Decreased amyloid-β and increased neuronal hyperactivity by immunotherapy in Alzheimer's models

Among the most promising approaches for treating Alzheimer's disease is immunotherapy with amyloid-beta (A beta)-targeting antibodies. Using in vivo two-photon imaging in mouse models, we found that two different antibodies to A beta used for treatment were ineffective at repairing neuronal dysfunction and caused an increase in cortical hyperactivity. This unexpected finding provides a possible cellular explanation for the lack of cognitive improvement by immunotherapy in human studies.