Parkinson’s disease is a common neurodegenerative disease in which α-synuclein deposits are aggregated in the brain, especially in the substantia nigra. Many studies indicate that this process may begin in the olfactory bulb and the enteric nervous system, and then spread through the vagus nerve and the olfactory route to further areas of the brain, many years before the onset of motor symptoms. This probably results in a much earlier occurrence of non-motor disorders, such as constipation or hyposmia. Intestinal inflammation in Parkinson’s disease may lead to increased intestinal permeability, referred to as leaky gut syndrome, which leads to microbial translocation and might trigger accumulation of α-synuclein in the enteric nervous system. Recently, more attention is paid to the influence of mutual interactions between the central nervous system and the intestines, which led to the definition of the gut–brain axis, involving neuronal, endocrine and immunological factors. Increased expression of proinflammatory cytokines in the intestines, glial intestinal reaction or the presence of α-synuclein deposits in the enteric nervous system are just some of the evidence for gastrointestinal involvement in the pathogenesis of Parkinson’s disease. Environmental exposure plays a key role in the formation of the composition and functioning of the intestinal microbiome and may increase susceptibility to neurodegenerative diseases such as Parkinson’s disease. Therefore, the intestinal microbiome in Parkinson’s disease has recently become a potential target in preventive strategies.