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In animal models, studies show that the lack of PINK1 resulted in abnormal mitochondrial morphology, loss of SNpc DA neurons, reduction in complex I activity, and enhanced vulnerability to oxidative stress (Kitada et al., 2007
Together, these results support the possibility that peripheral immune-metabolic alterations are linked to neurodevelopmental pathways implicated in ASD, consistent with emerging evidence that immune signaling can influence brain development
