Vargas · Annals of neurology 2005 · post-mortem and biofluid comparative study · n=17 (11 post-mortem cases, 6 living CSF donors; control n not stated in abstract)

Neuroglial activation and neuroinflammation in the brain of patients with autism.

Cited 2157 times in the scientific literature.

Level 4 - case-series / case-control

Comparative post-mortem and biofluid case series

PubMed 15546155 · doi:10.1002/ana.20315 · record verified 2026-08-31

What was done

Investigators evaluated neuroglial activation and cytokine profiles in post-mortem brain tissue and cerebrospinal fluid (CSF) from individuals with autism using immunocytochemistry, cytokine protein arrays, and ELISA. Morphological analyses were performed on autopsy tissues (cerebellum, midfrontal gyrus, and cingulate gyrus) from 11 autistic patients. Cytokine profiling was conducted on fresh-frozen brain tissue from 7 patients and on CSF from 6 living autistic patients.

What was found

Immunocytochemistry revealed marked activation of microglia and astroglia in the cerebral cortex, white matter, and cerebellum of autistic patients. Cytokine profiling demonstrated that macrophage chemoattractant protein-1 (MCP-1) and tumor growth factor-beta1 (TGF-beta1) were the most prevalent cytokines in brain tissue. CSF analysis showed a proinflammatory cytokine profile with a marked increase in MCP-1. The abstract reports no numerical values, concentrations, or statistical significance metrics.

Why it matters

This study provides direct post-mortem and CSF evidence of innate neuroimmune and neuroglial activation in the brains of individuals with autism, identifying neuroinflammation as a potential biological feature and therapeutic target in a subset of patients.

Limits

The sample size is very small (11 autopsy donors, 6 living CSF donors), and control group details and numbers are omitted from the abstract. No quantitative effect sizes, variances, or p-values are reported. Cross-sectional post-mortem and biofluid data cannot determine whether neuroinflammation is a primary cause or secondary consequence of autism pathology.

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