AI Article Synopsis
- Researchers found that regulating autophagy can help improve learning and memory by reducing beta-amyloid peptide (Aβ) buildup in the brain after a stroke.
- They focused on BACE1, an enzyme that influences Aβ production, to better understand how this regulation works.
- Experiments showed that oxygen-glucose deprivation or the autophagy inducer Rapamycin decreased BACE1 levels, while the autophagy inhibitor 3-methyladenine increased BACE1 levels, confirming the link between autophagy and BACE1 expression.
Article Abstract
Our previous findings have demonstrated that autophagy regulation can alleviate the decline of learning and memory by eliminating deposition of extracellular beta-amyloid peptide (Aβ) in the brain after stroke, but the exact mechanism is unclear. It is presumed that the regulation of beta-site APP-cleaving enzyme 1 (BACE1), the rate-limiting enzyme in metabolism of Aβ, would be a key site. Neuro-2a/amyloid precursor protein 695 (APP695) cell models of cerebral ischemia were established by oxygen-glucose deprivation to investigate the effects of Rapamycin (an autophagy inducer) or 3-methyladenine (an autophagy inhibitor) on the expression of BACE1. Either oxygen-glucose deprivation or Rapamycin down-regulated the expression of BACE1 while 3-methyladenine up-regulated BACE1 expression. These results confirm that oxygen-glucose deprivation down-regulates BACE1 expression in Neuro-2a/APP695 cells through the introduction of autophagy.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625509 | PMC |
| http://dx.doi.org/10.4103/1673-5374.165511 | DOI Listing |
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