The hypothesis that autism is associated with neuropathological changes was explored in the first reports published between 1980 and 1993 [7, 21, 22, 27, 42, 50, 51, 82, 90]. Since then, implementation of broader diagnostic terms such as Autism Spectrum Disorder (ASD), examination of larger cohorts, applications of stereology, and functional and structural magnetic resonance imaging (MRI) have resulted in the detection of several major types of pathology, most likely contributing to the clinical phenotype. An emerging concept of autism-related brain pathology integrates evidence of (a) abnormal acceleration of brain growth in early childhood [89], (b) minicolumn pathology [13, 14], (c) curtailed neuronal development [7, 108] and brain structure-specific delays of neuronal growth [111] with indications of abnormalities in brain cytoarchitecture [4, 7], metabolic modifications with abnormal amyloid protein precursor (APP) processing [5, 101], enhanced oxidative stress [17] and enhanced turnover of cell organelles with pigment accumulation and glial activation [68].
