Impaired 26S proteasome causes leaning and memory deficiency and induces neuroinflammation mediated by NF-κB in mice.

Background

Aging and many neurodegenerative disorders, including Alzheimer's disease (AD), show reduced proteasome activity, loss of synapses and increased neuroinflammation in the brain. However, whether proteasome dysfunction causes neuroinflammation remains less understood.

Methods

Here, we studied the effect of impaired 26S proteasome on neuroinflammation in the

Results

Our results revealed that impaired 26S proteasome led to AD-like cognitive deficiency and overt neuroinflammation in the synapses of the

Conclusions

These data indicate that impaired 26S proteasome causes AD-like cognitive deficiency and induces neuroinflammation mediated largely by NF-κB, which will help develop effective therapeutics and aid to better understand the pathogenesis of AD and many other neurodegenerative disorders where impaired proteasome is consistently coupled with neuroinflammation.