Direct electron transfer between Cyt c and heme-Aβ relevant to Alzheimer’s disease

Chandradeep Ghosh; Soumya Mukherjee; Somdatta Ghosh Dey

doi:10.1039/c3cc42700e

Direct electron transfer between Cyt c and heme-Aβ relevant to Alzheimer’s disease

Chandradeep Ghosh, Soumya Mukherjee, Somdatta Ghosh Dey

Hope Center for Neurological Disorders

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

Partially reduced oxygen species (PROS), produced by reduced heme bound Aβ peptides, can cause oxidative stress and synaptic damage in the brain, which is one of the key pathological features of Alzheimer’s disease. In situ oxidation of the heme center by a physiological redox agent like Cytochrome c (Cyt c) can significantly suppress neurotoxic PROS formation. Thus, Cyt c can potentially act as a neuroprotective agent against AD.

Original language	English
Pages (from-to)	5754-5756
Number of pages	3
Journal	Chemical Communications
Volume	49
Issue number	51
DOIs	https://doi.org/10.1039/c3cc42700e
State	Published - May 30 2013

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abstract = "Partially reduced oxygen species (PROS), produced by reduced heme bound Aβ peptides, can cause oxidative stress and synaptic damage in the brain, which is one of the key pathological features of Alzheimer{\textquoteright}s disease. In situ oxidation of the heme center by a physiological redox agent like Cytochrome c (Cyt c) can significantly suppress neurotoxic PROS formation. Thus, Cyt c can potentially act as a neuroprotective agent against AD.",

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AB - Partially reduced oxygen species (PROS), produced by reduced heme bound Aβ peptides, can cause oxidative stress and synaptic damage in the brain, which is one of the key pathological features of Alzheimer’s disease. In situ oxidation of the heme center by a physiological redox agent like Cytochrome c (Cyt c) can significantly suppress neurotoxic PROS formation. Thus, Cyt c can potentially act as a neuroprotective agent against AD.

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Direct electron transfer between Cyt c and heme-Aβ relevant to Alzheimer’s disease

Abstract

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