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Updated: Jan 8, 2026

Mouse Footpad Inoculation Model to Study Viral-Induced Neuroinflammatory Responses
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Basic Science and Pathogenesis.

Alexis M Rodríguez Rosas1, Diana L Baldenebro1, Carla E Angulo Rojo1

  • 1Universidad Autónoma de Sinaloa, Culiacan Rosales, SI, Mexico.

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|December 23, 2025
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Summary
This summary is machine-generated.

Gut microbiota dysbiosis is linked to type 2 diabetes (T2DM) and Alzheimer's disease (AD). This study characterized gut microbiota in individuals with T2DM and AD, revealing specific phylum alterations and diversity differences. Further research is needed to understand these connections.

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Area of Science:

  • Microbiology
  • Genomics
  • Immunology

Background:

  • The gut microbiota plays a crucial role in immune activity and metabolic regulation.
  • Dysbiosis of the gut microbiota is observed in both type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD).

Purpose of the Study:

  • To characterize the gut microbiota composition in individuals with T2DM and AD.
  • To investigate the differences in gut microbiota between healthy controls, T2DM patients, AD patients, and individuals with both conditions.

Main Methods:

  • 148 individuals were divided into four groups: Control (CTRL), T2DM, AD, and AD-T2DM.
  • DNA extraction from stool samples, 16S rRNA gene amplification (V4 region), and Illumina MiSeq sequencing were performed.
  • Phylum abundance, alpha diversity, and beta diversity analyses were conducted to compare microbial communities across groups.

Main Results:

  • Significant differences in Verrucomicrobiota abundance were observed in the AD group.
  • The AD-T2DM group showed a significant reduction in Bacteroidota compared to other groups.
  • Alterations in Firmicutes_A abundance and distinct beta diversity patterns were found in T2DM groups compared to controls.

Conclusions:

  • Gut microbiota dysbiosis in T2DM exacerbates with aging, leading to microbial diversity patterns similar to those in AD.
  • These age-related changes in gut microbiota may contribute to the dysregulation of molecular networks implicated in AD pathophysiology.