Evidence of neurodegeneration in autism spectrum disorder

Abstract

Autism spectrum disorder (ASD) is a neurological disorder in which a significant number of children experience a developmental regression characterized by a loss of previously-acquired skills and abilities. Loss of neurological function in ASD, as observed in affected children who have regressed, can be explained as neurodegeneration. Although there is research evidence of neurodegeneration or progressive encephalopathy in ASD, the issue of neurodegeneration in ASD is still under debate. Evidence of neurodegeneration in the brain in ASD includes: (1) neuronal cell loss, (2) activated microglia and astrocytes, (3) proinflammatory cytokines, (4) oxidative stress, and (5) elevated 8-oxo-guanosine levels. The evidence from this review suggests that neurodegeneration underlies the loss of neurological function in children with ASD who have experienced regression and loss of previously acquired skills and abilities, and that research into treatments to address the issue of neurodegeneration in ASD are warranted.

A two-phase study evaluating the relationship between Thimerosal-containing vaccine administration and the risk for an autism spectrum disorder diagnosis in the United States

“…The importance of postnatal loss of neurological function in those diagnosed with an ASD between 6 and 18 months of age, as observed in affected children who have regressed, is this phenomena is suggestive of neurodegeneration or a type of progressive encephalopathy with an etiological pathogenic basis occurring after birth [5]. To date, the etiology of ASD remains under debate.…”

The role of imbalance between urinary hexanoyl-lysine and total antioxidant capacity levels and its relation to plasma superoxide dismutase levels in autism spectrum disorder

“…When BBB disruption occurs, brain-specific proteins circulating inside the brain, are observed in the peripheral blood as an index for estimating the extent of the increase in BBB permeability and brain damage [81]. As described above, overproduction of ROS results in oxidative stress the imbalance between ROS and antioxidant capacity (referred to oxidative stress) became toxic to neurons, damaging DNA, proteins and lipids, inducing neurodegeneration [4] such as ASD [82]. Thus, the imbalance between the generation of ROS and TAC may disrupt BBB and be related to impaired social responsiveness through biochemical processes such as imbalance between increased urinary levels of HEL as oxidants and urinary levels of TAC as antioxidant in individuals with ASD.…”

Current Update on Synopsis of miRNA Dysregulation in Neurological Disorders

“…ASD is a type of NDD because many children with ASD undergo a developmental regression, as evidenced by loss of previously-acquired skills and abilities. Although the exact mechanism is not known, biological processes such as neuronal cell loss, release of proinflammatory cytokines, oxidative stress, and astrocytes and microglial activation have been suggested to contribute to neurodegeneration in ASD [95]. In addition, when changes occur in the way nerve cells and their synapses connect and organize, this ultimately affects the brain’s information processing ability, contributing to the pathogenesis of ASD [96].…”