Astaxanthin improves behavioural and immune dysfunction in the Shank3b mouse model of autism spectrum disorder.

Scientists tested a natural antioxidant called astaxanthin in mice with autism-like behaviours. The treatment improved social interaction, reduced repetitive behaviours, and helped with coordination. It also reduced brain inflammation and balanced immune system activity. The researchers suggest astaxanthin might be a safe treatment option for autism, though this was only tested in mice.

This preclinical study investigated astaxanthin (AST), a potent antioxidant and anti-inflammatory compound, in the Shank3b mouse model of autism spectrum disorder. AST treatment significantly improved core ASD-like behaviours including social interaction deficits, motor incoordination, and repetitive grooming. In the cerebellum, AST reduced pro-inflammatory cytokines and counteracted microglial hyperactivation. In peripheral immune compartments, AST modulated cytokine expression, with pro-inflammatory markers downregulated in bone marrow and spleen of treated mice, suggesting immune rebalancing.

ROC analysis indicated TNF and IFNγ expression in peripheral immune cells may serve as biomarkers of treatment response. Unlike N-acetylcysteine, AST did not induce pro-inflammatory effects, suggesting potential as a safe immunomodulatory therapy for ASD.

Results suggest astaxanthin may offer a novel, safe approach for addressing autism symptoms and immune dysfunction. However, human clinical trials are needed to establish safety, dosing, and efficacy. The immune biomarkers identified could potentially guide treatment decisions if validated in clinical populations.

Study conducted only in mouse model, limiting direct applicability to humans. Sample size not reported. Oxidative stress assays were not performed, missing key mechanistic data. Long-term safety and efficacy data not available. No comparison to standard autism treatments.

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by deficits in social communication and interaction, and repetitive behaviours. Numerous studies have associated ASD with immune dysregulation and inflammation, with neuroinflammatory processes reported in ASD individuals and mouse models. Altered immune cell profiles and cytokine levels have been observed in the peripheral blood (PB), supporting systemic immune dysfunction. Recently we showed that the administration of antioxidant molecule N-acetylcysteine (NAC) reduced oxidative stress and inflammation and counteracted behavioural deficits in two mouse models of ASD, providing a rationale for exploring other redox-active compounds.

Here, we investigated the effects of astaxanthin (AST), potent antioxidant and anti-inflammatory molecule, in the Shank3b model (Shank3bmice). AST treatment significantly improved core ASD-like behaviours, including social interaction deficits, motor incoordination, and repetitive grooming. In the cerebellum, AST reduced pro-inflammatory cytokines and counteracted microglial hyperactivation. In peripheral immune compartments, AST modulated cytokine expression.

Pro-inflammatory markers were downregulated in Shank3bmice in the bone marrow and spleen while they were elevated in Shank3b controls, suggesting immune rebalancing (i.e. adaptive modulation suppressing harmful inflammation while supporting protective immunity). As a limitation, oxidative stress assays were not performed here. Receiver operating characteristic (ROC) analysis suggests that TNF and IFNγ expression in peripheral immune cells may be promising biomarkers of treatment response. Notably, unlike NAC, AST did not induce pro-inflammatory effects in Shank3banimals.

These findings show that AST administration may counteract behavioural deficits and immune dysfunction in Shank3bmice, therefore suggesting its potential as a safe immunomodulatory therapy for ASD.