Young microbiota rejuvenates the aging brain

Heijtz, Rochellys Diaz; Gonzalez-Santana, Ayoze; Laman, Jon D.

doi:10.1038/s43587-021-00100-z

Cited by 5 publications

(1 citation statement)

References 15 publications

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“…This age-related gut microbiota status further accelerates aging [ 4 ]; thus, the intestinal tract is considered a key target organ for improving health in elderly animals and humans [ 11 ]. Previous data have shown that the transplantation of gut microbiota from young to old mice can decrease cognitive impairment, reverse differences in hippocampal metabolites, and reduce peripheral and brain inflammation, which can delay brain aging [ 12 ]. Moreover, it has been reported that related probiotics can prolong the lifespan of Drosophila melanogaster through microbiota-brain communication by preventing and treating neurodegeneration and cardiovascular disease, in addition to reducing physiological and oxidative stress [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Atp11b Deletion Affects the Gut Microbiota and Accelerates Brain Aging in Mice

Liu

Zhang²,

Shi³

et al. 2022

Brain Sciences

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The microbiota-gut-brain axis has attracted significant attention with respect to studying the mechanisms of brain aging; however, the specific connection between gut microbiota and aging remains unclear. The abnormal expression and mutation of proteins belonging to the P4-ATPase family, including Atp11b, results in a variety of neurological diseases. The results of our analysis demonstrate that there was a shift in the abundance of certain gut microbiota in Atp11b-knockout (KO) mice. Specifically, there was an increase in pro-inflammatory bacteria that accelerate aging and a decrease in probiotics that delay aging. Consequently, an enhanced oxidative stress response was observed, which was characterized by a reduction in the superoxide dismutase (SOD) activity and an increase in malondialdehyde (MDA) and reactive oxygen species (ROS) levels. In addition, our data demonstrate that there was a decrease in the number of cells in the dentate gyrus (DG) region of the hippocampus, and aggravation of aging-related pathological features such as senescence β-galactosidase (SA-β-Gal), p-HistoneH2AX (Ser139), and p16INK4. Moreover, KO mice show typical aging-associated behavior, such as memory impairment and slow pain perception. Taken together, we demonstrate a possible mechanism of aging induced by gut microbiota in Atp11b-KO mice, which provides a novel perspective for the treatment of aging through the microbiota-gut-brain axis.

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