An investigation of the molecular mechanisms engaged before and after the development of Alzheimer disease neuropathology in Down syndrome: a proteomics approach.

摘要: Down syndrome (DS) is one of the most common causes intellectual disability, owing to trisomy all or part chromosome 21. DS also associated with development Alzheimer disease (AD) neuropathology after age 40 years. To better clarify cellular and metabolic pathways that could contribute differences in brain, particular those involved onset neurodegeneration, we analyzed frontal cortex subjects without significant AD pathology comparison age-matched controls, using a proteomics approach. Proteomics represents an advantageous tool investigate molecular mechanisms underlying disease. From these analyses, investigated effects age, DS, have on protein expression levels. Our results show overlapping independent (including energy metabolism, oxidative damage, synthesis, autophagy) contributing aging, presence DS. Investigation pathomechanisms may provide putative targets for therapeutic approaches slow AD.