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Live-Cell Imaging Shows Proteasome Activation Improves Neuronal Survival in AD Model

AJAS · 2026 Biomedical and Health Sciences (inferred)

Lucas D'Cruz · Ohio Academy of Science, The

Overview

Alzheimer’s Disease (AD) is an incurable neurodegenerative disease (NDD) that affects ~11% of adults over the age of 65. AD, like many other NDDs, is characterized by a buildup of misfolded proteins intracellularly and extracellularly, partially due to an impaired ubiquitin-proteasome system (UPS). The proteasome is responsible for degrading misfolded proteins, and is further compromised by oxidative stress from excitotoxicity from excess glutamate levels. Compound A is a novel small molecule proteasome activator that has previously been shown to increase proteasome activity in cancer cells. Here, the effect of Compound A on proteasome activity and cell viability was examined to determine the drug’s efficacy in a cellular model of Alzheimer’s disease. Mouse hippocampal neuronal HT-22 cells were treated with Compound A, then assayed for 20S proteasome activity after 72 hours. To test the efficacy of Compound A for neuronal cell viability, untreated HT-22 cell viability was compared to cells treated with Compound A using propidium iodide staining and fluorescence microscopy (using the Satrorious IncuCyte Live-Cell Imager) over 88 hours. Results demonstrated that Compound A treatment trended toward a ~4.3-fold (p = 0.06) increase in proteasome activity after 72 hours. Additionally, Compound A outperformed 20 published proteasome activators in a comparative screen. Excitotoxicity-induced HT-22 cells treated with Compound A reduced neuronal death by 67% at 88 hours. Future tests of Compound A treatment will determine whether the drug decreases the presence of aggregating, misfolded proteins and whether Compound A has potential for therapeutic development for Alzheimer’s Disease or similar diseases.

Competition history

  • AJAS 2026 Category not listed

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Source: AAAS Annual Meeting (Confex) / American Junior Academy of Science

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