Alzheimer’s disease (AD) is a progressive brain disorder resulting in profound cognitive and memory impairments. Clinical studies indicate that diet and lifestyle are key risk factors for developing neurodegenerative disorders like AD. Metabolic imbalance is also implicated in AD. Recent studies have linked the metabolic hormone, leptin to an increased incidence of AD. Consequently, leptin dysfunction may be a key factor in AD pathogenesis. Thus leptin-based therapies may prove beneficial in treating AD.
Alzheimer’s disease (AD) is a progressive brain disorder that leads to profound cognitive and memory impairments. The prevalence of AD is predicted to rise rapidly in the future, which will pose a huge burden on health care services in the coming years. Evidence is growing that diet and lifestyle are key risk factors for developing AD and clinical studies indicate that metabolic dysfunction is a common trait in AD.
The last few decades has seen a marked increase in the incidence of both type 1 and type 2 diabetes in Western Societies resulting in a significant individual and societal health costs. Understanding those mechanisms that contribute to the development of obesity and disorders of glucose homeostasis are therefore critical areas of research. It is increasingly recognized that the brain contributes to the development of both diabetes and obesity.
A high proportion of the UK population is obese and this is associated with significantly increased risk of type 2 diabetes (T2D), cardiovascular disease and Alzheimer’s disease (AD). AD is also associated with increased risk of T2D and AD patients and AD animal models demonstrate disturbances in glucose metabolism. The aspartic protease BACE1 (beta-site amyloid precursor protein (APP)-cleaving enzyme) is thought to be the primary driver for the neurodegeneration and cognitive dysfunction associated with AD.