Brain-targeting liposome-based <i>APOE2</i> gene delivery exacerbates soluble amyloid-β accumulation in <i>App</i> ^NL-G-F mice.

ABSTRACT: Alzheimer's disease (AD) is the most common cause of late-life dementia characterized by progressive neurodegeneration and brain deposition of amyloid-β (Aβ) and phosphorylated tau. The APOE ε2 encoding apolipoprotein E (APOE2) is a protective allele against AD among the three genotypes (APOE ε2, ε3, ε4), while APOE4 is the strongest genetic factor substantially increasing AD risk. APOE regulates brain lipid homeostasis and maintaining synaptic plasticity and neuronal function, where APOE2 has a superior function compared to APOE3 and APOE4. Gene therapy that increases APOE2 levels in the brain is, therefore, a promising therapeutic strategy for AD treatment. We previously reported that PEGylated liposomes conjugated with transferrin

SUBMITTER: Wang N 

PROVIDER: S-EPMC11538761 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature