Research ReportErythropoietin attenuates Alzheimer-like memory impairments and pathological changes induced by amyloid β42 in mice

- EPO attenuates Aβ42-induced cognitive deficits in mice.
- EPO attenuates Aβ42-induced tau hyperphosphorylation through regulation of GSK-3β.
- EPO attenuates the Aβ42-induced mitochondrial dysfunction in the brain.
- EPO attenuates the Aβ42-induced neuronal apoptosis in the brain.

Amyloid beta (Aβ) is a key molecule in the neurodegenerative progression of Alzheimer׳s disease (AD). It is critical to develop a treatment that can arrest the Aβ-induced pathologic progression of AD. Erythropoietin (EPO) has various protective effects in the nervous system. However, the effect of EPO on Aβ-induced Alzheimer-like cognitive deficits and pathological changes remains unclear. In the present study, we observed that the treatment of mice with EPO (1000 IU/kg) attenuated Aβ42-induced cognitive deficits and tau hyperphosphorylation at multiple AD-related sites through the regulation of glycogen synthase kinase-3β (GSK-3β). We also observed that EPO attenuated the Aβ42-induced mitochondrial dysfunction and apoptosis in brain. These results indicate a potential role for EPO in AD therapy.