4‐Hydroxynonenal‐Derived Advanced Lipid Peroxidation End Products Are Increased in Alzheimer's Disease

@article{Sayre19974HydroxynonenalDerivedAL,
  title={4‐Hydroxynonenal‐Derived Advanced Lipid Peroxidation End Products Are Increased in Alzheimer's Disease},
  author={L. Sayre and Dawn A. Zelasko and P. Harris and G. Perry and R. G. Salomon and Mark A. Smith},
  journal={Journal of Neurochemistry},
  year={1997},
  volume={68}
}
Abstract: Recent studies have demonstrated oxidative damage is one of the salient features of Alzheimer's disease (AD). In these studies, glycoxidation adduction to and direct oxidation of amino acid side chains have been demonstrated in the lesions and neurons of AD. To address whether lipid damage may also play an important pathogenic role, we raised rabbit antisera specific for the lysine‐derived pyrrole adducts formed by lipid peroxidation‐derived 4‐hydroxynonenal (HNE). These antibodies… Expand
Protein‐Bound Acrolein
TLDR
The results suggest that protein‐bound acrolein is a powerful marker of oxidative damage to protein and support the hypothesis that lipid peroxidation and oxidativedamage to protein may play a crucial role in the formation of neurofibrillary tangles and to neuronal death in AD. Expand
Role of by-products of lipid oxidation in Alzheimer's disease brain: a focus on acrolein.
TLDR
Interestingly, data indicates that lipid peroxidation occurs in the brain of MCI and also in preclinical AD patients suggesting that oxidative damage may play an early role in the pathogenesis of AD. Expand
Increased F2‐isoprostanes in Alzheimer's disease: evidence for enhanced lipid peroxidation in vivo
Alzheimer's disease (AD) includes a group of dementing neurodegenerative disorders that have diverse etiologies but the same hallmark brain lesions. Since oxidative stress may play a role in theExpand
Four-Hydroxynonenal, a Product of Lipid Peroxidation, is Increased in the Brain in Alzheimer’s Disease
TLDR
This study reports an increase in mean free HNE in multiple brain regions in AD compared with age-matched control subjects and suggests that HNE may be an important substance in the pathogenesis of neuron degeneration in AD. Expand
The Lipid Peroxidation Product 4‐Hydroxynonenal Inhibits Neurite Outgrowth, Disrupts Neuronal Microtubules, and Modifies Cellular Tubulin
TLDR
It is shown that 4‐hydroxy‐2(E)‐nonenal (HNE), a major product of lipid peroxidation, inhibits neurite outgrowth and disrupts microtubules in Neuro 2A cells and that cellular tubulin is one of the major proteins modified by HNE and that the HNE adduction to tubulin occurs via Michael addition. Expand
4‐Hydroxynonenal Immunoreactivity is Increased in Human Hippocampus After Global Ischemia
TLDR
A marked increase in neuronal and glial 4‐HNE immunoreactivity was significantly increased in neurons and glia in the hippocampal formation after global ischemia, substantiates a role for lipid peroxidation in the pathogenesis of cerebral ischemIA. Expand
Crotonaldehyde accumulates in glial cells of Alzheimer’s disease brain
TLDR
The results suggest that increased oxidative stress and CRA formation in glial cells is implicated in the disease processes of AD. Expand
Potential implications of endogenous aldehydes in β‐amyloid misfolding, oligomerization and fibrillogenesis
TLDR
Formaldehyde, methylglyoxal and malondialdehyde and, to a lesser extent, 4‐hydroxynonenal are not only capable of enhancing the rate of formation of β‐amyloid β‐sheets, oligomers and protofibrils but also of increasing the size of the aggregates. Expand
Hydroxynonenal-generated crosslinking fluorophore accumulation in Alzheimer disease reveals a dichotomy of protein turnover.
TLDR
Findings directly implicate lipid crosslinking peroxidation products as accumulating not in the lesions or the lipofuscin pathways, but instead in a distinct pathway, GVD, that accumulates cytosolic proteins. Expand
12/15-lipoxygenase is increased in Alzheimer's disease: possible involvement in brain oxidative stress.
TLDR
Data show that the 12/15-LOX metabolic pathway is increased and correlates with an oxidative imbalance in the AD brain, implying that this enzyme might contribute to the pathogenesis of this neurodegenerative disorder. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 39 REFERENCES
E-4-hydroxy-2-nonenal is cytotoxic and cross-links cytoskeletal proteins in P19 neuroglial cultures.
TLDR
E-4-hydroxy-2-nonenal may contribute to neurodegeneration and neurofibrillary tangle formation in Alzheimer's disease. Expand
Evidence of neuronal oxidative damage in Alzheimer's disease.
TLDR
The presence of nitrotyrosine is demonstrated in neurofibrillary tangles of Alzheimer's disease and this findings further implicate nitric oxide expression and excitotoxicity in the pathogenesis of cell death in Alzheimer’s disease. Expand
Crosslinking of Apolipoprotein E by Products of Lipid Peroxidation
TLDR
Data suggest that HNE covalently crosslinks APOE in P19 neuroglial cultures to form a 50 kDa protein, and that similar modifications of APOE appear to occur in vivo. Expand
Glycated tau protein in Alzheimer disease: a mechanism for induction of oxidant stress.
  • S. Yan, X. Chen, +7 authors M. Smith
  • Chemistry, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1994
TLDR
It is proposed that in Alzheimer disease, AGEs in paired helical filament tau can induce oxidant stress, thereby promoting neuronal dysfunction, and being ideal substrates for nonenzymatic glycation. Expand
Advanced Maillard reaction end products are associated with Alzheimer disease pathology.
  • M. Smith, S. Taneda, +6 authors G. Perry
  • Chemistry, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1994
TLDR
Evidence is presented that antibodies against two Maillard end products, pyrraline and pentosidine, immunocytochemically label neurofibrillary tangles and senile plaques in brain tissue from patients with Alzheimer disease contain modifications typical of advanced Maillard reaction end products. Expand
Advanced glycation end products contribute to amyloidosis in Alzheimer disease.
TLDR
The results suggest that the in vivo half-life of beta-amyloid is prolonged in AD, resulting in greater accumulation of AGE modifications which in turn may act to promote accumulation of additional amyloid. Expand
Heme oxygenase-1 is associated with the neurofibrillary pathology of Alzheimer's disease.
TLDR
The increase in heme oxygenase-1 protein in association with the neurofibrillary pathology of Alzheimer's disease and other diseases characterized by neurofigrillary tangles supports the notion that the generation of free radicals and oxidative stress plays a role in the pathogenesis of neurofibillary pathology. Expand
Non-enzymatically glycated tau in Alzheimer's disease induces neuronal oxidant stress resulting in cytokine gene expression and release of amyloid β-peptide
TLDR
Insight is provided into how PHF-tau disturbs neuronal function, and a growing body of evidence that oxidant stress contributes to the pathogenesis of AD is added. Expand
Structural definition of early lysine and histidine adduction chemistry of 4-hydroxynonenal.
TLDR
The structures of first-formed His- and Lys-based adducts were elucidated by correlating NMR spectral properties with those obtained on models with reduced chiral center content, in some cases following hydride reduction. Expand
Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes.
TLDR
This review provides a comprehensive summary on the chemical properties of 4-hydroxyalkenals and malonaldehyde, the mechanisms of their formation and their occurrence in biological systems and methods for their determination, as well as the many types of biological activities described so far. Expand
...
1
2
3
4
...