Glucose metabolism is of central importance in maintaining the anti-oxidant ability of neurons to protect themselves from internal and external damage. When glucose metabolism is altered experimentally, neurons undergo many of the changes that are seen in Parkinson’s disease (PD) neurons. We hypothesize that a decrease in glucose metabolism in neurons, caused by aging and other genetic factors, could be the primary event that results in neuronal death in PD.
Using tissue donated by patients who suffered from PD, we will look at changes in glucose metabolism in the brain. We will compare any changes we see to the severity of symptoms suffered by the patient, and the changes that have occurred in the brain. If our hypothesis is correct, we should see a correlation between the advancement of neuropathological features in the brain (“Braak staging”) and the extent of glucose metabolism perturbation.
Relevance to Diagnosis/Treatment of Parkinson’s Disease:
Currently there are few, if any comprehensive studies examining glucose metabolism in PD patients, despite increasing evidence to suggest that changes may occur. Through this study, and further work, we will be able to characterize metabolic changes in PD, opening an entirely new avenue for therapeutics and research. This study has the potential to yield new and exciting diagnostic approaches to PD and hopefully take us a step closer to curing this debilitating disease.
At the end of this study, we aim to have identified any changes to glucose metabolism in PD that may be occurring, which can be used for further research to look at these mechanisms in more detail.
Using brain tissue donated by individuals who suffered from Parkinson’s disease (PD), and tissue from age-matched individuals without PD, we have investigated the breakdown of the sugar glucose in two areas of the brain that are known to be affected in disease (as seen by pathology) and another region that remains unaffected. Our results suggest that the efficiency of glucose breakdown in PD could be changed compared to people without PD. 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 important in the events that cause nerve cells to die in this disease. Our data although preliminary, opens up possibilities for biomarker development for disease progression and the potential for development of new therapeutic strategies.