Abstract
Parkinson's Disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra. Recent evidence supports the involvement of the gastrointestinal tract in PD pathogenesis, including alterations in microbiota and intestinal permeability. Apart from being the preferred energy source for colonic epithelial cells, butyrate is involved in anti-inflammatory, enteroendocrine and epigenetic mechanisms that influence colonic and systemic health, including brain function. A few studies using oral administration of sodium butyrate indicate beneficial effects in PD animal models; however, prebiotic fibers that generate butyrate locally in the gut may be more effective. The design and selection of butyrogenic prebiotic fibers would allow preclinical studies to evaluate how gut-derived butyrate could affect PD pathophysiology. This review describes potential benefits of increasing gut butyrate production in PD through a prebiotic approach. Moreover, physico-chemical features of prebiotic fibers that target butyrogenic colonic bacteria are discussed.
Highlights
Parkinson’s disease (PD) is a relentlessly progressive neurodegenerative disease of aging, with a considerable burden of disability
Researchers have provided evidence that supports a role for the gastrointestinal tract and the enteric nervous system (ENS) in the pathogenesis of PD [3, 4]. α-Synuclein aggregates are present in Substance P containing neurons in the sigmoid colonic submucosal neurons in patients with PD [5]
Butyrate reduction was accompanied by decrease in abundance of butyrogenic bacteria from Firmicutes, such as Roseburia and E. rectale (Clostridium Cluster XIVa)
Summary
Parkinson’s disease (PD) is a relentlessly progressive neurodegenerative disease of aging, with a considerable burden of disability. If the SCFA mixture dosage utilized corresponds to levels that can be reached through gut-microbiota production In this regard, oral administration of 100 mg/kg of sodium butyrate (NaB), but not 1,200 mg/kg, attenuated social deficits in an autism mouse model [64], indicating that distinct outcomes may take place by changing SCFA concentration. Oral administration of 100 mg/kg of sodium butyrate (NaB), but not 1,200 mg/kg, attenuated social deficits in an autism mouse model [64], indicating that distinct outcomes may take place by changing SCFA concentration Another consideration is that orally delivered butyrate is mainly absorbed in the upper gastrointestinal tract and could have distinctly different outcomes from the colonic-produced butyrate
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