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Journal Article Ppublish 5 citations

PubMed: 39262376 DOI: 10.1080/19490976.2024.2395907

Fecal microbiota transplantation derived from mild cognitive impairment individuals impairs cerebral glucose uptake and cognitive function in wild-type mice: and TXNIP-GLUT signaling pathway.

Gut Microbes 16(1):2395907

Authors: Tao Wang, Ling Hao, Kexin Yang, Wenjing Feng, Zhiting Guo, Miao Liu, Rong Xiao

Affiliations

  • School of Public Health, Capital Medical University, Beijing, China.
  • School of Public Health, Capital Medical University, Beijing, China. Institute for Nutrition and Food Hygiene, Beijing Center for Disease Prevention and Control, Beijing, China.

Abstract

Gut microbiome dysbiosis has been widely implicated in cognitive impairment, but the identity of the specific bacterial taxa and mechanisms are not fully elucidated. Brain glucose hypometabolism coincides with the cognitive decline. This study explored the link among cognition, gut microbiota and glucose uptake based on the fecal microbiota transplantation from mild cognitive impairment individuals (MCI-FMT) and investigated whether similar mechanisms were involved in 27-hydroxycholesterol (27-OHC)-induced cognitive decline. Our results showed that the MCI-FMT mice exhibited learning and memory decline and morphological lesions in the brain and colon tissues. There were reduced F-fluorodeoxyglucose uptake, downregulated expression of glucose transporters (GLUT1,3,4) and upregulated negative regulator of glucose uptake (TXNIP) in the brain. MCI-FMT altered the bacterial composition and diversity of the recipient mice, and the microbial signatures highlighted by the increased abundance of recapitulated the negative effects of MCI bacterial colonization. However, inhibiting or TXNIP increased the expression of GLUT1 and GLUT4, significantly improving brain glucose uptake and cognitive performance in 27-OHC-treated mice. Our study verified that cognitive decline and abnormal cerebral glucose uptake were associated with gut microbiota dysbiosis; we also revealed the involvement of and molecular mechanisms of TXNIP-related glucose uptake in cognitive deficits caused by 27-OHC.

MeSH

Dysbiosis, Fecal Microbiota Transplantation, Brain, Colon, Cognitive Dysfunction, Cognition Disorders, Gastrointestinal Microbiome, Transplantation, Cognition, Microbiota

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