<p>TORCH-associated encephalopathy in children with autism spectrum disorder (ASD) is accompanied by a pronounced neurometabolic syndrome characterized by neuronal damage, mitochondrial energy deficiency, and disturbances in methylation processes. In the present study, children with ASD and confirmed TORCH-related central nervous system injury demonstrated significantly elevated serum levels of neuron-specific enolase (NSE), lactate, ammonia, and homocysteine, reflecting neuronal injury, mitochondrial dysfunction, and metabolic dysregulation. These alterations were more pronounced than in children with idiopathic autism and in healthy controls, suggesting a possible contribution of infection-related neuroinflammatory mechanisms to ASD pathology. The combined assessment of NSE, lactate, ammonia, and homocysteine represents a biologically relevant set of biochemical predictors for TORCH-induced encephalopathy in children with ASD. Elevated levels of these markers were closely associated with the severity of cognitive, emotional, and adaptive impairments, as well as with more severe clinical forms of autism. Thus, an integrated biochemical profiling approach may serve as a valuable basis for early risk stratification, differential diagnosis, and the development of personalized metabolic and neuroprotective therapeutic strategies in children with autism associated with TORCH infections.</p>