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Additionally, BIM, PUMA, and tBID can directly engage with BAX and BAK to initiate apoptosis [43, 44]

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These mechanisms affect synaptic plasticity, energy metabolism, and the integrity of the gutbrain barrier

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elegantly demonstrated that neural stem cell secretomes inhibit microglial activation via BDNF/VEGF signaling, but their work neglected gastrointestinal dysbiosis, overlooking the bidirectional crosstalk now recognized as central to ASD pathophysiology [42]