Abstract: Sporadic or late-onset Alzheimer’s disease (LOAD) occurs in 1 of 10 people over 65 years of age and comprises 95% of all AD patients. Unlike earlyonset AD, which is caused by defined single gene mutations, the mechanisms and events underlying risk for LOAD are not fully understood and no substantial disease-modifying interventions are currently available. Age is the most prominent risk factor for LOAD, and interacting age-related and LOAD-associated factors contribute to its pathogenesis. Among these factors are changes in bioenergetic cell functions, which metabolize substrates and produce energy stored in adenosine triphosphate. Our findings and the work of others have suggested that disturbances of these bioenergetic functions are both inherent and acquired during the aging process and contribute to LOAD dementia later in life (Ryu et al., 2021a, b; Cohen and Sonntag, 2024). Identifying these abnormal bioenergetic functions may lead to the development of agents or approaches to reduce the risk for LOAD.