Alzheimer's disease (AD) is a neurodegenerative disorder characterized by widespread dementia. Despite extensive research on the pathogenesis of AD over the past fifty years, the underlying mechanisms responsible for AD-related cellular damage and cognitive impairment remain elusive. Currently, multiple studies have confirmed alterations in glucose metabolism patterns within nerve cells in individuals with AD. This metabolic transition plays a crucial role in cell survival and disease progression, even occurring decades before pathological changes and cognitive dysfunction manifest. This article provides an overview of potential mechanisms through which glucose metabolism reprogramming contributes to AD development in various types of nerve cells and brain regions, as well as their interplay, aiming to establish a foundation for further investigation into AD while offering insights and ideas for the development of novel preventive and therapeutic approaches.