Figure 1.

In examining the underpinnings and evolution of Alzheimer’s disease (AD), one observes substantial influence from lifestyle and risk-associated genes. A notable precursor event to AD is calcium dyshomeostasis, which plays a crucial role in the synthesis of amyloid beta (Aβ) and phosphorylated Tau (pTau). The formation of toxic oligomers from Aβ can subsequently amalgamate into amyloid plaques. Similarly, pTau oligomers can lead to the establishment of neurofibrillary tangles. Such occurrences are widely regarded as pivotal to the process of neurodegeneration. Concurrently, these and other associated phenomena generate reactive oxygen species (ROS), which not only underscore neuroinflammation, a hallmark of neurodegeneration, but also potentially exacerbate or catalyze further pathological events pertinent to AD.