Reduction of aluminum ion neurotoxicity through a small peptide application e NAP treatment of Alzheimer's disease

Reduction of aluminum ion neurotoxicity through a small peptide application e NAP treatment of Alzheimer's disease

Alzheimer's disease (AD) is the most common cause of dementia in late life. It is difficult toprecisely diagnose AD at early stages, making biomarker search essential for furtherdevelopments. The objective of this study was to identify protein biomarkers associatedwith aluminum ions toxicity (AD-like toxicity) in a human neuroblastoma cell model, SHSY5Yand assess potential prevention by NAP (NAPVSIPQ). Complete proteomic techniqueswere implemented. Four proteins were identified as up-regulated with aluminum iontreatment, CBP80/20-dependent translation initiation factor (CTIF), Early endosome antigen1 (EEA1), Leucine-rich repeat neuronal protein 4 (LRRN4) and Phosphatidylinositol 3-kinase regulatory subunit beta (PI3KR2). Of these four proteins, EEA1 and PI3KR2 weredown-regulated after NAP-induced neuroprotective activity in neuroblastoma cells. Thus,aluminum ions may increase the risk for neurotoxicity in AD, and the use of NAP is suggestedas a treatment to provide additional protection against the effects of aluminumions, via EEA1 and PI3KR2, associated with sorting and processing of the AD amyloidprecursor protein (APP) through the endosomal system.