Pickering Andrew M
bioRxiv. 2024 Oct 20:2024.10.17.618893. doi: 10.1101/2024.10.17.618893.
The aging brain experiences a significant decline in proteasome function, The proteasome is critical for many key neuronal functions including neuronal plasticity, and memory formation/retention. Treatment with proteasome inhibitors impairs these processes. Our study reveals a marked reduction in 20S and 26S proteasome activities in aged mice brains driven by reduced functionality of aged proteasome. This is matched by a decline in 20S proteasome but an increase in 26S proteasome. Our data suggests this may be a compensatory response to reduced functionality. By overexpressing the proteasome subunit PSMB5 in the neurons of mice, enhancing proteasome function, we slowed age-related declines in spatial learning and memory as well neuromuscular declines. We then showed acute treatment with a proteasome activator to rescue spatial learning and memory deficits in aged mice. These findings highlight the potential of proteasome augmentation as a therapeutic strategy to mitigate age-related cognitive declines.
衰老的大脑在蛋白酶体功能方面会出现显著下降。蛋白酶体对于许多关键的神经元功能至关重要,包括神经元可塑性以及记忆形成/保留。用蛋白酶体抑制剂进行治疗会损害这些过程。我们的研究表明,衰老小鼠大脑中20S和26S蛋白酶体活性显著降低,这是由衰老蛋白酶体功能降低所驱动的。这与20S蛋白酶体的下降相匹配,但26S蛋白酶体有所增加。我们的数据表明,这可能是对功能降低的一种补偿性反应。通过在小鼠神经元中过表达蛋白酶体亚基PSMB5来增强蛋白酶体功能,我们减缓了与年龄相关的空间学习和记忆下降以及神经肌肉衰退。然后我们表明,用蛋白酶体激活剂进行急性治疗可挽救衰老小鼠的空间学习和记忆缺陷。这些发现凸显了增强蛋白酶体作为一种减轻与年龄相关的认知衰退的治疗策略的潜力。