Title:Diabetes Mellitus and Energy Dysmetabolism in Alzheimer’s Disease:
Understanding the Relationships and Potential Therapeutic Targets
Volume: 19
Issue: 8
Author(s): Adejoke Y. Onaolapo, Folusho O. Ojo, Olufunto O. Adeleye, Joshua Falade and Olakunle J. Onaolapo*
Affiliation:
- Department of Anatomy, Behavioural Neuroscience Unit, Neurobiology Subdivision, Ladoke Akintola University of
Technology, Ogbomoso, Oyo State, Nigeria
Keywords:
Amyloid beta proteins, antihyperglycaemic agent, cognitive impairment, dysmetabolism, lipid dysmetabolism, tau phosphorylation.
Abstract: Over the last century, there has been a gradual but sustained increase in life expectancy
globally. A consequence of increased life expectancy is an associated rise in the prevalence of agerelated
chronic debilitating neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's
disease, Huntington's disease, and multiple sclerosis. These disorders, which are generally
characterised by the loss of motor/sensory neurons and cognitive decline, have continued to confound
researchers who are working tirelessly to define their pathogenetic mechanisms and develop
effective therapies. In the last few years, there has been increasing evidence of the existence of a
relationship between energy metabolism and neurodegeneration, with reports that type 2 diabetes
mellitus increases the risk of AD. Evidence from preclinical and epidemiologic studies has associated
dysmetabolism and dysmetabolic syndromes with the development of neurodegenerative changes.
More recently, diabetes mellitus and energy dysmetabolism have been linked to the aetiopathogenesis
of AD. Moreover, metabolic hormones, including ghrelin, leptin, insulin, and insulin-like
growth factor (IGF)-1, have been reported to play key roles in the regulation of neuronal injury and
loss in neurodegenerative diseases like AD. In this narrative review, we examine the current scientific
evidence regarding the role of dysmetabolism (including diabetes mellitus and metabolic syndrome)
in AD and how it impacts disease progression and the development of novel therapies in
AD.