Obesity and Alzheimer’s Disease: A Bridge between Two Worlds

Abstract

Obesity and Alzheimer’s disease (AD) are two chronic illnesses with far reaching effects. Although both diseases are manifested in physiologically different ways, they share many molecular similarities and affect millions of individuals. Three mechanistic links for these two diseases include: brain derived neurotrophic factor (BDNF), insulin, and chronic inflammation. BDNF has long been associated with neuronal growth and synaptic plasticity but has also been linked to hunger control. Studies independently investigating obesity and AD have shown down-regulation of BDNF in both pathologies. While insulin functions as a critical regulator of blood glucose, insulin resistance and feedback inhibition of insulin production have both been described in the initiation and maintenance of obesity and AD. Lastly, chronic inflammation may lead to and result from AD and obesity. For example, brain inflammation in AD may lead to neurodegeneration, while obesity may also place the body in a state of chronic inflammation. This review seeks to elucidate and bridge the gap between obesity and AD, thus identifying new therapeutic targets common to both diseases.