Selenium Nanoparticles-Enriched Lactobacillus casei ATCC 393 Prevents Cognitive Dysfunction in Mice Through Modulating Microbiota-Gut-Brain Axis

Oct 17, 2022International journal of nanomedicine

Selenium Nanoparticle-Enhanced Lactobacillus casei May Prevent Memory Problems in Mice by Changing Gut Bacteria and Brain Communication

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Abstract

Thirteen weeks of treatment with ATCC 393-SeNPs significantly improved cognitive dysfunction in mice with Alzheimer's disease.

ATCC 393-SeNPs reduced amyloid beta aggregation and hyperphosphorylation of TAU protein, which are associated with Alzheimer's disease.
The treatment prevented neuronal death by affecting key signaling pathways related to brain health.
ATCC 393-SeNPs improved intestinal barrier function and increased antioxidant capacity compared to standard ATCC 393.
The intervention restored gut microbiota balance and boosted levels of short-chain fatty acids and neurotransmitters.
ATCC 393-SeNPs inhibited microglial activation and provided protection against oxidative stress and neuroinflammation.

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PURPOSE: The bidirectional communication between the gut and the central nervous system mediated by gut microbiota is closely related to the occurrence and development of neurodegenerative diseases, including Alzheimer's disease (AD). Selenium (Se) has been identified as playing a role against AD. Probiotics have beneficial effects on host brain function and behavior by modulating the microbiota-gut-brain axis. Herein, we evaluated the protective effects ofATCC 393 (ATCC 393) and selenium nanoparticles-enrichedATCC 393 (ATCC 393-SeNPs) against D-galactose/aluminum chloride-induced AD model mice. Lactobacillus casei L. casei L. casei L. casei

METHODS: The Morris Water Maze (MWM) test was used to assess cognitive function of mice. The morphology and histopathological changes, antioxidant capacity and immune responses in the brain and ileum were evaluated. The alterations in intestinal permeability of the mice were determined using FITC-dextran. Gut microbiota composition was assessed using 16s rRNA sequencing.

RESULTS: Thirteen weeks intervention withATCC 393 orATCC 393-SeNPs significantly improved cognitive dysfunction, and minimized amyloid beta (Aβ) aggregation, hyperphosphorylation of TAU protein, and prevented neuronal death by modulating Akt/cAMP-response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway. Moreover, compared withATCC 393,ATCC 393-SeNPs further effectively mitigated intestinal barrier dysfunction by improving antioxidant capacity, regulating immune response, restoring gut microbiota balance, and increasing the level of short-chain fatty acids and neurotransmitters, thereby inhibiting the activation of microglia and protecting brain neurons from neurotoxicity such as oxidative stress and neuroinflammation. L. casei L. casei L. casei L. casei

CONCLUSION: These findings indicated that targeting the microbiota-gut-brain axis withATCC 393-SeNPs may have therapeutic potential for the deficits of cognitive function in the AD model mice. Thus, we anticipate thatATCC 393-SeNPs may be a promising and safe Se nutritional supplement for use as a food additive to prevent the neurodegenerative disease. L. casei L. casei

Key numbers

13 weeks

Cognitive Improvement

Duration of ATCC 393 or ATCC 393-SeNPs treatment in AD model mice.

0.3 mg/kg

Reduction in Aβ Aggregation

Selenium content in the ATCC 393-SeNPs diet administered to mice.

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Selenium Nanoparticles-Enriched Lactobacillus casei ATCC 393 Prevents Cognitive Dysfunction in Mice Through Modulating Microbiota-Gut-Brain Axis

Abstract

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