Are We What We Eat? Impact of Diet on the Gut–Brain Axis in Parkinson’s Disease

Abstract

Parkinson’s disease is characterized by motor and non-motor symptoms, such as defects in the gut function, which may occur before the motor symptoms. To date, there are therapies that can improve these symptoms, but there is no cure to avoid the development or exacerbation of this disorder. Dysbiosis of gut microbiota could have a crucial role in the gut–brain axis, which is a bidirectional communication between the central nervous system and the enteric nervous system. Diet can affect the microbiota composition, impacting gut–brain axis functionality. Gut microbiome restoration through probiotics, prebiotics, synbiotics or other dietary means could have the potential to slow PD progression. In this review, we will discuss the influence of diet on the bidirectional communication between gut and brain, thus supporting the hypothesis that this disorder could begin in the gut. We also focus on how food-based therapies might then have an influence on PD and could ameliorate non-motor as well as motor symptoms.

Nutrition and Gut–Brain Pathways Impacting the Onset of Parkinson’s Disease

“…This gut information is in turn transferred to the CNS in order to produce a response [ 52 , 55 ]. Accumulating evidence suggests that this microbiome–gut–brain axis might play a key role in the underlying pathological mechanisms of PD [ 35 , 36 , 41 ].…”

“…Results suggested an altered microbiome in PD participants by showing a reduction in their number of Prevotellaceae bacteria compared to controls. Strikingly, this alteration was associated with the severity of the motor symptoms [ 29 , 35 ]. Further findings linking gut dysbiosis and PD pathogenesis showed that PD patients may exhibit not only a decreased abundance of Prevotella but also an increased abundance of Lactobacilliceae [ 35 , 74 ].…”

“…Strikingly, this alteration was associated with the severity of the motor symptoms [ 29 , 35 ]. Further findings linking gut dysbiosis and PD pathogenesis showed that PD patients may exhibit not only a decreased abundance of Prevotella but also an increased abundance of Lactobacilliceae [ 35 , 74 ]. These alterations may be associated with reduced levels of ghrelin, an important gut hormone involved in the survival and efficacy of dopaminergic neurons [ 74 ].…”

“…The accumulating evidence showing a bidirectional link between bacteria in the gut and neurons in the CNS (known as the “microbiota–gut–brain axis”) has resulted in an ongoing redefinition of health and disease, including neurodegenerative diseases [ 33 , 34 ]. In particular, recent studies have suggested that alterations in the composition of the gut microbiota (known as gut dysbiosis) might be a potential trigger for neuroinflammation, which in turn may lead to the development of PD [ 35 , 36 , 37 , 38 ]. In line with this hypothesis, α-Syn aggregation may start in the gut and then be spread from the gastrointestinal tract to the midbrain via the vagus nerve, resulting in the selective death of SNc [ 38 , 39 ].…”

“…Increasing evidence suggests that specific nutritive patterns may influence (positively or negatively) the microbiota–gut–brain axis and, in turn, the risk of developing PD [ 44 , 46 ]. These nutritive patterns include dietary macronutrients (carbohydrates, proteins, and fats) [ 35 , 46 , 47 ], the intake levels of omega-3 (ω3) fatty acids [ 48 ], fruits, and vegetables [ 45 , 49 ], and the adherence to specific diets (e.g., Mediterranean diet or Western diet) [ 44 , 50 ].…”