One major proposed mechanism to explain changes associated with cellular and organismal aging is that oxidative damage to lipid, protein and nucleic acids accumulates as cells become less capable of coping with oxidative stress. This potentially leads to membrane instability, accumulation of damaged proteins and acquired mutation, all of which may contribute to cellular dysfunctions associated with aging and aging related diseases.
The role of oxidative stress as it contributes to neuronal dysfunction in the context of aging and Alzheimer’s disease (AD) is of particular interest and has generated enormous observational and experimental literature. Despite this, large scale clinical trials of antioxidative therapy have not yet produced a compelling therapy for AD. Additionally, specific mechanisms which contribute to oxidative stress in the brain are not clear. The large volume of literature and heterogeneity of results makes a comprehensive understanding of the changes occurring in the human brain in Alzheimer’s disease elusive.
To address this, we are conducting analyses and meta-analyses to map the network of oxidative stress-related changes in the brain and blood in AD to try to better define the changes to determine if there is a broad dysregulation or a more-specific pattern to explain reported changes.
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