Glucose metabolism in Brain and Neurodegenerative diseases: Multifactorial effects

Metabolic dysfunctions are one of the major contributors to the development of Alzheimer’s Disease (AD). They are one of the main causes of the inflammatory processes in the brain that potentially lead to neurodegeneration. In particular, glucose metabolic dysfunction is related to AD. It is known that diabetes TII is a risk factor to develop AD and vice versa. The brain is an organ that requires major glucose consumption to function (120 g glucose per day) and so it is important to research brain glucose metabolism to explore the relation to the development of Alzheimer’s Disease.

Investigations over the last few years into post-mortem AD brains have observed insulin resistance, as well as a decrease in the expression of several glucose transporters in AD brains. For these reasons, some investigators have referred to AD as a novel diabetes TIII. Glucose metabolic dysfunction in brain could cause several disturbances that may lead to neurodegeneration, including mitochondrial disturbances, post-translational modifications in key proteins, oxidative stress, generation of a pro-inflammatory state, among others.

Mechanisms underlying the molecular signalling or trigger for the above-mentioned effects are still unknown. Thus, the aim of this research topic is to shed light into some of these effects and potentially propose some molecular mechanism that could explain, at least in part, this relation. We encourage research into glucose metabolism and neuroinflammation, the influence of hormones in glucose metabolism in the brain. We also encourage papers, not only associated with Alzheimer’s disease, but also other neurodegenerative diseases such as Parkinson’s Disease.

Topic editor Prof. Ivan Nalvarte is the chairman at Nordic JoinCell. All other Topic Editors declare no competing interests with regards to the Research Topic subject.