Alzheimer's disease is ranked as one of the most important neurodegenerative disorders, causing devastating effects on populations of the aged across the world. Apart from causing cognitive and motor disturbances, this disease in the aged population presents a significant challenge in diagnosis and treatment. Although some advances have been made in the understanding of pathophysiology, the etiology of AD comprises a complex interplay among genetic and environmental factors. Genetic predisposition is not the sole cause of AD; major players are also environmental factors, which most commonly include exposure to neurotoxic agents like heavy metals, pesticides, and metal-based nanoparticles. It leads to abnormal accumulation and aggregation of β-amyloid peptides, along with phosphorylation of tau proteins in AD, which play major roles in defining the disease characteristics. Furthermore, AD pathogenesis encompasses the environmental factors that cause oxidative stress and epigenetic changes. Current research fits within the frame of understanding the role of these environmental factors in epidemiological and experimental data. The development of genome-wide and exposome-wide studies has established insight into gene-environment interaction. This means that the development of this research is paramount in promoting the role of precision medicine in neurodegenerative diseases. This paper integrates the very disparate insights from human epidemiological studies and experimental models into the building of a more comprehensive understanding of AD. It is through the examination of the synergistic effects of biometal dyshomeostasis, GE interactions, and environmental etiologies that approaches to intervention are made more probable in alleviating these devastating illnesses and managing patient outcomes.
Samynathan et al. (2024) studied this question.