Evidence map›Paper›PMID 42213276›Full record

ArticleJournal of molecular neuroscience : MN2026

Biochemical Predictors in the Blood Serum of Children with TORCH Encephalopathy and Autism.

Nodirakhon Khusenova, Yakuthon Madjidova, Shukhrat Usmanov, Latofat Ziyakhodjaeva, Gulnora Rixsiyeva, Rano Yunusova, Taj Mohammad

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Article in Journal of molecular neuroscience : MN, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Nodirakhon KhusenovaDepartment of Neurology, Child Neurology and Medical Genetics, Tashkent State Medical University, Tashkent, Uzbekistan. nadira_088@hotmail.com.
Yakuthon MadjidovaDepartment of Neurology, Child Neurology and Medical Genetics, Tashkent State Medical University, Tashkent, Uzbekistan.
Shukhrat UsmanovDepartment of Neurology, Child Neurology and Medical Genetics, Tashkent State Medical University, Tashkent, Uzbekistan.
Latofat ZiyakhodjaevaDepartment of Neurology, Child Neurology and Medical Genetics, Tashkent State Medical University, Tashkent, Uzbekistan.
Gulnora RixsiyevaDepartment of Infectious Diseases, Children's Infectious Disease and Pulmonology, Tashkent State Medical University, Tashkent, Uzbekistan.
Rano YunusovaDepartment of Hospital Pediatrics, Tashkent State Medical University, Tashkent, Uzbekistan.
Taj MohammadCentre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi, 110025, India. tajmohammad.tk@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

Autism Spectrum DisorderEnthesopathyBiomarkersChildChild BehaviorChild, PreschoolCognitionEmotionsFemaleHumansMaleBiomarkersAutism spectrum disorderBiochemical predictorsChildrenMitochondrial dysfunctionNeurometabolic markersTORCH encephalopathy

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.