**10. The metal ion theory**

Metal dyshomeostasis has a role in the development and pathophysiology of illnesses, including as cancer and neurodegenerative disorders. A number of these compounds are employed in clinical studies. Ionosphere and metal chelators are

*Iron Oxide Nanoparticles: A Mighty Pioneering Diagnostic Tool But Is It Really Safe… DOI: http://dx.doi.org/10.5772/intechopen.112074*

well-known modulators of transition metal homeostasis. Other medications besides the metal-binding ones can also target the homeostasis of transition metals. The balance of redox transition metals, primarily copper (Cu), iron (Fe), and other trace metals, is changing, according to current findings. In AD, their brain levels are observed to be elevated. Other neurological diseases also involve copper, manganese, aluminum, and zinc. The cholinergic theory Acetyl-cholinesterase inhibitors (AChEIs) and the impact of apo-lipo-protein E (APOE) genotype in Alzheimer's disease patients. The AchEI drugs are the cornerstone of AD treatment, and the most significant risk factor for AD is the APOE genotype [36].

### **11. Role of iron in AD**

Iron is the most abundant transition element on Earth and one of the most important minerals in the body. It plays an indispensable role in many physiological and pathological processes of the body. Iron homeostasis is even more crucial in the brain to maintain its normal function. Iron dyshomeostasis within the brain can cause oxidative stress and inflammatory responses, leading to cell damage and finally neurological diseases. Ferroptosis, a programmed cell death process associated with iron dysregulation, has been supposed to be linked to neurological diseases, especially neurodegenerative diseases. Till date, it is impossible to explain AD with a single pathological path. Currently, metal dyshomeostasis in AD has been extensively studied. Studies have found intracellular iron deposition even before the formation of senileplaques and neurofibrillary tangles (NFT), and ferroptosis is proposed to be one of key causes of neuronal loss in AD patients [38].
