Alzheimer’s disease (AD) is the most common cause of dementia, with an estimated 6.9 million Americans aged 65 and older currently living with Alzheimer's dementia. Postmortem studies of AD brains have shown that mitochondrial dysfunction plays an important role in the pathogenesis of AD. The electron transport chain (ETC) within mitochondria, comprising five complexes, plays a crucial role in ATP production through oxidative phosphorylation. Recent findings have observed alterations in the function of these complexes in AD brains, leading to impaired energy metabolism and increased oxidative stress. This study aimed to investigate these claims through Western blot analysis of various complexes, using postmortem human brain Broca area 8 tissue from both Alzheimer's disease (AD) and non-disease (ND) models. Our results showed a significant decrease in the protein expression of complexes I, III, IV, and V in the Alzheimer's disease (AD) brain compared to the non-disease (ND) brain. Furthermore, our analysis of sex-based differences revealed no significant variations in complex protein levels between males and females in Broca area 8. Additionally, we will test this on Broca area 22 tissue using our various samples to see if there is a similar trend between AD and ND brains. A comparative study between these two areas will help us understand how AD is affected region by region and see if there is a similar trend in sex-based differences. These findings can contribute to future research on mitochondrial dysfunction in AD, helping to regulate and understand the underlying mechanisms, and identifying new targets for therapeutic development.