Objective: To identify intestinal bacteria that are changed in DLB alone or in both DLB and cognitive decline in Parkinson’s disease (PD).

Background: Gut microbiota in dementia with Lewy bodies (DLB) has not been reported.

Method: Gut microbiota was analyzed in 28 patients with DLB.

Results: Similar to PD, short chain fatty acids-producing genera were decreased in DLB. In contrast to PD, Ruminococcus torques and Collinsella were increased in DLB. Gut microbiota in DLB was similar to that in Hoehn and Yahr stages 3 and 4 (HY3&4). Random forest models showed that high Ruminococcus torques, low Bifidobacterium, and high Collinsella in DLB were essential to differentiate DLB from HY3&4. In concordance with DLB, Ruminococcus torques was high and Bifidobacterium was low in arbitrary defined PD dementia (PDD+). In contrast to DLB, however, Collinsella was low in PDD+.

Conclusion: High Ruminococcus torques in DLB and PDD+ degrades intestinal mucin, which may subsequently allow abnormal aggregation of intestinal α-synuclein. Bifidobacterium is also low in Alzheimer’s disease, and oral supplementation of Bifidobacterium ameliorates cognitive impairment in Alzheimer’s disease. Both Ruminococcus torques and Collinsella produce ursodeoxycholate, which exerts anti-inflammatory, anti-oxidant, and anti-apoptotic effects. Ursodeoxycholate generated by Ruminococcus torques and Collinsella in DLB may attenuate neuroinflammation to prevent dopaminergic cell death in the substantia nigra, but Ruminococcus torques alone in PD may not be sufficient to attenuate nigral neuroinflammation. Modulation of these bacteria may retard the development and progression of DLB and cognitive decline in PD.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/gut-dysbiosis-in-patients-with-dementia-with-lewy-bodies/