Particle Creation by Black Holes by Stephen Hawking
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Ferroptosis and Alzheimer's Disease: A Closer Look
What's this about?
This paper reviews research on a type of cell death called ferroptosis and how it might relate to Alzheimer’s disease. Alzheimer’s damages memory and thinking, mostly in older people.
What is Ferroptosis?
Ferroptosis is a way cells can die when too much iron and harmful molecules build up inside. It causes cells to shrink and parts called mitochondria to clump. This is different from other known types of cell death.
How Iron and Fats Cause Ferroptosis:
Too much iron in cells creates toxic molecules called ROS. This can start ferroptosis. Some proteins like HSPB1 help control iron and stop this.
Certain fats in cells can react and damage mitochondria, also causing ferroptosis. An enzyme called GPX4 normally stops this. Antioxidants like vitamin E help too.
ROS from excess iron accelerates the process.
Amino Acids are Protective:
Amino acids called GSH shield cells from damage. GSH requires the amino acid cysteine. Low GSH allows cell damage and ferroptosis.
Connecting Ferroptosis to Alzheimer’s Disease:
In Alzheimer’s, GSH is low in parts of the brain, suggesting early disease. More iron is also seen, which could start ferroptosis.
Proteins called Aβ and Tau in Alzheimer’s brain may interact with fats and worsen cell damage from ferroptosis.
Some genes linked to ferroptosis are more active in Alzheimer’s patients. Understanding ferroptosis could reveal new treatments.
Possible Alzheimer’s Treatments:
1. Remove excess iron with drugs called chelators - some success seen.
2. New drugs can target damaging fats - CMS121 fixes Aβ damage. Vitamin E slowed Alzheimer's for some.
3. Increase GSH to shield cells and repair damage - looks promising in models.
Other Ways to Protect the Brain:
Substances like Ginkgolide B and salidroside raise GPX4 levels, shielding cells. The amino acid cysteine helps make GSH through the Xc system, protecting the brain.
The Future:
More research on ferroptosis and the immune system could explain Alzheimer’s better. Important brain genes involved in ferroptosis are also being studied. Drugs to stop ferroptosis show potential. Understanding ferroptosis and Alzheimer's may lead to better treatments or prevention.
Author Contributions:
- Qi Han: Analyzed data
- Li Sun: Designed experiments and led project
- Qi Han & Ke Xiang: Edited the paper
Key References:
1. Scheltens et al. (2021). Recent review on Alzheimer’s disease. The Lancet.
2. Pleen & Townley (2022). Update on Alzheimer’s clinical trials. Journal of Neurology.
3. Trejo-Lopez et al. (2022). Details on brain changes in Alzheimer's. Neurotherapeutics.
4. Dixon et al. (2012). Introduced ferroptosis concept. Cell.
5. Mou et al. (2019). Ferroptosis in cancer. Journal of Hematology & Oncology.
6. Huang et al. (2020). Amyloid toxicity via ferroptosis. Cell Death & Disease.
7. Bao et al. (2021). Iron's role in Alzheimer’s memory loss. Cell Death & Differentiation.
8. Hirschhorn & Stockwell (2019). History of ferroptosis discovery. Free Radical Biology & Medicine.
9. Shao et al. (2021). Ginkgolide B for cognitive protection. Biochemical and Biophysical Research Communications.
10. Okada et al. (2019). Memantine protects the brain. Pharmacology Research & Perspectives.
See original paper for full citations. Links provided where available.
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