Lipid peroxidation triggers neurodegeneration: A redox proteomics view into the Alzheimer disease brain
Open accessAbstract
Lipid peroxidation involves a cascade of reactions in which production of free radicals occurs selectively in the lipid components of cellular membranes. Polyunsaturated fatty acids easily undergo lipid peroxidation chain reactions, which, in turn, lead to the formation of highly reactive electrophilic aldehydes. Among these, the most abundant aldehydes are 4-hydroxy-2-nonenal (HNE) and malondialdehyde, while acrolein is the most reactive. Proteins are susceptible to posttranslational modifications caused by aldehydes binding covalently to specific amino acid residues, in a process called Michael adduction, and these types of protein adducts, if not efficiently removed, may be, and generally are, dangerous for cellular homeostasis. In the present review, we focused the discussion on the selective proteins that are identified, by redox proteomics, as selective targets of HNE modification during the progression and pathogenesis of Alzheimer disease (AD). By comparing results obtained at different stages of the AD, it may be possible to identify key biochemical pathways involved and ideally identify therapeutic targets to prevent, delay, or treat AD.
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Lipid peroxidation is increased in Alzheimer disease and amnestic mild cognitive impairment brain or cerebrospinal fluid and in preclinical Alzheimer disease hippocampus, as shown by elevated protein-conjugated HNE, F2-isoprostanes, and F4-isoprostanes.
“Increased lipid peroxidation (a term explained in Table 1) in AD and aMCI brains or CSF and in PCAD hippocampus is further evidenced by rises in the levels of protein-conjugated HNE, F2-isoprostanes, and F4-isoprostanes8,11,12,13,15,16,19–23.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [22]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredLipid peroxidation and possibly other oxidative damage in synaptic membranes account for loss of long-term potentiation and other synaptic functions involved in learning and memory.
“These considerations support the notion that lipid peroxidation, and perhaps other forms of oxidative damage in synaptic membranes, accounts for the loss of long-term potentiation (LTP) and other synaptic functions involved in learning and memory12,15,16,20–22,34,35.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [22]
Section 1 says lipid peroxidation impairs membrane receptors and other membrane functions and may contribute to brain dysfunction. Section 2.1 reports that a lipid-peroxidation product alters glutamate transport in rat neocortical synaptosomes. These passages support a connection to impaired neuronal function, but the copy does not say that oxidative damage in synaptic membranes accounts for loss of long-term potentiation or other learning-and-memory functions. (LLM, conf=0.82)
Experimental — accuracy not yet measuredInjured neurons and oligodendrocytes have a low capacity for consuming FFAs and sequestering them into lipid droplets, making them more vulnerable to lipid-induced cytotoxicity in chronic inflammation.
“Injured neurons and oligodendrocytes have a low capacity for consuming FFAs and sequestering them into LDs61, making them more vulnerable to lipid-induced cytotoxicity in chronic inflammation62,63.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [62]
Section 1, “Lipid peroxidation and neurodegeneration” (page unavailable), says lipid peroxidation damages neuronal membranes and produces compounds that cause cellular damage. It does not establish the claimed vulnerability of oligodendrocytes or place that damage in chronic inflammation. The separate claim about FFA consumption and lipid-droplet sequestration is attached to citation 61, not to this source. (LLM, conf=0.83)
Experimental — accuracy not yet measured3-Nitrotyrosine and protein carbonyls are used as biomarkers of oxidative damage in the brain of Alzheimer's disease and mild cognitive impairment.
“3-nitrotyrosine and protein carbonyls, these last produced mainly by the action of free radicals on the peptide chain or by oxidation of amino acids, are used as biomarkers of oxidative damage in the brain of AD and MCI [18,24,31,32,33].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [33]
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Self-citation
- Authors
- Sultana, R., Perluigi, M., & Butterfield, D. A.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Butterfield, D. Allan
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2013-09
- Volume
- 62
- Pages
- 157-169
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3573239
- OpenAlex
- W2159518687
- Cited by
- 478
- References
- 173
- Citations by year
- 2026: 27 · 2025: 30 · 2024: 35 · 2023: 29 · 2022: 44 · 2021: 54 · 2020: 49 · 2019: 30 · 2018: 38 · 2017: 30 · 2016: 29 · 2015: 35 · 2014: 36 · 2013: 11 · 2012: 1
- FWCI
- 2.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Funders
- NIH (AG-05119, AG-029839)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- lipid peroxidation, Alzheimer's disease, neurodegeneration, 4-hydroxynonenal, malondialdehyde, acrolein, protein aldehyde adducts, redox proteomics, polyunsaturated fatty acids, oxidative stress, therapeutic target
- MeSH terms
- Aldehydes, Alzheimer Disease, Fatty Acids, Unsaturated, Gene Expression Regulation, Humans, Malondialdehyde, Nerve Degeneration, Protein Processing, Post-Translational, Proteins, Lipid Peroxidation
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