Disturbances in metal-ion regulation have been implicated in a variety of neurodegenerative disorders including Alzheimer’s Disease (AD).  Endogenous metal ions, including copper, iron, and zinc, as well as exogenous metal ions, like aluminum, have been found to accumulate in the regions of the brain most affected by these diseases.  Profiling experiments on neuronal tissue from AD patients have also implicated a variety of microRNAs (miRNA) in disease initiation and progression.  Although research has shown a variety of structural and functional roles for these enriched transition metal levels, the effect of excess metal ion exposure on microRNA (miRNA) mediated changes in gene expression has yet to be fully established. Herein, we study the effects of excess copper, iron and manganese exposure on the dysregulation of selected miRNA in cultured neuronal cells and the downstream effects on the expression and/or modification of two Alzheimer’s disease related proteins, amyloid precursor protein (APP) and hyperphosphorylated tau.<br/>

Metal ion induced alterations in amyloid precursor protein expression and tau hyperphosphorylation via microrna mediated pathways

251st National Meeting (2016)

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