Kinesin protein interacts with mitochondria in the cerebral cortex. Individuals who inherit Presenilin-1,2 mutations present AD characteristics earlier than the age of 40-45. Families with these mutations exhibit autosomal dominant heredity, with a 50% probability of each generation developing AD. These mutations lead to plaque creation, tangles, cell loss, and dementia. However, genetic mutations are responsible for less than 2% of AD cases. Education is a controversial marker for AD, with individuals with a higher educational level having a lower probability of developing the disease, potentially due to the highly stable network of neuronal synapses in their brain. Metal ions are also significant AD risk factors and negatively impact disease development. When proteins and lipid membranes with toxic effects are affected, reactive oxygen species are produced, and metalloprotein Aβ amyloid peptides are present. Zinc and Copper are released by cortical neurons in the brain and can lead to Aβ accumulation and deposits through interactions with histidine amino acids. Additionally, Fe 2+ and Cu 2+ can react with Aβ to produce H2O2, which contributes to oxidative stress. Zn 2+ and Cu 2+ also enhance Aβ interactions with cell membranes, increasing its toxicity. Moreover, Fe 3+ and Cu 2+ can interact with Aβ to induce oxidative stress, while Aβ oligomerization can create Calcium channels that disrupt calcium homeostasis and further contribute to oxidative stress .