The Beneficial Role of Thiamine in Parkinson Disease

Lương, Khanh vinh quốc; Nguyễn, Lan

doi:10.1111/cns.12078

Cited by 47 publications

(13 citation statements)

References 139 publications

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“…Around 10% of the population had an inadequate vitamin B1 intake, which is an issue as studies suggest a relationship between thiamin and dopamine levels. A reduced dopamine release is associated with thiamin deficiency (32,33). Thiamin deficiency is associated with neuronal loss, and a decrease in the activity of thiamin-dependent enzymes has been demonstrated in neurodegenerative disorders, including PD (34).…”

Section: Discussionmentioning

confidence: 99%

Dietary Intake of Parkinson's Disease Patients

Baert

Matthys

Mellaerts³

et al. 2020

Front. Nutr.

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Background and Aims: Dietary management, as an adjuvant therapy in Parkinson's disease (PD), provides clear benefits to patients. However, baseline information about the usual dietary intake of Parkinson's patients is lacking. Methods: We conducted an observational cross-sectional study, investigating the dietary intake in Belgian PD patients, as well as their medication use and knowledge of possible food-drug interactions. A dietary record of 2 non-consecutive days, allowing the calculation of usual intake, was used. Medication use and knowledge of food-drug interactions were investigated using a self-administered questionnaire. Results: The nutrient (both macro and micro) intake in this study was similar to the dietary pattern of the general Belgian population. However, results showed that the PD population had a high dietary fiber intake of 26.2 ± 7.7 g/day, which is in line with the recommended intake. The majority of the PD patients had an inadequate intake of vitamin D and iron (respectively, 55.9 and 76.5% of all participants). When looking into the knowledge about food-drug interactions, the majority of the PD patients claimed to be aware of the food-drug interaction between dietary proteins and levodopa. However, only 18.2% of the patients took all doses of levodopa out of meals. Conclusion: Our results show that monitoring of dietary intake in PD patients is of importance to detect possible micronutrient insufficiencies. Patients should receive professional guidance in optimizing their diet to accommodate for different complaints inherent to PD, including constipation. Furthermore, the knowledge of patients regarding the importance of correct medication intake should be improved.

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Section: Discussionmentioning

confidence: 99%

Dietary Intake of Parkinson's Disease Patients

Baert

Matthys

Mellaerts³

et al. 2020

Front. Nutr.

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“…Thiamin (also known as vitamin B1) is widely used in neuropharmacology. In particular, its administration causes a transient improvement in cognitive function of some patients affected by neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD) 1 2 3 4 5 . The importance of thiamin administration in elderly is supported by the fact that the levels of thiamin and its coenzyme form, thiamin diphosphate (ThDP), are decreased with age 6 .…”

mentioning

confidence: 99%

Molecular mechanisms of the non-coenzyme action of thiamin in brain: biochemical, structural and pathway analysis

Mkrtchyan

Aleshin

Parkhomenko

et al. 2015

Sci Rep

114

124

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Thiamin (vitamin B1) is a pharmacological agent boosting central metabolism through the action of the coenzyme thiamin diphosphate (ThDP). However, positive effects, including improved cognition, of high thiamin doses in neurodegeneration may be observed without increased ThDP or ThDP-dependent enzymes in brain. Here, we determine protein partners and metabolic pathways where thiamin acts beyond its coenzyme role. Malate dehydrogenase, glutamate dehydrogenase and pyridoxal kinase were identified as abundant proteins binding to thiamin- or thiazolium-modified sorbents. Kinetic studies, supported by structural analysis, revealed allosteric regulation of these proteins by thiamin and/or its derivatives. Thiamin triphosphate and adenylated thiamin triphosphate activate glutamate dehydrogenase. Thiamin and ThDP regulate malate dehydrogenase isoforms and pyridoxal kinase. Thiamin regulation of enzymes related to malate-aspartate shuttle may impact on malate/citrate exchange, responsible for exporting acetyl residues from mitochondria. Indeed, bioinformatic analyses found an association between thiamin- and thiazolium-binding proteins and the term acetylation. Our interdisciplinary study shows that thiamin is not only a coenzyme for acetyl-CoA production, but also an allosteric regulator of acetyl-CoA metabolism including regulatory acetylation of proteins and acetylcholine biosynthesis. Moreover, thiamin action in neurodegeneration may also involve neurodegeneration-related 14-3-3, DJ-1 and β-amyloid precursor proteins identified among the thiamin- and/or thiazolium-binding proteins.

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“…These intestinal bacteria are prominent producers of SCFAs, such as butyrate as well as folate (vitamin B9) and thiamine (vitamin B1) which are important for maintenance of epithelial barrier function 71,72 . Interestingly, all of these SCFAs are associated with the amelioration of PD pathology [72][73][74] . For molecular mimicry in the pathophysiology of PD, Tobacco Mosaic virus (TMV) 43 has been implicated but needs more investigation to make absolute conclusion.…”

Section: Alzheimer's Diseasementioning

confidence: 99%

The Role of the Gut-Brain Axis in Neurodegenerative Diseases and Relevance of the Canine Model: A Review

Ambrosini¹,

Borcherding²,

Kanthasamy³

et al. 2019

Preprint

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Identifying appropriate animal models is critical in developing translatable in vitro and in vivo systems for therapeutic development and investigating disease pathophysiology. These animal models should have direct biological and translational relevance to the underlying disease they are supposed to mimic. Aging dogs naturally develop a cognitive decline in many aspects including learning and memory, but also exhibit human-like individual variability in the aging process. Neurodegenerative processes that can be observed in both human and canine brains include the progressive accumulation of β-amyloid (Aβ) found as diffuse plaques in the prefrontal cortex, including the gyrus proreus, the hippocampus, and in the cerebral vasculature. A growing body of epidemiological data shows that human patients with neurodegenerative diseases have concurrent intestinal lesions, and histopathological changes in the gastrointestinal (GI) tract occurs decades that evolve before neurodegenerative changes. Gut microbiome alterations also have been observed in many neurodegenerative diseases including Alzheimer’s and Parkinson’s diseases, and inflammatory CNS diseases. Interestingly, only recently has the dog gut microbiome been recognized to more closely resemble in composition and in functional overlap with the human gut microbiome as compared to rodent models. This article aims to review the physiology of the gut-brain axis (GBA), and its involvement with neurodegenerative diseases in dogs and humans. Additionally, we outline the advantages and disadvantages of traditional in vitro and in vivo models and discuss future research directions investigating major human neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases using dogs.

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The Beneficial Role of Thiamine in Parkinson Disease

Cited by 47 publications

References 139 publications

Dietary Intake of Parkinson's Disease Patients

Dietary Intake of Parkinson's Disease Patients

Molecular mechanisms of the non-coenzyme action of thiamin in brain: biochemical, structural and pathway analysis

The Role of the Gut-Brain Axis in Neurodegenerative Diseases and Relevance of the Canine Model: A Review

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