The Effect Of FPR2 Deficiency In The ICV-STZ Mouse Models Of Alzheimer’s Disease

Background: Alzheimer’s disease is a common neurological degenerative disease and pathologically mainly shows up as the extracellular senile plaques and the intracellular neurofibrillary tangles(NFTs)made up by hyper-phosphorylated tau protein.With the global population aging aggravated,AD has become an important threat to the health of the elderly.Formyl peptide receptor 2(FPR2)is a representative G protein-coupled receptor,mainly expressed on the surface of macrophages in mammals.Studies have shown that Aβ can specifically activate FPR2,promote the migration and activation of glial cells,and thus promote the inflammatory response in the brain of AD patients.Activated FPR2 can produce neurotoxic effects by the release of nitric oxide,hydrogen peroxide,glutamic acid and cytokines,while the FPR2 receptor forms more betaamyloid deposition through Aβ42 reuptake,which is the core component of senile plaques.However,it is unclear whether FPR2 is involved in tau hyperphosphorylation in AD.Strategy: Build ICV-STZ(intracerebroventricular injecttion of Streptozotocin)mice models to detect whether FPR2 have an effect on tau hyperphosphorylation.Using Morris water maze and other behavioral experiments to detect whether the learning and memory ability of mice were affected.By using Western blotting,the level of tau hyperphosphorylation in the mice hippocampus was detected.Immunofluorescence staining was used to evaluate the tau hyperphosphorylation in brain of ICV-STZ mice.Results: The deficiency of FPR2 may reverse the loss of learning ability of AD mice model and can also reduce tau hyperphosphorylation.Conclusions: Results of the study suggested that FPR2 is involved with the learning impairment and tau hyperphosphorylation in ICV-STZ AD mouse model.FPR2 may become a new potential target for AD prevention and therapy.