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Basic Science and Pathogenesis.

Maalavika Govindarajan1, Chetan Aware1, Kira Ivanich1

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Summary
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Inducible nitric oxide synthase knockout (iNOS-KO) may protect cerebral blood flow (CBF) in Alzheimer's Disease (AD) models. This neuroprotective role persists despite gut dysbiosis induced by fecal microbiome transplantation (FMT) from mild cognitive impairment (MCI) patients.

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Area of Science:

  • Neuroscience
  • Microbiology
  • Genetics

Background:

  • Inducible Nitric Oxide Synthase (iNOS) exacerbates Alzheimer's Disease (AD) pathology.
  • Gut dysbiosis is linked to AD, with bacteria like E. Coli inducing iNOS.
  • A novel iNOS knockout (iNOS-KO) 3xTg-AD mouse model was developed to study iNOS's role.

Purpose of the Study:

  • To investigate the neuroprotective potential of iNOS-KO against AD progression.
  • To determine if iNOS-KO can preserve cerebral blood flow (CBF) despite gut dysbiosis.
  • To assess the impact of fecal microbiome transplantation (FMT) from mild cognitive impairment (MCI) patients on iNOS-KO/3xTg-AD mice.

Main Methods:

  • Fecal samples from MCI patients and healthy controls (HC) were used for FMT in iNOS-KO/3xTg-AD mice.
  • Mice underwent antibiotic treatment before FMT.
  • 16S rRNA sequencing analyzed microbial composition; 7T MRI with CASL-EPI measured global CBF.

Main Results:

  • FMT successfully imprinted donor microbial signatures in recipient mice, with FMT-MCI mice showing increased pathobionts.
  • Despite induced gut dysbiosis, CBF levels were comparable across all groups (FMT-MCI, FMT-HC, and controls).
  • The preservation of CBF is attributed to the iNOS knockout.

Conclusions:

  • MCI patients exhibit higher gut dysbiosis compared to HC.
  • iNOS-KO demonstrates a potential neuroprotective role by preserving CBF in an AD model, even with dysbiosis.
  • iNOS emerges as a potential therapeutic target for mitigating AD risk and pathology.