Gerasimov KA, Ignasheva YE, Dobryakova YV, Korotkova TA, Koryagina AA, Markevich VA, Bolshakov AP (2026) Overexpression of WNT3a in the hippocampus can partly alleviate deficits in animal models of Alzheimer’s Disease. Neurochem Res 51(3):174. doi: 10.1007/s11064-026-04793-9 PMID: 42185674
Objective: To investigate whether enhancing WNT signaling through hippocampal overexpression of the WNT3a ligand can mitigate functional deficits in two distinct animal models of Alzheimer’s disease (AD) pathology.
Summary: The authors used a rat model of cholinergic deficit, induced by intraseptal 192-IgG-SAP injections, and a transgenic 5XFAD mouse model of amyloidosis. Findings demonstrate that targeted WNT3a overexpression in the hippocampus can partially alleviate synaptic and functional deficits in AD models by directly modulating synaptic plasticity, primarily through the restoration of the Wnt/β-catenin pathway.
Usage: Rat model with intraseptal 192-IgG-SAP (IT-01) injections
Related Products: 192-IgG-SAP (Cat. #IT-01)