2-Minute Neuroscience: Autism
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Autism is characterized by impairments in social communication and interaction and restricted and repetitive behaviors. In this video, I discuss the neuroscience of autism along with potential factors and mechanisms involved in the development of autism.
TRANSCRIPT:
Autism, also known as autism spectrum disorder, is characterized by symptoms that include impairments in social communication and interaction and restricted and repetitive behaviors. Although the neuroscience of autism is still poorly understood, autism is considered to be a complex developmental disorder that involves atypical brain organization starting early in development.
Individuals with autism often experience a period of unusually rapid brain growth in infancy and early childhood. This accelerated brain growth is linked to an atypical pattern of connectivity between brain regions. A number of studies report that alterations in brain circuitry involved with social interaction and attention can be detected well before the symptoms of autism begin to appear. At this point, however, it’s unclear how brain overgrowth and atypical connectivity might be linked to the occurrence of autism symptoms.
Research suggests that the risk of autism is strongly influenced by genetics, yet studies consistently report that environmental factors also play a large role. Although a number of potential environmental factors have been identified, the risk factors for autism are far from definitive, and it remains unclear which factors are responsible for causing an increase in autism risk, and which are associated in a non-causal way. The risk factors that are most strongly linked to autism are associated with the prenatal or perinatal period. Thus, it’s possible they might be responsible for disruptions to typical neural development, leading to symptoms of autism months or years later. How these risk factors might interfere with neural development is still uncertain, but hypotheses have suggested potential mechanisms such as epigenetic effects, inflammation, oxidative stress, or damage caused by oxygen deficiency. More work needs to be done, however, to fully elucidate the genetic and environmental risk factors for autism, as well as the mechanisms for the development of autism symptoms.
REFERENCES:
Lord C, Brugha TS, Charman T, Cusack J, Dumas G, Frazier T, Jones EJH, Jones RM, Pickles A, State MW, Taylor JL, Veenstra-VanderWeele J. Autism spectrum disorder. Nat Rev Dis Primers. 2020 Jan 16;6(1):5. doi: 10.1038/s41572-019-0138-4. PMID: 31949163.
Lord C, Elsabbagh M, Baird G, Veenstra-Vanderweele J. Autism spectrum disorder. Lancet. 2018 Aug 11;392(10146):508-520. doi: 10.1016/S0140-6736(18)31129-2. Epub 2018 Aug 2. PMID: 30078460; PMCID: PMC7398158.
Modabbernia A, Velthorst E, Reichenberg A. Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses. Mol Autism. 2017 Mar 17;8:13. doi: 10.1186/s13229-017-0121-4. PMID: 28331572; PMCID: PMC5356236.
Muhle RA, Reed HE, Stratigos KA, Veenstra-VanderWeele J. The Emerging Clinical Neuroscience of Autism Spectrum Disorder: A Review. JAMA Psychiatry. 2018 May 1;75(5):514-523. doi: 10.1001/jamapsychiatry.2017.4685. PMID: 29590280.
TRANSCRIPT:
Autism, also known as autism spectrum disorder, is characterized by symptoms that include impairments in social communication and interaction and restricted and repetitive behaviors. Although the neuroscience of autism is still poorly understood, autism is considered to be a complex developmental disorder that involves atypical brain organization starting early in development.
Individuals with autism often experience a period of unusually rapid brain growth in infancy and early childhood. This accelerated brain growth is linked to an atypical pattern of connectivity between brain regions. A number of studies report that alterations in brain circuitry involved with social interaction and attention can be detected well before the symptoms of autism begin to appear. At this point, however, it’s unclear how brain overgrowth and atypical connectivity might be linked to the occurrence of autism symptoms.
Research suggests that the risk of autism is strongly influenced by genetics, yet studies consistently report that environmental factors also play a large role. Although a number of potential environmental factors have been identified, the risk factors for autism are far from definitive, and it remains unclear which factors are responsible for causing an increase in autism risk, and which are associated in a non-causal way. The risk factors that are most strongly linked to autism are associated with the prenatal or perinatal period. Thus, it’s possible they might be responsible for disruptions to typical neural development, leading to symptoms of autism months or years later. How these risk factors might interfere with neural development is still uncertain, but hypotheses have suggested potential mechanisms such as epigenetic effects, inflammation, oxidative stress, or damage caused by oxygen deficiency. More work needs to be done, however, to fully elucidate the genetic and environmental risk factors for autism, as well as the mechanisms for the development of autism symptoms.
REFERENCES:
Lord C, Brugha TS, Charman T, Cusack J, Dumas G, Frazier T, Jones EJH, Jones RM, Pickles A, State MW, Taylor JL, Veenstra-VanderWeele J. Autism spectrum disorder. Nat Rev Dis Primers. 2020 Jan 16;6(1):5. doi: 10.1038/s41572-019-0138-4. PMID: 31949163.
Lord C, Elsabbagh M, Baird G, Veenstra-Vanderweele J. Autism spectrum disorder. Lancet. 2018 Aug 11;392(10146):508-520. doi: 10.1016/S0140-6736(18)31129-2. Epub 2018 Aug 2. PMID: 30078460; PMCID: PMC7398158.
Modabbernia A, Velthorst E, Reichenberg A. Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses. Mol Autism. 2017 Mar 17;8:13. doi: 10.1186/s13229-017-0121-4. PMID: 28331572; PMCID: PMC5356236.
Muhle RA, Reed HE, Stratigos KA, Veenstra-VanderWeele J. The Emerging Clinical Neuroscience of Autism Spectrum Disorder: A Review. JAMA Psychiatry. 2018 May 1;75(5):514-523. doi: 10.1001/jamapsychiatry.2017.4685. PMID: 29590280.
