Alzheimer’s disease is a progressive neurodegenerative disorder characterized by cognitive decline and widespread cellular dysfunction. While individual pathological features such as mitochondrial impair-ment, lysosomal dysfunction, and altered brain activity have been studied extensively, how these changes relate to one another across disease progression remains less clear. In this work, we integrate cellular-and neural-level data to examine how Alzheimer’s disease evolves across multiple biological scales. Using literature-derived measurements of mitochondrial function, lysosomal properties, organelle interactions, and oxidative stress, together with publicly available electroencephalography (EEG) data, we analyze trends across control, mild cognitive impairment, early Alzheimer’s disease, and late Alzheimer’s disease stages. We observe a progressive decline in mitochondrial ATP production, increased oxidative stress, and disrupted calcium regulation, accompanied by impaired lysosomal acidification and increased lyso-some number. Altered interactions between mitochondria and the endoplasmic reticulum emerge as a key feature of disease progression, linking metabolic stress to cellular dysfunction. Age- and sex-dependent analyses reveal distinct trajectories of mitochondrial dysfunction, with males exhibiting stronger age-related increases in oxidative stress and altered organelle coupling. At the neural level, individuals with Alzheimer’s disease show reduced alpha-band EEG power compared to controls, reflecting disrupted brain network activity. These results provide a unified, multi-scale view of Alzheimer’s disease progression, connecting intracellular pathology to large-scale neural dysfunction. This framework highlights poten-tial early markers of disease and suggests that targeting mitochondrial health, lysosomal function, and organelle communication may be important for future therapeutic strategies.