There has been increased discussion about the gut-brain axis in veterinary neurology and the paper we are going to talk about is one of the newest in the chain of publications. Dr. Curtis Dewey and associates published a study (JAVMA 2026) in which they evaluated microbiome of dogs pre and post treatment with FMT. Additionally, the owners were requested to complete the DISHAA questionnaire (cognitive function questionnaire) multiple times throughout the 90 day study period.
Unfortunately, only 6 of the initial 11 dogs completed the full study, which is the biggest downfall to data interpretation. In those 6 dogs, 4 improved and 2 worsened on their DISHAA scores. Three of the 4 dogs that improved also demonstrated an increased microbiome richness and diversity suggesting there might be a link. However, the small study precludes much clinical application. Unfortunately, some increases in unfavorable GI bacteria were also noted in dogs with improvement which drives the question “how much influence did the FMT make on the dog’s improvement?” It is well accepted that epileptic dogs will have a marked improvement in seizure frequency when enrolled in a study, regardless of the treatment provided. Without a blinded study, caregiver bias is a major concern when we rely on observational data such as the seizure frequency or cognitive functionality.
Potential mechanisms proposed for beneficial effects of FMT include decreased intestinal/systemic inflammation, increased production of short-chain fatty acids (SCFAs), improved intestinal and blood-brain barrier integrity, enhanced clearance of cerebral β-amyloid, and decreased formation of neurofibrillary tangles.
SCFAs—particularly acetate, butyrate, and propionate—are of particular interest because of their roles in intestinal and blood-brain barrier integrity and regulation of inflammatory cytokines. The authors note that some responding dogs developed increased abundance of SCFA-associated organisms and P hiranonis, a keystone organism involved in normal bile acid metabolism.
However, the study did not measure SCFA concentrations, inflammatory biomarkers, blood-brain barrier function, β-amyloid burden, or other mechanistic endpoints. Consequently, these mechanisms remain hypotheses rather than demonstrated effects of FMT in these dogs.
Based on the small study it is reasonable to consider the results as a proof of concept study rather than a pilot study. Proof of what concept? That we can successfully, and with few side effects, administer FMT to dogs with signs of CCDs. That the GI microbiota can change over time but whether or not it is directly related to the FMT remains to be seen.
How can we use this information clinically? I really try to pick topics that will be clinically useful to those of us in the field and this well…isn’t! I chose this article because it is useful to point to studies like this when discussing frustration over the “lack of treatment options” for specific diseases with owners. This is evidence of progress. We’re studying this complex disease and although we don’t have an answer that will result in a demonstrable improvement in quality of life for dogs progressing through CCDs, we are trying! Keep your ear tuned for future studies that build on this one and help us manage our aging population.
Thanks for reading! I hope you have a great week and I look forward to working with you soon!