Dynamic Brain Changes in Autism: Review of Telencephalic Structures
In this chapter of morphological differences in postmortem brains from autistic and normal individuals, we identified consistent reports of abnormalities in neuronal neurogenesis and neurodegeneration. Postmortem studies observed since 1985 found abnormalities throughout the brain, but for the sake of this chapter, our focus is on telencephalon, which includes cerebral cortex, amygdala and basal ganglion, and related pathways. Postmortem studies have examined cortical and subcortical regions, ventricular features and neurotransmitter, and neurotrophic factors. In this chapter we make several important observations on the development and progression of autism disorder derived from postmortem studies. (1) The changes in telencephalon occur in all cortical, subcortical, and connections between these regions. (2) There is accelerated growth and evidence of enhanced neurogenesis and brain size in children and toddlers. (3) There is evidence of neuropathology in brains from adolescents and adult patients. (4) Serotonin neurons, trophic factors, and glial cells appear to be involved in these developmental changes. The findings are grouped into three developmental stages: (1) neonate and toddlers (1–10 years), (2) adolescent (11–19 years), and (3) adult (20–60 years). Unfortunately, postmortem studies frequently have only a few cases and results may not be identified by the age of the donor. However, consistent findings were identified from the published studies we reviewed. We propose a hypothetical sequence of development events to describe autism. Serotonin fibers entering the telencephalon are increased: à increase in cell proliferation, neuronal and glial maturation in ventricles, and cortical columns; à increased brain size; à increased microglia activation and receptor downregulation; and trophic factor depletion à increase in neuronal dystrophy and degeneration. These steps are part of a neuroplasticity scheme and serve to help in understanding the dynamics of the disease.
KeywordsMigration Anisotropy Dopamine Dementia Serotonin
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