Title : The Oral Iron Chelator, Deferasirox, Reverses the Age-Dependent Alterations in Iron and Amyloid-β Homeostasis in Rat Brain: Implications in the Therapy of Alzheimer's Disease.

Pub. Date : 2016

PMID : 26484920






4 Functional Relationships(s)
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1 We have shown in this study that chelatable iron accumulates in the aged rat brain along with overexpression of transferrin receptor 1 (TfR1) and ferritin, accompanied by significant alterations in amyloid-beta (Abeta) peptide homeostasis in the aging brain, such as an increased production of the amyloid-beta protein precursor, a decreased level of neprilysin, and increased accumulation of Abeta42. Iron transferrin receptor Rattus norvegicus
2 We have shown in this study that chelatable iron accumulates in the aged rat brain along with overexpression of transferrin receptor 1 (TfR1) and ferritin, accompanied by significant alterations in amyloid-beta (Abeta) peptide homeostasis in the aging brain, such as an increased production of the amyloid-beta protein precursor, a decreased level of neprilysin, and increased accumulation of Abeta42. Iron transferrin receptor Rattus norvegicus
3 When aged rats are given daily the iron chelator, deferasirox, over a period of more than 4 months starting from the 18th month, the age-related accumulation of iron and overexpression of TfR1 and ferritin in the brain are significantly prevented. Iron transferrin receptor Rattus norvegicus
4 The analysis of the results together suggests that iron accumulation and oxidative stress interact at multiple levels that include transcriptional and post-transcriptional mechanisms to bring about changes in the expression levels of TfR1 and ferritin and also alterations in Abeta peptide metabolism in the aging rat brain. Iron transferrin receptor Rattus norvegicus