Mice with the Alzheimer's disease-associated APOE4 and the APOE2 genes were more likely to die from COVID-19 than those with the APOE3 gene. Those with APOE4 and APOE2 genes had more virus replication in the lungs, higher inflammation, and increased tissue damage following coronavirus infection.
Inhibiting the NHE6 gene abolished the formation of amyloid-beta plaques in mouse models of Alzheimer's disease.
ApoE2 appears to have neuroprotective properties and could be key in the fight against Alzheimer's disease, according to a new study.
A new study reports even low levels of APOE4 can increase beta-amyloid plaques in the brain and neuronal damage in mouse models of Alzheimer's disease. However, introducing APOE2 can reduce amyloid deposits and other associated damage.