Lipid peroxidation triggers neurodegeneration: a redox proteomics view into the Alzheimer disease brain.
TLDR
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.About:
This article is published in Free Radical Biology and Medicine.The article was published on 2013-09-01 and is currently open access. It has received 397 citations till now. The article focuses on the topics: Lipid peroxidation & Cellular homeostasis.read more
Citations
More filters
Journal ArticleDOI
Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease
TL;DR: Current research on the interplay and sequence of oxidative damage related to impaired brain glucose metabolism and proteostasis defects are summarized and potential pharmacological interventions to retard AD progression are suggested.
Journal ArticleDOI
13 reasons why the brain is susceptible to oxidative stress.
TL;DR: 13 reasons why the brain is susceptible to oxidative stress are rationalised and key reasons include inter alia unsaturated lipid enrichment, mitochondria, calcium, glutamate, modest antioxidant defence, redox active transition metals and neurotransmitter auto-oxidation.
Journal ArticleDOI
The development of the concept of ferroptosis.
TL;DR: The history of observations consistent with the current definition of ferroptosis, as well as the advances that contributed to the emergence of the concept, are described.
Journal ArticleDOI
Neuron-Astrocyte Metabolic Coupling Protects against Activity-Induced Fatty Acid Toxicity
Maria S. Ioannou,Jesse Jackson,Shu-Hsien Sheu,Chi-Lun Chang,Aubrey V. Weigel,Hui Liu,H. Amalia Pasolli,C. Shan Xu,Song Pang,Doreen Matthies,Harald F. Hess,Jennifer Lippincott-Schwartz,Zhe Liu +12 more
TL;DR: These findings reveal that FA metabolism is coupled in neurons and astrocytes to protect neurons from FA toxicity during periods of enhanced activity, which could underlie both homeostasis and a variety of disease states of the brain.
Journal ArticleDOI
Ferroptosis and Its Role in Diverse Brain Diseases.
TL;DR: This review summarizes current research on ferroptosis, its underlying mechanisms, and its role in the progression of different neurologic diseases and provides valuable information regarding treatment and prevention of these devastating diseases.
References
More filters
Journal ArticleDOI
Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes.
TL;DR: 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.
Book ChapterDOI
Determination of aldehydic lipid peroxidation products: malonaldehyde and 4-hydroxynonenal
TL;DR: This chapter discusses the methods used for the qualitative and quantitative determination of aldehydes in biological systems and focuses on 4-hydroxynonenal and malondialdehyde, which are in many instances the most abundant individual aldehyde resulting from lipid peroxidation.
Journal ArticleDOI
THE HEME OXYGENASE SYSTEM:A Regulator of Second Messenger Gases
TL;DR: This review highlights the current information on molecular and biochemical properties of HO-1 and HO-2 and addresses the possible mechanisms for mutual regulatory interactions between the CO- and NO-generating systems.
Journal ArticleDOI
Oxidative stress hypothesis in alzheimer's disease
TL;DR: Supporting indirect evidence comes from a variety of in vitro studies showing that free radicals are capable of mediating neuron degeneration and death, suggesting that therapeutic efforts aimed at removal of ROS or prevention of their formation may be beneficial in AD.
Journal ArticleDOI
Gene regulation and DNA damage in the ageing human brain.
TL;DR: This article showed that DNA damage is markedly increased in the promoters of genes with reduced expression in the aged cortex, and these gene promoters are selectively damaged by oxidative stress in cultured human neurons, and show reduced base-excision DNA repair.