Alzheimer's disease (AD) research aims to understand its pathogenesis for better diagnostics and treatments. Neurons, reliant on oxidative phosphorylation (OXPHOS) for energy, are severely impacted by mitochondrial dysfunction, closely linked to AD. A key feature of AD is amyloid aggregates, mainly Aβ(1-42) peptides, accumulating within neurons early in the disease. These soluble Aβ oligomers trigger mitochondrial OXPHOS hyperactivity, possibly causing oxidative stress. However, their structure inside mitochondria remains unclear. Using advanced X-ray fluorescence imaging and tomography at ID16A, we aim to map amyloid assembly and explore its impact on mitochondrial function. This, along with label-free 3D nanoscale imaging, could reveal the role of metal ions in neuronal cells, connecting mitochondrial respiration to fibrillation. Insights could aid in diagnosing, delaying, and preventing AD. Preliminary data show promising results.