Lipid peroxidation and advanced glycation end products in the brain in normal aging and in Alzheimer's disease
Clicks: 179
ID: 120094
2002
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
30.0
/100
179 views
21 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #191 of 438 articles by views in acta neuropathologica
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 438 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
The cellular distribution of malondialdehyde (MDA) was assessed immunohistochemically in brain specimens from young and normal elderly subjects as well as patients with Alzheimer's disease (AD). MDA was increased in the cytoplasm of neurons and astrocytes in both normal aging and AD, but was rarely detected in normal young subjects. By electron microscopic immunohistochemistry, neuronal MDA formed cap-like linear deposits associated with lipofuscin, while glial MDA deposits surrounded the vacuoles in a linear distribution. In the hippocampus, neuronal and glial MDA deposition was marked in the CA4 region but mild in CA1. By examination of serial sections stained with anti-MDA and antibodies against an advanced glycation end product, N ε-(carboxymethyl)lysine (CML), neuronal and glial MDA deposition was colocalized with CML in AD, but only neuronal MDA was colocalized with CML in normal aged brains. Glial MDA, although abundant in the aged brain, typically was not colocalized with CML. In AD cases, MDA was colocalized with tau protein in CA2 hippocampal neurons; such colocalization was rare in CA1. MDA also was stained in cores of senile plaques. Thus, while both MDA and CML accumulate under oxidative stress, CML accumulation is largely limited to neurons, in normal aging, while MDA also accumulates in glia. In AD, both MDA and CML are deposited in both astrocytes and neurons.
| Reference Key |
dei2002actalipid
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Rika Dei;Akinori Takeda;Hisayoshi Niwa;Mei Li;Yuji Nakagomi;Masaki Watanabe;Toshiaki Inagaki;Yukihiko Washimi;Yoshinari Yasuda;Katsunori Horie;Toshio Miyata;Gen Sobue;Rika Dei;Akinori Takeda;Hisayoshi Niwa;Mei Li;Yuji Nakagomi;Masaki Watanabe;Toshiaki Inagaki;Yukihiko Washimi;Yoshinari Yasuda;Katsunori Horie;Toshio Miyata;Gen Sobue; |
| Journal | acta neuropathologica |
| Year | 2002 |
| DOI |
doi:10.1007/s00401-002-0523-y
|
| URL | |
| Keywords |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.