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Epidemiological studies associate milk consumption with an increased risk of Parkinson’s disease (PD) and type 2 diabetes mellitus (T2D). PD is an  α -synucleinopathy associated with mitochondrial dysfunction, oxidative stress, deficient lysosomal clearance of  α -synuclein ( α -syn) and aggregation of misfolded  α -syn. In T2D,  α -syn promotes co-aggregation with islet amyloid polypeptide in pancreatic  β -cells. Prion-like vagal nerve-mediated propagation of exosomal  α -syn from the gut to the brain and pancreatic islets apparently link both pathologies. Exosomes are critical transmitters of  α -syn from cell to cell especially under conditions of compromised autophagy. This review provides translational evidence that milk exosomes (MEX) disturb  α -syn homeostasis. MEX are taken up by intestinal epithelial cells and accumulate in the brain after oral administration to mice. The potential uptake of MEX miRNA-148a and miRNA-21 by enteroendocrine cells in the gut, dopaminergic neurons in substantia nigra and pancreatic  β -cells may enhance miRNA-148a/DNMT1-dependent overexpression of  α -syn and impair miRNA-148a/PPARGC1A- and miRNA-21/LAMP2A-dependent autophagy driving both diseases. MiRNA-148a- and galactose-induced mitochondrial oxidative stress activate c-Abl-mediated aggregation of  α -syn which is exported by exosome release. Via the vagal nerve and/or systemic exosomes, toxic  α -syn may spread to dopaminergic neurons and pancreatic  β -cells linking the pathogenesis of PD and T2D.

Synergistic Effects of Milk-Derived Exosomes and Galactose on α-Synuclein Pathology in Parkinson’s Disease and Type 2 Diabetes Mellitus