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Amyloid-β precursor protein facilitates the regulator of calcineurin 1-mediated apoptosis by downregulating proteasome subunit α type-5 and proteasome subunit β type-7
Amyloid-beta precursor protein may help cell death control by lowering specific protein breakdown components
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Abstract
APP overexpression significantly increased RCAN1 levels in cells and transgenic mice.
- Individuals with Down syndrome develop Alzheimer's disease neuropathology due to trisomy of chromosome 21.
- Amyloid-β protein, linked to neuritic plaques, is produced from amyloid-β precursor protein (APP).
- APP overexpression reduced the expression of two proteasome subunits, potentially leading to impaired degradation of RCAN1.
- Inhibition of RCAN1 expression diminished APP-induced neuronal cell death.
- The findings suggest that APP regulates neuronal apoptosis through the proteasome pathway, contributing to Alzheimer's disease in Down syndrome.
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