Autism is a disease that has affected families around the world and has become an ever-growing problem in the United States. Autism is known as a complex, developmental disability linked to abnormal biology and chemistry in the brain. Experts believe that Autism presents itself during the first three years of a person’s life. The condition is the result of a neurological disorder that has an effect on normal brain function, affecting development of the person’s communication and social interaction skills. However, the exact mechanisms in which the disease functions remains unknown. In the United States, autism has been on an unusually steep rise since 1970. It is the goal of researchers to determine what has caused this sharp increase. In order to explain this, researchers have turned to examining the disease mechanistically.
Researchers have learned from twin and sibling studies that genetic factors play a role in autism. However, the genetic factors cannot be the sole reason autism develops in young children. Thus, experimental factors are proposed to be the cause for the increase in autistic individuals. These factors can include diet, exercise, vaccine sensitivity, or anything outside the body that could alter the interior. Being that this brings about a broad category of factors that could lead to autism, researchers have hypothesized a “redox/methylation” hypothesis.
In this hypothesis, researchers have noted that environmental factors lead to oxidative stress. Because neuronal cells exhibit the most sensitivity to oxidative stress, the brain is affected the most with autism. Given the correct risk genes, a number of adaptive responses involving sulfur metabolism are initiated once oxidative stress has taken its course. This leads to an inhibition of methionine synthase, which greatly reduces methylation activity. Most importantly, this affects DNA methylation and dopamine-stimulated phospholipid methylation. This decrease in DNA methylation disrupts epigenetic events that are characteristic of normal development. The decrease in dopamine-stimulated phospholipid methylation restricts the frequency-dependent synchronization of neuronal networks. Thus, communication between neurons is altered. This is linked to the lack of attention and cognition.
Although the “redox/methylation” hypothesis is purely speculation, the research has led to areas of interest involved with autism. The hypothesis has found a general explanation for autism but does lack in areas regarding specific cases of autism. However, the “redox/methylation” hypothesis does provide a starting point at which researchers can hope to build upon. In order to validate the hypothesis, the specific causes of autism need to be identified.
Autism's Growing Behavior
