中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (12): 2251-2252.doi: 10.4103/1673-5374.284994

• 观点:退行性病与再生 • 上一篇    下一篇

重新设计促红细胞生成素以治疗阿尔茨海默病

  

  • 出版日期:2020-12-15 发布日期:2020-08-04

Targeting the transferrin receptor to develop erythropoietin for Alzheimer’s disease

Rachita K. Sumbria   

  1. Department of Biopharmaceutical Sciences, School of Pharmacy and Health Sciences, Keck Graduate Institute, Claremont; Department of Neurology, University of California, Irvine, CA, USA
  • Online:2020-12-15 Published:2020-08-04
  • Contact: Rachita K. Sumbria, PhD, rsumbria@kgi.edu.
  • Supported by:
    This work was supported by grants from the National Institute of Health, NIA R21AG055949 and R01AG062840.

摘要: orcid: 0000-0002-7459-0723 (Rachita K. Sumbria)

Abstract: 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 pro- jected to grow to 13.8 million by 2050 (Gaugler et al., 2019). Amy- loid-beta (Aβ) plaque accumulation, one of the major pathological hallmarks of AD, can begin > 20 years before clinical symptoms of AD. By the time AD is clinically diagnosed, neuronal loss and neu- ropathological lesions (Aβ plaques and tau tangles) have already occurred in many brain regions (Gaugler et al., 2019). AD demen- tia 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.