中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (5): 988-989.doi: 10.4103/1673-5374.297074

• 观点:退行性病与再生 • 上一篇    下一篇

潘多拉魔盒:来自微生物的淀粉样蛋白会加速阿尔茨海默病吗?

  

  • 出版日期:2021-05-15 发布日期:2020-12-29

A crate of Pandora: do amyloids from bacteria promote Alzheimer’s disease?

Vu Thu Thuy Nguyen, Kristina Endres*   

  1. Department of Psychiatry and Psychotherapy, University Medical Center Johannes 
    Gutenberg-University Mainz, Mainz, Germany
  • Online:2021-05-15 Published:2020-12-29
  • Contact: Kristina Endres, PhD, kristina.endres@unimedizin-mainz.de.
  • Supported by:
    This work was supported by funding from the MWWK, Germany (research consortium NeuroDegX).

摘要: https://orcid.org/0000-0002-1099-8287 (Kristina Endres) 

Abstract: AD is the predominant neurodegenerative disease within the elderly. Over 50 million patients suffer from dementia currently world-wide and an estimated tripling of numbers within the next 30 years is expected. Only one to maximally five percent of all cases of AD are based on mutations in the amyloid precursor protein (APP) gene or within the presenilin genes (PS1/PS2) and therefore are called familial (FAD). The majority of cases has to be designated as sporadic, which frankly only means that the origin of these cases is still enigmatic. Within the last 5 to 10 years new ideas have been born in regard to underlying causes of the sporadic manifestation by the re-discovery of our microbial commensals as important factors of health and disease of human beings. A growing number of studies reports on altered oral or gut microbial communities in AD patients as compared to unaffected, cognitively normal age-matched controls. However, still only restricted consensus of findings arises from these studies: Ruminococcus and S24-7 seem to be occasionally decreased while Odoribacter, Blautia, and Alistipes have repeatedly been shown to be increased in gut microbiota of patients or rodent disease models (Endres, 2019). Altered counts of single representatives of families or genera do not tell so much about physiologically relevant communities, functional interactions, or metabolites capable of triggering or preventing pathological alterations.