مقالات پذیرفته شده در هفتمین کنگره بین المللی زیست پزشکی
Fecal microbiota transplant as a potential treatment for Alzheimer’s disease (AD)
Fecal microbiota transplant as a potential treatment for Alzheimer’s disease (AD)
Nasrin Zare,1,*seyed Mohammad moein ghaemmaghami,2Ali Khodadadi,3Farzaneh Karampour,4
1. faculty of medical school najafabad branch Islamic azad university 2. faculty of medical school najafabad branch Islamic azad university 3. faculty of medical school najafabad branch Islamic azad university 4. faculty of medical school najafabad branch Islamic azad university
Introduction: Alzheimer’s disease (AD) is a neurodegenerative disorder that affects millions of people worldwide and can lead to cognitive impairment and progressive memory loss. The disease is characterized by the accumulation of tau-protein and β-amyloid plaques in the central nervous system (CNS), which affect neurons in the cortex of the brain, especially the hippocampus. AD worsens memory and can lead to people becoming unable to function independently in society. Given that AD is associated with abnormal gut microbiota, microbiota-targeted interventions such as fecal microbiota transplantation (FMT) might represent a potentially attractive therapeutic option against AD. The purpose of this study was to evaluate the significance of fecal microbiota transplantation (FMT) as a potential therapeutic option against Alzheimer’s disease (AD).
Methods: Our study was conducted on the PubMed database using the keywords “Fecal Microbiota Transplantation” and “Alzheimer Disease” since 2020. Out of 25 papers related to this topic, 15 were reviewed.
Results: Some previous studies have shown that the pathogenesis of Alzheimer’s disease (AD) is associated with the gut microbiome through the brain-gut axis. The imbalance of intestinal flora can stimulate microglia as cells of innate immunity and cause the secretion of pro-inflammatory cytokines. Additionally, short-chain fatty acids as metabolites of intestinal flora could regulate the synthesis of hormones. Therefore, microbiota-mediated intestinal and systemic immune aberrations and alteration in peripheral circulating hormones contribute to the pathogenesis of AD. Furthermore, The bacterial community and genetic background might be correlated to AD severity and progression. These findings provide a novel framework for understanding the role of gut microbiota in AD. Findings have suggested that FMT seems a possible treatment route because it could improve cognitive function in AD by glial reactivation, slowing Aβ plaque deposition, recovering synaptic dysfunction and neuroinflammation, and decreasing the tau-protein.
Conclusion: The protective effects of FMT may be related to reversing alterations of gut microbiota and its metabolites. However, more research in this area may lead to both novel treatments and a better understanding of the mechanisms behind Alzheimer's disease.