ArticleScientific reports2025
Treadmill training protects valproic acid-induced autistic features via cerebellar AMPK/PPAR-γ dependent pathway and improves mitochondrial activity in mice.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Physical Activity and Purkinje Cells: Mechanisms of Cerebellar Plasticity and Neuroprotection.Journal of functional morphology and kinesiology · 2026Review
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9 authors.
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Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with impaired sociality and stereotypic behavior. Endurance training could modulate mitochondrial dysfunction sharing in the pathophysiology of ASD. We investigated the neuroprotective effects of training on VPA-induced ASD in mice. Forty mice were divided into control, Training, VPA, and VPA + Training groups. Mice were subjected to neurobehavioral tests. Assessment of the protein content of serum CRP, irisin, meteorin-like protein (metrnl), cerebellar inflammatory markers, serotonin, and BDNF was done by ELISA. MDA and catalase were also investigated using a colorimetric technique. Cerebellar citrate synthase (CS) enzyme activity was also measured. Cerebellar AMPK, PPAR-ɣ, and metrnl gene expressions were assessed via RT-PCR. Cerebellar immunohistochemical studies of GFAP, Bax, and PPAR-γ markers were conducted. Statistical methods were used in the data analysis, including one-way ANOVA, and t-tests. The VPA group showed significant impairments in social interaction, and cognition in neurobehavioral tests (P = 0.000). A significant increase of CRP, MDA, and inflammatory markers associated with a significant reduction in irisin, metrnl, catalase, CS, serotonin, and BDNF (P = 0.000) was noticed. Besides, cerebellar AMPK and PPAR-γ gene expressions were down-regulated. Significant cerebellar degenerative changes were also observed (P = 0.000). Training dramatically reversed VPA-induced neurobehavioral, biochemical, and cerebellar degenerative changes. Endurance training has anti-inflammatory, anti-apoptotic, and antioxidant properties. Adipo-myokines release, enhanced mitochondrial activity, and activation of AMPK and PPAR-γ pathways could be involved mechanisms. Training programs are a promising strategy for addressing the social and neurobehavioral impairments linked to ASD, according to the muscle-brain interplay.
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