This article is a summary in Spanish of the publication by Dr Daniel A. Rossignol and Dr Richard E Frye: https://www.frontiersin.org/articles/10.3389/fphys.2014.00150/full?s=08#B79

The autism spectrum disorders (ASD) are traditionally considered behavioral disorders, but recent research suggests that they may involve physiological abnormalities in the brainsuch as oxidative stress, mitochondrial dysfunction, and immune dysregulation/inflammation. These abnormalities have been observed in peripheral biomarkers such as blood and urine samples, but more recent studies have identified them in brain tissue from individuals with ASD.

Many of the brain regions affected in ASD are involved in speech and hearing processing, social behavior, memory, and sensory-motor coordination. A growing body of evidence links oxidative stress, mitochondrial dysfunction, and immune dysregulation/inflammation in the brains of individuals with ASD, leading to implies that ASD has a biological basis with features of known medical disorders. This understanding may pave the way for new testing and treatment strategies for individuals with ASD.

Numerous studies have shown evidence of oxidative stress in postmortem brain samples from individuals with Autism Spectrum Disorder (ASD).

These studies reported decreased glutathione (GSH), oxidative damage to proteins, lipids, and DNA, as well as alterations in the activity of enzymes vital for redox metabolism. Despite some limitations, such as small sample sizes and inconsistencies in the brain areas analyzed in the studies, the findings are robust in ASD subjects and brain regions, suggesting a pervasive presence of oxidative stress in the ASD brain.

Mitochondrial dysfunction has been observed in the brain of individuals with Autism Spectrum Disorder (ASD) using magnetic resonance techniques and post-mortem brain samples. The studies have reported a decrease in the activities of electron transport chain (ETC) complexes and tricarboxylic acid (TCA) cycle enzymes., as well as differences in the expression of mitochondrial genes in ASD brains compared to controls.

MRS studies have detected abnormal energy metabolites in the frontal cortex and reduced levels of N-acetyl-aspartate (NAA) in global white and gray matter and other brain areas. ETC dysfunction has been found in several brain regions, with ETC complex I being the most commonly reported as depressed. Also, changes in genes that control mitochondrial dynamics have been observed. These findings consistently demonstrate mitochondrial dysfunction in the brains of individuals with ASD.

Research has observed inflammation and immune dysregulation in both brain tissue and cerebrospinal fluid (CSF) samples.

Research has observed inflammation and immune dysregulation in both brain tissue and cerebrospinal fluid (CSF) samples from individuals with Autism Spectrum Disorder (ASD). These studies have found increases in cytokines, expression of genes related to the immune system, activation of microglial cells, and other biomarkers of inflammation.

The strongest evidence for immune system activation comes from histological evidence of microglial cell changes in various brain regions and neuroimaging. The alteration in immune regulation is supported by elevations in proinflammatory cytokines in brain tissue and CSF, as well as elevated expression of genes that regulate proinflammatory pathways in individuals with ASD. Most of the research points to an activation of the innate immune system in the brains of individuals with ASD. This supports further research into the role of inflammation and immune dysregulation in the brains of children with ASD.

Recent studies have found physiological abnormalities in individuals with Autism Spectrum Disorder (ASD), pointing to a clear biological basis. These abnormalities include oxidative stress, mitochondrial dysfunction, and immune dysregulation. A significant percentage of these studies have been published since 2010, with many examining possible interactions between these abnormalities in the brains of individuals with ASD.

Some studies have reported links between oxidative stress and mitochondrial dysfunction, as well as oxidative stress and inflammation in the brains of individuals with ASD. It has been suggested that some of these physiological abnormalities may explain certain ASD symptoms, such as speech processing, memory, social interaction, and sensory-motor coordination. Treatments targeting these abnormalities have shown improvements in autism using nutritional supplements and medications., although additional studies are needed to determine its long-term effectiveness.

In conclusion, the reviewed studies support the presence of oxidative stress, mitochondrial dysfunction, and inflammation/immune dysregulation in the central nervous system (CNS) of individuals with Autism Spectrum Disorder (ASD). Despite the limitations, these findings suggest that these physiologic abnormalities may play an important role in the pathologic mechanisms that alter brain function in ASD. Interestingly, similar abnormalities have been found in other neurocognitive and psychiatric diseases, including Alzheimer's, Parkinson's, multiple sclerosis, amyotrophic lateral sclerosis, and Friedreich's ataxia. Since these pathophysiological mechanisms appear to be shared among multiple cognitive and behavioral disorders, future research should investigate the similarities.