Background: The prevalence of neurogastroenterological diseases, i.e., disorders of gut brain interaction, has increased over the last decades. Altered gastrointestinal (GI) motility is a key feature of this group of diseases and is affecting all anatomical segments of the GI tract, ranging from swallowing disorders to fecal incontinence. Considering the ongoing demographic transformation in developed countries worldwide, it is highly relevant to understand the age-dependency of motility disorders per se and its pathophysiological mechanisms with a special focus on neurodegeneration. This review summarizes the most relevant findings and open research questions in the field of age-dependent changes in GI motility with a strong focus on studies performed on humans or with biological material obtained from humans. Summary: While the basic function of the GI tract including motility in most of its segments is largely unaltered by aging per se, there is clear evidence supporting an age-dependent increase in the prevalence of constipation and fecal incontinence, the latter mainly affecting women. When, however, the large percentage of elderly patients suffering from frequent chronic diseases such as diabetes, Parkinson’s disease, or cerebrovascular disease are included, a clear increase in “secondary” motility disorders also affecting the esophagus or the stomach is evident. Studies regarding the pathophysiology of geriatric dysmotility are often limited by the heterogenous clinical history of the studied patients and by coincident impairments of interoceptive sensory function. However, a loss in the number of cholinergic neurons together with changes in the number of interstitial cells of Cajal, certain subtypes of enteric glia, changes in immune cell function, and changes in the endocrine signaling throughout the GI tract have been reported. Key Messages: The overall prevalence of swallowing disorders, impaired gastric emptying, constipation and fecal incontinence is high among elderly patients. The pathophysiology most likely includes a variety of factors ranging from degeneration of enteric neurons and the non-neuronal cell populations involved in GI motility up to age-dependent metabolic and neuroendocrine changes and dietary factors. Deciphering the effects of “healthy aging” but also of the numerous typical chronic diseases of the elderly on GI motility is an ongoing challenge and prerequisite for improving patients’ medical care and quality of life.

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