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In Wernickes encephalopathy there is AKGDH and thiamine deficiency associated with increased oxidative stress markers, lipid peroxidation resulting in neuronal cell death in pons, thalamus and cerebellum [67, 69]

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39 Additionally, there is established evidence of alterations in glutamate circuits and GABAergic circuits in ASD patients, as manifested by increased numbers of excitatory synapses and spine densities, significantly reduced levels of glutamic acid decarboxylase, and GABAA and GABAB receptor alterations in the postmortem brains of patients with autism