Chronic Exposure to Thermally Processed Food-Derived Carbon Polymers Accelerated Neuroinflammation in Alzheimer Disease Mice through Microbe-Gut-Brain Axis.

Carbon-based polymers (CPs) were identified and isolated as an emerging dietary risk factor from processed foods, specifically roasted lamb.

• CPs are described as 'thermally processed food-derived carbon polymers'
• Roasted lamb was used as the representative processed food source for CP isolation
• CPs are characterized as 'carbon-based polymers' distinct from other food processing byproducts
• The study frames CPs as an 'emerging dietary risk factor' warranting biosafety reevaluation

Prolonged exposure to CPs induced gut microbiota dysbiosis in transgenic AD mice.

• The study used transgenic APPswe/PSEN1dE9 mice as the AD model
• Chronic (prolonged) CP exposure was the experimental condition
• Gut microbiota dysbiosis was identified as a primary consequence of CP exposure
• The dysbiosis was associated with elevated endotoxin (LPS) production and perturbed tryptophan metabolism

CP exposure led to intestinal inflammation associated with elevated LPS and disrupted tryptophan metabolism.

• Elevated endotoxin (LPS) production was observed following CP-induced microbiota dysbiosis
• Tryptophan metabolism was perturbed by CP exposure
• These alterations collectively led to intestinal inflammation
• The intestinal inflammation was identified as upstream of systemic and neurological effects

CP-induced gut dysbiosis facilitated LPS entry into blood circulation, triggering systemic inflammation and increased blood-brain barrier permeability.

• LPS translocated from the gut into blood circulation following CP-induced intestinal inflammation
• Systemic inflammation was triggered by circulating LPS
• Blood-brain barrier (BBB) permeability was increased as a consequence of systemic inflammation
• Increased BBB permeability was identified as the mechanism by which peripheral inflammation reached the central nervous system

Chronic CP exposure accelerated neuroinflammation and synaptic dysfunction in APPswe/PSEN1dE9 transgenic AD mice via the LPS-TLR4-NF-κB signaling pathway.

• The transgenic mouse model used was APPswe/PSEN1dE9
• Both neuroinflammation and synaptic dysfunction were accelerated by CP exposure
• The LPS-TLR4-NF-κB signaling pathway was identified as the mechanistic pathway mediating these effects
• The pathway links peripheral LPS signaling through Toll-like receptor 4 (TLR4) to nuclear factor kappa B (NF-κB) activation in the brain

The study proposes a microbe-gut-brain axis mechanism by which dietary CPs from processed foods may accelerate Alzheimer disease progression.

• The mechanistic sequence identified was: CP exposure → gut microbiota dysbiosis → intestinal inflammation → systemic LPS circulation → BBB disruption → neuroinflammation
• This constitutes a 'microbe-gut-brain axis' as described in the paper title
• The findings provide 'a scientific basis for reevaluating the biosafety of dietary CPs in humans, especially for at-risk populations'
• Processed foods are noted as 'increasingly associated with the prevalence of neurodegenerative diseases, including Alzheimer disease'