Discovery Shows Intestinal Bacteria Involved In The Development Of Dementia With Lewy Bodies

National University Corporation Tokai National University Organization Nagoya University Graduate School of Medicine (Dean, Hiroshi Kimura), Omics Medical Science Associate Professor Masaaki Hirayama, Neurogenetic Information Professor Kinji Ohno, Assistant Professor Hiroshi Nishiwaki et al. Okayama Noh Neurology Clinic Director Kenichi Kashiwabara, Iwate Medical University Neurology Geriatrics Professor Tetsuya Maeda, Fukuoka University Noh Neurology Professor Yoshio Tsuboi et al. We discovered that it may be related to the onset of dementia with Lewy bodies *2 , which is one of *1 . Dementia with Lewy bodies (DLB) is the second most common form of dementia after Alzheimer’s disease. It has almost the same morbidity rate among the elderly as Parkinson’s disease *3 (PD), and positive symptoms such as hallucinations have become a social problem. DLB is a disease related to PD and REM sleep behavior disorder *4 (RBD), which develops when α-synuclein accumulates in the brain. The research group has clarified the possibility that α-synuclein, which is abnormally accumulated due to changes in the enteric plexus, has prion properties and spreads from the dorsal vagal nucleus to the locus coeruleus and substantia nigra to cause RBD and PD. (Mov Disord 35:1626,2020; mSystems 5:e00797-20,2020; npj Parkinson’s Dis 8:65,2021). This research group analyzed the intestinal microbiota and fecal bile acids of 278 patients with DLB, PD, and RBD. As a result, intestinal bacteria that produce short-chain fatty acids (SCFA) are reduced, and Akkermancia *5 , which degrades the intestinal mucosa, is produced.

A feature of elevated s was common in PD and DLB patients. However, Ruminococcus torques *6 and Collinsella *7 , which were unchanged in PD, were increased in his DLB. In addition, in the random forest model *8 that distinguishes between DLB and PD, high levels of Ruminococcus torques and Collinsella, which suppress intestinal permeability, and low levels of Bifidobacterium *9 , which is also observed in Alzheimer’s disease, are characteristic of his DLB. I understand. Since Ruminococcus torques and Collinsella are major secondary bile acid producers, quantification of bile acids in feces revealed higher production of ursodeoxycholic acid (UDCA) in DLB. Therefore, these bacteria and their metabolites may be involved in the development and progression of DLB.