Microplastics, fragments of plastic less than 5 mm in size, are increasingly prevalent in the environment and human diets. This review explores the impact of microplastic exposure on the gut-brain-axis, focusing on microbial dysbiosis, gut inflammation, immune activation, translocation to other organs, and neurological effects. Microplastics are now a permanent feature of the global environment, and their effects on the gut, brain, and overall body are critical for understanding their role in neurodegenerative diseases like Alzheimer's and Parkinson's. Microplastics can enter the body through ingestion, contaminating drinking water and food. Studies show humans ingest up to 5 grams of microplastics weekly, but research on their health effects is still in its early stages. Microplastics disrupt the gut microbiome, leading to dysbiosis, increased gut permeability, and systemic inflammation. These changes can affect the gut-brain-axis, contributing to neuroinflammation and neurodegeneration. Microplastics can cross the gut barrier and enter the bloodstream, reaching organs such as the brain, liver, and kidneys. They can cause structural and functional changes in tissues, including the brain, leading to neurotoxicity and neurodegeneration. Microplastics also activate the immune system, promoting inflammation and altering immune cell function. This immune activation can contribute to neuroinflammation and the progression of neurodegenerative diseases. The gut microbiome plays a crucial role in maintaining gut health and the gut-brain-axis. Microplastics can alter the microbiome, leading to dysbiosis and increased susceptibility to diseases. The interaction between microplastics and the gut microbiome is complex, with microplastics promoting the growth of certain bacteria and altering microbial biofilms. Microplastics can be absorbed by the gut lining and transported throughout the body, leading to accumulation in various organs. The shape and size of microplastics influence their uptake and distribution. Studies show that smaller microplastics are more readily absorbed, while larger ones may be less so. Microplastics can also interact with environmental and gastrointestinal factors, forming coronas that may enhance their toxicity. Microplastics can cause cellular stress, leading to oxidative stress and inflammation. They can damage intestinal cells, alter mucin production, and disrupt the gut barrier, contributing to a "leaky gut" condition. This condition can lead to systemic inflammation and neuroinflammation, exacerbating neurodegenerative diseases. The immune system responds to microplastics by activating inflammatory pathways, leading to the release of pro-inflammatory cytokines and immune cell infiltration. This immune activation can contribute to neuroinflammation and the progression of neurodegenerative diseases. Microplastics can cross the blood-brain barrier, leading to neuroinflammation, microglial activation, and neurotoxicity. They can also contribute to the aggregation of proteins like α-synuclein, which is associated with neurodegenerativeMicroplastics, fragments of plastic less than 5 mm in size, are increasingly prevalent in the environment and human diets. This review explores the impact of microplastic exposure on the gut-brain-axis, focusing on microbial dysbiosis, gut inflammation, immune activation, translocation to other organs, and neurological effects. Microplastics are now a permanent feature of the global environment, and their effects on the gut, brain, and overall body are critical for understanding their role in neurodegenerative diseases like Alzheimer's and Parkinson's. Microplastics can enter the body through ingestion, contaminating drinking water and food. Studies show humans ingest up to 5 grams of microplastics weekly, but research on their health effects is still in its early stages. Microplastics disrupt the gut microbiome, leading to dysbiosis, increased gut permeability, and systemic inflammation. These changes can affect the gut-brain-axis, contributing to neuroinflammation and neurodegeneration. Microplastics can cross the gut barrier and enter the bloodstream, reaching organs such as the brain, liver, and kidneys. They can cause structural and functional changes in tissues, including the brain, leading to neurotoxicity and neurodegeneration. Microplastics also activate the immune system, promoting inflammation and altering immune cell function. This immune activation can contribute to neuroinflammation and the progression of neurodegenerative diseases. The gut microbiome plays a crucial role in maintaining gut health and the gut-brain-axis. Microplastics can alter the microbiome, leading to dysbiosis and increased susceptibility to diseases. The interaction between microplastics and the gut microbiome is complex, with microplastics promoting the growth of certain bacteria and altering microbial biofilms. Microplastics can be absorbed by the gut lining and transported throughout the body, leading to accumulation in various organs. The shape and size of microplastics influence their uptake and distribution. Studies show that smaller microplastics are more readily absorbed, while larger ones may be less so. Microplastics can also interact with environmental and gastrointestinal factors, forming coronas that may enhance their toxicity. Microplastics can cause cellular stress, leading to oxidative stress and inflammation. They can damage intestinal cells, alter mucin production, and disrupt the gut barrier, contributing to a "leaky gut" condition. This condition can lead to systemic inflammation and neuroinflammation, exacerbating neurodegenerative diseases. The immune system responds to microplastics by activating inflammatory pathways, leading to the release of pro-inflammatory cytokines and immune cell infiltration. This immune activation can contribute to neuroinflammation and the progression of neurodegenerative diseases. Microplastics can cross the blood-brain barrier, leading to neuroinflammation, microglial activation, and neurotoxicity. They can also contribute to the aggregation of proteins like α-synuclein, which is associated with neurodegenerative