Increases in levels of SPTAN1 and SPTBN1 and their breakdown products have been observed in senile plaques in Alzheimer’s disease [124, 125] and in Parkinson’s disease Lewy body protein products [126] which could lead to aggregation of misfolded proteins and resultant neurotoxicity in brains of adult subjects with ASD. This evidence concerns the gene SPTBN1 and early-onset autosomal dominant Alzheimer disease.