Targeting the Transferrin Receptor to Develop Erythropoietin for Alzheimer’s Disease

Alzheimer’s disease (AD) is the sixth leading cause of death in the United States with approximately 5.8 million Americans currently living with AD. Due to the lack of a disease modifying treatment for AD and the aging baby boomer generation, this number is projected to grow to 13.8 million by 2050 (Gaugler et al., 2019). Amyloid-beta (Aβ) plaque accumulation, one of the major pathological hallmarks of AD, can begin \u3e 20 years before clinical symptoms of AD. By the time AD is clinically diagnosed, neuronal loss and neuropathological lesions (Aβ plaques and tau tangles) have already occurred in many brain regions (Gaugler et al., 2019). AD dementia correlates highly with neuronal loss, and therefore, reduction of neuropathological lesions in the AD brain at the time of clinical diagnosis alone cannot reverse AD dementia. We propose that a therapy that combines a reduction of neuropathological lesions of AD along with neuronal repair and neurogenesis may be required to treat AD dementia