Alzheimers disease (AD) is a neurological disorder that causes the buildup of amyloid-beta plaques and neurofibrillary tangles in the brain. One key mechanism designed to mitigate the buildup of these misfolded proteins is the ubiquitin-proteasome system (UPS). In healthy individuals, the UPS marks these amyloid-beta plaques and neurofibrillary tangles with ubiquitin markers, facilitating their subsequent degradation by the proteasome complex. The UPS is critical for the degradation of the proteins, and its dysfunction has been observed in AD. In this paper, a potential treatment for diminishing dysfunction of the ubiquitin-proteasome system is composed for Alzheimers disease individuals. This research paper explores the correlation between impaired UPS and AD, focusing on its role in degrading damaged proteins. The paper also collects evidence suggesting that enhancing the ubiquitin-proteasome system can have a positive impact on clearing amyloid-beta plaques and neurofibrillary tangles. Additionally, potential UPS-based treatments for AD, such as PA28 activators and natural compounds, are investigated.
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Yan et al. (2024) studied this question.
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