Abstract
Epidemiological and biochemical studies strongly implicate a role for cholesterol in the pathogenesis of Alzheimer's disease (AD). Mutation in the PS-1 and APP genes, which increases production of the highly amyloidogenic amyloid β-peptide (Aβ42), is the major cause of familial AD. The AD brain is under significant oxidative stress, including protein oxidation and lipid peroxidation. In the present study, protein oxidation and lipid peroxidation were compared in the brain homogenates from knock-in mice expressing mutant human PS-1 and APP in relation to the intake of dietary cholesterol. The APP and PS-1 mice displayed increased oxidative stress as measured by protein oxidation and lipid peroxidation, independent of dietary cholesterol. These results are discussed with reference to proposed therapeutic strategies of AD.
Original language | English |
---|---|
Pages (from-to) | 148-150 |
Number of pages | 3 |
Journal | Neuroscience Letters |
Volume | 368 |
Issue number | 2 |
DOIs | |
State | Published - Sep 23 2004 |
Bibliographical note
Funding Information:This research was supported in part by NIH to D.A.B. [AG-10836; AG-05119] and G.L.W. [AG10546; Alzheimer’s Assoc., IIRG-01-2654]
Keywords
- Alzheimer's disease
- Amyloid precursor protein
- Aβ(1-42)
- Cholesterol
- Lipid peroxidation
- Oxidative stress
- Presenilin-1
- Protein carbonyl
ASJC Scopus subject areas
- General Neuroscience