Selenium attenuates A beta production and A beta-induced neuronal death
A-Ryeong Gwon1, Jong-Sung Park, Jun-Hyung Park
1College of Pharmacy, Sungkyunkwan University, 300 Cheoncheon-dong, Suwon 440-746, Republic of Korea.
Neuroscience Letters
|December 23, 2009
Summary
Selenium supplementation can reduce beta-amyloid production and protect neurons from toxicity. This suggests selenium may help prevent neuronal degeneration in Alzheimer's disease.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Alzheimer's disease (AD) is characterized by amyloid-beta (A beta) peptide accumulation.
- A beta production and subsequent neuronal death are key pathological events in AD.
Purpose of the Study:
- To investigate the effects of selenium on amyloid-beta (A beta) metabolism.
- To determine selenium's role in preventing A beta-induced neuronal death.
Main Methods:
- Assessed the impact of selenium on A beta 40, A beta 42, and soluble amyloid precursor protein beta (sAPP beta) levels.
- Measured beta-secretase (BACE1) and gamma-secretase activities.
- Evaluated selenium's protective effects against 4-Hydroxynonenal (HNE) and A beta toxicity in primary neuronal cultures.
Main Results:
- Selenium significantly reduced A beta 40, A beta 42, and sAPP beta production.
- Selenium inhibited beta-secretase and gamma-secretase activities.
- Selenium blocked HNE-induced transcription of beta-secretase (BACE1).
- Selenium protected primary neurons from HNE and A beta-mediated toxicity.
Conclusions:
- Selenium limits beta-amyloid production by reducing secretase activities.
- Selenium exhibits neuroprotective properties against A beta and oxidative stress.
- Selenium may offer a therapeutic strategy for Alzheimer's disease by mitigating A beta pathology and neuronal death.
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