prefrontal cortex result in hindered synaptogenesis, diminished neuroplasticity, and a slowdown in neurogenesis (38)

The serotonin-degrading enzyme monoamine oxidase-A does not generally increase with age (not to the extent of MAO-B increase), although levels increase during perimenopause, a period of heightened depression vulnerability [74]