“Alzheimer’s disease (AD), the most generic form of dementia, is an irreversible, progressive brain disorder that destroys neuronal cells. AD is the fifth leading cause of death for people aged sixty-five and older [1]. Scientists do not yet fully understand the cause of this disease, which is likely to involve several factors and can affect each person differently. Health care providers often fail to diagnose AD at an early stage; thus, researchers are currently working on a diagnostic framework in which AD onset can be detected based on biological changes in the brain and body even before any symptoms appear [2]. Early AD identification remains challenging as the conventional biomarkers for AD can overlap with the classical aging process.

Recent studies suggest that dysfunctional glucose metabolism is often found in AD brains. An aged-matched comparison between regular and AD brains showed reduced glucose utilization, evidenced in APP (AD model) mice [7]. Thus, glucose utilization could be an early important imaging marker for AD detection. Under normal physiological conditions, brain cells use a relatively higher percentage of glucose for their function and energy source [8]. Alteration in cerebral glucose metabolic rate and glucose consumption are reflected in the synaptic excitability and neuronal activity [9]. In the AD brain, a lesser extent of glucose utilization was detected by positron emission tomography (PET) using 18F-fluorodeoxyglucose (FDG) as a tracer [10]. Specifically, a reduction in glucose consumption at the hippocampal and posterior cingulate of the brain was observed in the early AD stages [11,12,13].

NIH National Library of Medicine (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9455726/)