This week, our neurochemistry class moved away from typical discussion of neurodegenerative diseases to focus on autism, a neurodevelopmental disease. The prevalence of autism has increased 600% over the last two decades. Autism is one of three autism spectrum disorders (the other two are Asperger syndrome and pervasive developmental disorder, not otherwise specified (PDD-NOS)). Children usually first start showing signs of social/emotional impairment, repetitive behavior, limited interests, and atypical eating patterns before the age of two. Unfortunately little is known about the cause of the disease, which limits the treatment and therapy options available. Scientists do believe that the increase of autism can be attributed to a combination of both genetics and the environment. Overall, autism is thought to result from disorganized connections between neurons in the brain. Several hypotheses attempt to explain the cause of the disorganization in the brain.
One of the hypotheses currently suggested is that decreased acetylcholine signaling is responsible for the development of autism. It has been observed that autistic patients have fewer acetylcholine receptors in the brain. These receptors are responsible for relaying signals about pain and producing anti-inflammatory signals. More research needs to be done to further clarify how acetylcholine contributes to the development of autism. Most of the other hypotheses about the pathogenesis of autism involve the mother and the influence of prenatal environment. Some studies suggest that maternal infection while the fetus is in utero may increase the likelihood of developing autism. Other studies support the belief that increased prenatal stress will increase the likelihood of developing autism. The hypothesis discussed in the article “Autism as a disorder of deficiency of brain-derived neurotropic factor and altered metabolism of polyunsaturated fatty acids” is that maternal nutrition, specifically polyunsaturated fatty acids (PUFAs), plays a significant role in the development of autism. PUFAs control energy use in the brain and the amount of acetylcholine that is released. Memory, learning, neurite growth, and synapse formation are all promoted by increases in PUFAs. PUFAs also prevent cell death and inflammation. Additionally, PUFAs are known to increase brain-derived neurotrophic levels, which are important for brain development, learning and memory. Researchers believe that PUFAs and BDNF are involved in the development of autism because levels of PUFAs and BDNF are significantly decreased in autistic patients compared to healthy controls. PUFAs are also decreased in patients with conditions such as schizophrenia, attention deficit hyperactivity disorder (ADHD), and dyslexia. It is believed that supplementing the mother’s and the child’s diet with polyunsaturated fatty acids could improve autistic symptoms and possibly reduce the likelihood of developing autism.
Parents of children with autism know there are very few treatment options available currently. Most autistic children participate in early, intensive therapy (at least 25-40 hours per week) in order to improve language skills, imitation, play, and motor skills. 3-25% of children with autism will no longer be on the autism spectrum after early behavioral therapy intervention. However, intervention is only effective in reversing or treating autism in some cases. Further research into the effects PUFAs and BDNF administration could provide a new avenue for treatment to prevent or reverse the development of autism in a greater percentage of children.
Hope for Autism
