Oxidative damage to cellular macromolecules, including, nucleic acids, proteins, and lipids, is a feature of aging as well as many neurodegenerative diseases including Alzheimer’s disease (AD). Together these data support a role for lipid peroxidation in the progression of AD. A time- and concentration-dependent decrease in survival and a concentration dependent decrease in glucose uptake were observed in primary cortical cultures treated with HHE. Extractable HHE was significantly elevated in the hippocampus/parahippocampal gyrus (HPG) of PCAD and LAD subjects and protein-bound HHE was significantly higher in MCI, PCAD, and LAD HPG. Levels of extractable and protein-bound HHE were increased in multiple regions in the progression of AD. In the present study levels of extractable and protein-bound HHE were quantified in the hippocampus/parahippocampal gyrus (HPG), superior and middle temporal gyri (SMTG), and cerebellum (CER) of MCI, PCAD, LAD, and normal control (NC) subjects. However, there has been limited study of a third member, 4-hydroxyhexenal (HHE), a diffusible lipid peroxidation product of the ω-3 polyunstataturated fatty acids (PUFAs). Multiple studies have demonstrated elevations of α, β-unsaturated aldehydes including, 4-hydroxynonenal (HNE) and acrolein, in vulnerable regions of mild cognitive impairment (MCI), preclinical Alzheimer’s disease (PCAD), and late-stage Alzheimer’s disease (LAD) brain.
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