Our results indicate that DREAM inhibition markedly improves ATF6 processing in the hippocampus and that it might contribute to a delay in memory decline in HD mice.
Here we aimed to explore whether ATF5 is also expressed by neurons in human brain both in basal conditions and in Huntington's disease (HD), where UPR has been described to be partially impaired due to defective ATF6 processing.
Our results suggest that the ATF6α/Rheb pathway is altered in Huntington's disease as the decrease in ATF6α processing is accompanied by a decrease in the accumulation of Rheb.