Abstract
Neuropathological studies have demonstrated that the presence of neurofibrillary tangles (NFTs) is one of the most prominent pathologic characteristics of Alzheimer's disease (AD). The microtubule-associated protein tau is the major component of NFTs, and its abnormal hyperphosphorylation leads to the destabilization of microtubules, impaired axonal transport, and eventual death of the neurons. The hematopoietic cytokine erythropoietin (Epo) is now considered as a viable agent with regard to central nervous system injury in a variety of cellular systems. Here we report that Epo prevented tau hyperphosphorylation in SH-SY5Y cells exposed to the beta-amyloid peptide and that this effect may depend on the PI3K/Akt-GSK-3beta pathway. This study provides new molecular insight into the neuroprotective effect of Epo and suggests its possible therapeutic role in the management of AD.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
