Giulia Colombo MicrobiotaMi

MicrobiotaMi Comment 30_21  by Giulia Colombo

Related Journal Article:  Age-related cognitive decline is associated with microbiota-gut-brain axis disorders and neuroinflammation in mice

This article was published in the: Behav Brain Res. 2021 Mar 26;402:113125. doi: 10.1016/j.bbr.2021.113125. Epub 2021 Jan 7. PMID: 33422597

A gut matter: the parallel aging of the microbiota and the brain

Age-related cognitive decline is associated with chronic low grade neuroinflammation that may result from a complex interplay among many factors, such as bidirectional communication between the central nervous system (CNS) and gut microbiota. This usually occurs through the immune, the neuroendocrine and the vagal pathways. Wu et al. compared 2-month-old (young) and 15-month-old (aged) mice to explore the potential association between age-related cognitive decline and the microbiota-gut-brain axis disorder.

Aged mice exhibit deficits in learning and memory, paralleled by a decrease in hippocampal neuronal and synaptic density. They also exhibit significant dysbiosis of the gut microbiota, that is a reduction in diversity and a loss of beneficial microbic taxa. Widespread disruptions of the intestinal barrier and blood-brain barrier is also present and can be the cause of increased intestinal, low-grade systemic and cerebral inflammation. In fact, plasma and brain levels of lipopolysaccharide – an essential component of Gram-negative bacteria’s wall and inflammatory signal for the immune system – are significantly higher in aged mice compared with young mice, with increasing expression of Toll-like receptor 4 (TLR4), myeloid differential protein-88 (MyD88) and nuclear translocation of nuclear factor κB (NF-κB) in intestinal and brain tissues. The activation of the TLR4/MyD88/NF-κB signalling pathway probably underlies the overproduction of the pro-inflammatory cytokines IL-1β, IL-6 and TNFα as measured in aged mice’s blood.

These data show that microbiota-gut-brain axis dysfunction that occurs through LPS-induced activation of the TLR4/NF-κB signalling pathway can be implicated in age-related neuroinflammation and cognitive decline. Given that the two-way biochemical communication of the microbiota-gut-brain axis has been shown to play an important role in regulating neuroethology and cognition in humans, also neurodegenerative diseases may be triggered or worsened by gut-microbiota dysbiosis through a chronic low-level inflammatory disorder.

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