Abstract
Oral administration of hydrogen water ameliorates Parkinson’s disease (PD) in rats, mice, and humans. We previously reported that the number of putative hydrogen-producing bacteria in intestinal microbiota is low in PD compared to controls. We also reported that the amount of hydrogen produced by ingestion of lactulose is low in PD patients. The decreased hydrogen production by intestinal microbiota may be associated with the development and progression of PD. We measured the amount of hydrogen production using gas chromatography by seven bacterial strains, which represented seven major intestinal bacterial groups/genera/species. Blautia coccoides and Clostridium leptum produced the largest amount of hydrogen. Escherichia coli and Bacteroides fragilis constituted the second group that produced hydrogen 34- to 93-fold lower than B. coccoides. Bifidobacterium pseudocatenulatum and Atopobium parvulum constituted the third group that produced hydrogen 559- to 2164-fold lower than B. coccoides. Lactobacillus casei produced no detectable hydrogen. Assuming that taxonomically neighboring strains have similar hydrogen production, we simulated hydrogen production using intestinal microbiota that we previously reported, and found that PD patients produce a 2.2-fold lower amount of intestinal hydrogen compared to controls. The lower amount of intestinal hydrogen production in PD was also simulated in cohorts of two other countries. The number of hydrogen-producing intestinal bacteria may be associated with the development and progression of PD. Further studies are required to prove its beneficial effect.
Highlights
We found that fecal counts of putative hydrogen-producing bacteria were low in Parkinson’s disease (PD) patients [11]
Among the twelve fecal bacterial groups/genera/species that we previously analyzed by qRT-PCR of 16S or 23S rRNA (YIF-Scan) (Table 2 in [11]), we quantified the amount of hydrogen production of six bacterial strains (Blautia coccoides JCM 1395, Clostridium leptum ATCC 29065, Bacteroides fragilis ATCC 25285, Escherichia coli W3110, Bifidobacterium pseudocatenulatum ATCC 27919 and Atopobium parvulum ATCC 33793) representing six most dominant bacterial groups/genera/species according to YIF-Scan (Blautia coccoides group, Clostridium leptum subgroup, Bacteroides fragilis group, Enterobacteriaceae, Bifidobacterium, and Atopobium cluster), respectively
As the count of Lactobacillus was significantly higher in PD [11], we analyzed hydrogen production by a representative strain Lactobacillus casei ATCC 334
Summary
Pathological hallmark of PD is abnormally aggregated α-synuclein protein (Lewy body) in dopaminergic neurons in substantia nigra in the midbrain [1]. Braak et al observed in autopsies of idiopathic PD patients and healthy elderly people that α-synuclein pathology begins in the dorsal nucleus of vagus nerve, and ascends to raphe nuclei, locus ceruleus, substantia nigra, and cerebral cortex [1]. In 44.6% of PD patients, constipation starts on average 18.1 years before the onset of motor symptoms [2]. Rapid eye movement (REM) sleep behavior disorder and depression precede the onset of motor symptoms approximately 10 and 5 years, which represent abnormalities in Raphe nucleus and locus ceruleus, respectively [3]. Accumulating evidence supports the notion that abnormal α-synuclein first aggregates in the neural plexus in the gastrointestinal tract, and ascends into the central nervous system
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