The gastrointestinal (GI) tract has its own autonomy through the enteric (or intrinsic) nervous system (ENS), also called the “little brain”. There is a bi-directional communication between the gut and the brain through the autonomic nervous system (ANS) represented by the sympathetic and parasympathetic nervous systems. The vagus nerve (VN) is a key parasympathetic component of the ANS. The gut can also communicate with the brain through the circumventricular organs. The gut microbiota is also able to target the brain, i.e. the microbiota-gut-brain axis through the ANS (Fig. 1), in particular through its interaction with the VN [1]. This communication allows physiological relationships, which are involved in the control of GI functions such as secretion, motility, sensitivity, immunity, intestinal permeability, and satiety, but which can become, under certain conditions, pathological. Accumulating evidence has suggested a bidirectional link between gastrointestinal inflammation and neurodegeneration, in accordance with the concept of the gut-brain axis [2].

Parkinson's disease (PD) is a clinical syndrome characterized by bradykinesia, resting tremor, rigidity and postural instability due to the death of dopamine cells in the substantia nigra (SN) [3]. Its pathological hallmark is cytoplasmic eosinophilic Lewy body depositions. PD is characterized by the accumulation and aggregation of α-synuclein not only in the central nervous system (CNS) but also in the VN and ENS of patients [4], [5], [6]. Indeed, non-motor GI manifestations are observed in PD patients since the entire GI tract is affected, inducing complications, from oral issues (drooling and swallowing problems), to dysphagia, gastroparesis and constipation [7]. An abnormal microbiota-gut-brain interaction contributes to the pathogeny of PD [8]. Excessive stimulation of the innate immune system resulting from gut dysbiosis and/or small intestinal bacterial overgrowth and increased intestinal permeability may induce systemic inflammation, while activation of enteric neurons and enteric glial cells may contribute to the initiation of α-synuclein misfolding [8]. This supports the hypothesis that PD originates in the gut to spread to the CNS, in particular through the VN according to Braak's hypothesis [9].

This review will focus on the microbiota-gut-brain axis and its pathological implication in PD as well as therapeutic potential implications targeting this axis.