Cited by 777Alzheimer's disease research and treatmentsAntioxidant Activity and Oxidative StressDementia and Cognitive Impairment Research

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Increased Lipid Peroxidation Precedes Amyloid Plaque Formation in an Animal Model of Alzheimer Amyloidosis

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Praticò, Domenico, Uryu, Kunihiro, Leight, Susan, Trojanoswki, John Q., Lee, Virginia M.-Y.·2001·The Journal of Neuroscience

DOI 10.1523/jneurosci.21-12-04183.2001PMC PMC6762743

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Abstract

Oxidative stress is a key feature in the Alzheimer's disease (AD) brain and manifests as lipid peroxidation (LPO). Isoprostanes (iPs) are specific and sensitive markers of in vivo LPO. To determine whether amyloid beta (Abeta) deposition in vivo is associated with increased LPO, we examined iP levels in a transgenic mouse model (Tg2576) of AD amyloidosis. Urine, plasma, and brain tissues were collected from Tg2576 and littermate wild-type (WT) animals at different time points starting at 4 months of age and continuing until 18 months of age. Levels of urinary 8,12-iso-iPF(2alpha)-VI were higher in Tg2576 than in WT animals as early as 8 months of age and remained this high for the rest of the study. A similar pattern was observed for plasma levels of 8,12-iso-iPF(2alpha)-VI. Homogenates from the cerebral cortex and hippocampus of Tg2576 mice had higher levels of 8,12-iso-iPF(2alpha)-VI than those from WT mice starting at 8 months of age. In contrast, a surge of Abeta 1-40 and 1-42 levels as well as Abeta deposits in Tg2576 mouse brains occurred later, at 12 months of age. A direct correlation was observed between brain 8,12-iso-iPF(2alpha)-VI and Abeta 1-40 and 1-42. Because LPO precedes amyloid plaque formation in Tg2576 mice, this suggests that brain oxidative damage contributes to AD pathogenesis before Abeta accumulation in the AD brain.

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Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
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“Indeed, the recent demonstration of rare Ab plaques as well as scant amounts of formic acid-extractable Ab in 8-month-old Tg2576 mouse brains prompts cautious interpretation of our data with respect to whether LPO precedes or is linked to the initial stages of AD-like amyloidosis in Tg2576 mice ( Kawarabayashi et al.,…”
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Authors: Praticò, D., Uryu, K., Leight, S., Trojanoswki, J. Q., & Lee, V. M.-Y.
Affiliations: University of Pennsylvania (US)
ORCID: Praticò, Domenico
Uryu, Kunihiro
Lee, Virginia M.-Y.
Venue: The Journal of Neuroscience
Publisher: Society for Neuroscience
Published: 2001-06-15
Volume: 21
Issue: 12
Pages: 4183-4187
ISSN: 0270-6474 (ISSN-L)
1529-2401
DOI: 10.1523/jneurosci.21-12-04183.2001
PMC: PMC6762743
OpenAlex: W1954454186
Cited by: 777
References: 24
Citations by year: 2026: 4 · 2025: 15 · 2024: 17 · 2023: 29 · 2022: 19 · 2021: 32 · 2020: 23 · 2019: 27 · 2018: 16 · 2017: 24 · 2016: 24 · 2015: 28 · 2014: 32 · 2013: 37 · 2012: 48
FWCI: 22.76
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-sa
creativecommons.org/licenses/by-nc-sa/4.0/ (vor, 183 d)
Locations: Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: American Heart Association
National Institutes of Health (AG-11542)
National Institute on Aging (P01AG011542, AG 11542)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: lipid peroxidation, isoprostanes, amyloid-beta, amyloid plaques, Alzheimer's disease, Tg2576 mice, oxidative stress, Aβ40, amyloid-beta 42, brain oxidative damage, pathogenesis
MeSH terms: Aging, Alzheimer Disease, Amyloidosis, Animals, Brain, Cerebellum, Cerebral Cortex, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Female, Hippocampus, Male, Mice, Transgenic, Peptide Fragments, Lipid Peroxidation, Dinoprost, Amyloid beta-Peptides, Mice, Plaque, Amyloid

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Increased Lipid Peroxidation Precedes Amyloid Plaque Formation in an Animal Model of Alzheimer Amyloidosis

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