Dr Laura Dunn and colleagues have just published a study looking at disruptions in the way that neurons in the brains of people with Parkinson’s handle glucose:
In contrast to other cell types neurons utilise glucose through an alternate pathway and maintains their anti-oxidant ability to protect themselves from various stresses, both internal and external. Neurons undergo many of the changes seen in Parkinson’s disease (PD) when glucose metabolism is altered in experimental models. MRI and PET-scan studies have shown decreased glucose metabolism in PD patients. For this reason we hypothesised that altered glucose metabolism in neurons could be a primary event in neuronal death in PD.
Using tissue donated by patients who suffered from PD we studied changes in glucose metabolism in the brain and compared this to age-matched individuals without PD. Alzheimer’s disease (AD) patients was also investigated as a disease control. Our data suggest that efficiency of glucose breakdown in two areas of the brain is altered early on in PD disease progression. Importantly, this is not seen in either control or AD tissue. As this breakdown is known to affect the amount of free radicals in the brain, our data suggests that changes to glucose breakdown could be key early events that cause vulnerable nerve cells to die. Our data opens up possibilities for novel biomarker development for PD progression and also point towards a new avenue for PD therapeutics.
Read all about their work online on the Neurobiology of Aging website: