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Redox activeiron is utilized in biology for various electron transferand catalytic reactions essential for life, yet this same chemistrymediates the formation of partially reduced oxygen species (PROS).Oxidative stress derived from the iron accumulated in the amyloidplaques originating from amyloid β (Aβ) peptides and neurofibrillarytangles derived from hyperphosphorylated tau proteins has been implicatedin the pathogenesis of Alzheimer’s disease (AD). Altered hemehomeostasis leading to dysregulation of expression of heme proteinsand heme deposits in the amyloid plaques are characteristic of theAD brain. However, the pathogenic significance of heme in neurodegenerationin AD has been unappreciated due to the lack of detailed understandingof the chemistry of the interaction of heme and Aβ peptides.As a result, the biochemistry and biophysics of heme complexes ofAβ peptides (heme–Aβ) remained largely unexplored. [ABSTRACT FROM AUTHOR]