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• W2532488312 abstract "Neurodegenerative disorders, e.g., Alzheimer’s disease (AD), are typically late-life while neurodevelopmental disorders, e.g., autism spectrum disorder (ASD) and fragile X syndrome (FXS), manifest early in life. ASD and FXS have partial overlap of behavioral symptoms. FXS is strongly associated with mental retardation while ASD can co-occur with high cognitive function. AD includes progressive loss of cognitive function. Amyloid-β (Aβ) precursor protein (APP) and metabolites are usually associated with AD pathogenesis. Excess Aβ is neurotoxic and can lead to atrophy of brain regions in AD, such as amygdala, which is enlarged in ASD, but not FXS. We previously reported differing levels of APP products in ASD and FXS vs. controls. We measured levels of soluble-fraction APP metabolites (Aβ, sAPPα, sAPPtotal) in brain samples from subjects with AD, ASD, FXS, and age-matched controls (no known neurological disorders). Tissues were homogenized in a “non-detergent” buffer, homogenates centrifuged, and supernatant collected and subjected to ELISA analyses. Data was analyzed by generalized linear models followed by ANOVA. We herein report notable biochemical differences between the developmental disorders and a parallel between AD and FXS. Specifically, we found elevated soluble Aβ and total APP in FXS brain samples compared to ASD and controls. Soluble Aβ levels were significantly higher in AD brain samples than controls. Further, we detected increased levels of sAPPα and total sAPP vs. controls in AD brains, but these differences were not significant. The developmental disorder FXS, while often displaying ASD symptoms, is more strongly associated with mental retardation. We found elevated levels of neurotoxic Aβ peptide and total APP in both FXS and AD samples vs. age-matched controls, while Aβ levels in ASD brains were reduced from controls. Age-matched controls account for non-specific effects of age on Aβ levels. ASD may partially be the result of early-life “Aβ deficiency”, and FXS-associated mental retardation may be due to early-life Aβ excess, in parallel with presumed effects of neurotoxic Aβ accumulation in AD. An analysis of relative frequency of AD in people with ASD may illuminate if early-life low Aβ levels may influence late-life risk for this form of neurodegeneration." @default.
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• W2532488312 date "2016-07-01" @default.
• W2532488312 modified "2023-09-27" @default.
• W2532488312 title "P4-305: Novel Parallels and Distinctions Among App Metabolite Pathways in Alzheimer's Disease and Neurodevelopmental Disorders" @default.
• W2532488312 doi "https://doi.org/10.1016/j.jalz.2016.07.048" @default.
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