Milk and Parkinson disease: Could galactose be the missing link

Abstract

Epidemiological evidence has linked the consumption of milk and dairy products to an increased risk of developing Parkinson’s disease (PD). However, the potential pathogenetic mechanisms remain to date yet to be ascertained.

Galactose (D-Gal) is a hexose sugar which, when given orally and by other routes of administration, is picked up by the brain after a few hours. For doses above 100 mg/kg, it appears that galactose can cause biochemical and neuropathological alterations in neurons and astrocytes, similar to those observed in PD. These quantities can be reached and surpassed with the simple daily consumption of two glasses of milk, the main dietary source of D-Gal in humans.

It is likely that, relative to other neurons, dopaminergic neurons are more vulnerable to D-Gal induced damage, because of their greater vulnerability to oxidative stress.

Mitochondrial dysfunction plays a critical role in both PD and D-Gal toxicity, and mutations of the genes commonly involved in PD and in mitochondrial homeostasis could enhance this mechanism.

If this hypothesis were to be confirmed, dietary interventions, such as reducing the sources of galactose in the diet, and/or increasing the intake of protective molecules, could help reduce the occurrence of this disease in the aging population.