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10.1016/j.stem.2008.01.014 26 InoueM

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However, emerging evidence suggests that abnormalities in the balance between excitatory (glutamate-mediated), and inhibitory (GABA-mediated) neurotransmission may be a common pathophysiological mechanism and hence a treatment target in ASD 4,5,6

Likewise, the currently available human transcriptomic datasets provide only indirect support for the proposed model, because they are predominantly based on peripheral blood immune-cell profiling and therefore capture systemic inflammatory responses rather than direct pancreas-specific remodeling of mitochondrial, ER, lysosomal, or secretory-granule interactions in acinar cells (98)