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High Levels of Alzheimer Beta-Amyloid Precursor Protein (APP) in Children With Severely Autistic Behavior and Aggression

Pediatric Neurology-RI 1757, Riley Hospital for Children, Indiana University School of Medicine, 702 Barnhill Drive, Indianapolis

Demao Chen, PhD

Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN

Martin R. Farlow, MD

Department of Neurology, Indiana University School of Medicine, Indianapolis, IN

David W. Dunn, MD

Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN

Bryan Maloney, BA

Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN

Jennifer A. Zimmer, MD

Department of Neurology, Indiana University School of Medicine, Indianapolis, IN

Debomoy K. Lahiri, PhD

Department of Psychiatry, Indiana University School of Medicine, Indianapolis, IN

Autism is characterized by restricted, repetitive behaviors and impairment in socialization and communication. Although no neuropathologic substrate underlying autism has been found, the findings of brain overgrowth via neuroimaging studies and increased levels of brain-derived neurotrophic factor (BDNF) in neuropathologic and blood studies favor an anabolic state. We examined acetylcholinesterase, plasma neuronal proteins, secreted beta-amyloid precursor protein (APP), and amyloid-beta 40 and amyloid-beta 42 peptides in children with and without autism. Children with severe autism and aggression expressed secreted beta-amyloid precursor protein at two or more times the levels of children without autism and up to four times more than children with mild autism. There was a trend for children with autism to show higher levels of secreted beta-amyloid precursor protein and nonamyloidogenic secreted beta-amyloid precursor protein and lower levels of amyloid-beta 40 compared with controls. This favors an increased -secretase pathway in autism (anabolic), opposite to what is seen in Alzheimer disease. Additionally, a complex relationship between age, acetylcholinesterase, and plasma neuronal markers was found. (J Child Neurol 2006;21:444—449; DOI 10.2310/7010.2006.00130).

Journal of Child Neurology, Vol. 21, No. 6, 444-449 (2006)
DOI: 10.1177/08830738060210062201


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